Title of Invention

A NOVEL SYNERGISTIC POLYHERBAL COMPOSITION,USEFUL FOR TREATING HEPATITIS NON A TO G VIRUS INFECTION(S) AND A PROCESS FOR PREPARING SUCH COMPOSITION

Abstract

A synergistic polyherbal composition useful for treating Hepatitis virus infection caused by Hepatitis non-A to G virus, said composition comprising extract of Rheum emodi Wall. in the range of (25-250) mg , Phyllantus amarus Linn, in the range of (25-250) mg, Eclipta alba Hassk. in the range of (25-250) mg, Andrographis paniculate Nees. in the range of (25-250) mg, and Picrorhiza kurroa Royle ex Benth. in the range of (25-250) mg, and optionally Fumaria officinalis in the range of (5-50) mg, Tinospora cordiofolia Miers. in the range of (5-50) mg, Terminalia chebula Retz. in the range of (5-50) mg, Cichorium intybus Linn, in the range of (10-50) mg , Tephrosea purpurea Linn, in the range of (10-50) mg, and Boerhaavia diffusa Linn, in the range of (10-50)mg; the combined extract thus obtained is mixed with pharmaceutically acceptable neutral agents and converted into suitable pharmaceutically acceptable dosage form.

Full Text

FIELD OF THE INVENTION The present invention relates to a novel herbal composition used for treating acute non A to G viral hepatitis and a process for the preparation of the composition, a method of treating acute non A to G viral hepatitis. The present novel herbal composition is derived essentially from four plants namely: (1) Phyllanlhus amarus; (2) Eclipta alba; (3) Andrographis paniculata; (4) Picrorhiza kurroa. In addition, the present invention provides a novel composition comprising essentially extracts from plants namely: (1) Phyllanlhus amarus; (2) Eclipla alba; (3) Andrographis paniculata; (4) Picrorhiza kurrora and (5) Rheum emodi and a process for preparing such composition. The present novel composition is the safe and effective herbal pharmaceutical preparation for the treatment of acute non A to G viral hepatitis. Further, the said composition also acts as a hepatoprotective agent and improves the liver cell line functions. BACKGROUND OF THE INVENTION The Ayurvedic system of Indian medicine provides many formulations for treating many disorders/diseases in human being. A few of the plants have already been investigated for the beneficial medicinal properties. Phyllanthus amarus: Phyllanlhus amarus is a herbaceous plant which occurs as a winter weed throughout the hotter paits of India. The plant is bitter and astringent in taste and the extract of the roots and the leaves are used as a remedy for jaundice and other liver disorders. and other liver disorders. Eclipta alba: Eclipta alba is a herbaceous plant which grows in moist conditions throughout India. The extracts of Eclipta alba are largely used for the treatment of the liver and the gall bladder. The plant juice and extracts are used hi combination with other aromatics in the treatment of jaundice. Andrographis paniculata: Andrographis paniculata is an annual herb which is grown as a hedge plant throughout the plains of India. The plant is reputed in the Ayurvedic system of Medicine to be useful hi the treatment of sluggish liver and jaundice. Picrorrhiza kurroa: "/*. kurroa is a perennial herb found hi the Alpine Himalayas from Kashmir to Sikkim. Its use hi the Ayurvedic system of medicine is described as being used in the disease states of jaundice, liver disorders and urinary disorders. Fumaria officinalis: This plant, reputed to be useful in disorders of the liver, is found throughout India, from the Indo-gangetic plain to the Nilgiri Hills. Tinospora cordifolia: This species is a succulent climbing shrub and it occurs hi most districts of Southern India. The extracts of T. cordifolia are effective hi promoting the regeneration of liver tissue, and preventing fibrous changes in the incidence of hepatotoxicity. The crude drug itself, and the tincture prepared from it are now official in the Indian pharmacopea. Terminalia chebula: The fruits of this large deciduous tree are used for its purgative, tonic and carminative properties. In combination with Embellica myrobalans and Belleric myroballan, under the Indian name TREPHALA, these fruits are used as adjuncts to other medicines hi the treatment of almost all disease state hi the Ayurvedic system of medicine. Cichorum intybus: This is a rough and glandular perennial herb found throughout northwest India. The root of the plant is known to be useful hi the disease states of the enlargement of the liver and the spleen. Tephrosia purpurea: The root of this branched herbaceous plant has been found to be useful in the treatment of sluggish liver by improving its function and hi enlarged spleen. Rheum emodi: Rheum emodi is a plant grown hi sub Himalayan regions of India and its neighbouring countries. The traditional preparation consists of dried rhizome of the plant and roots which are cut into pieces and dried. Rhubarb root contains a large proportion, of Chrysophanic acid, sometimes called Chrysophan, an allied substance Emodin, a glucoside rhapantiein, a tannin named Rheo tannic acid several resins, an albuminoid principle, mucilage, extractives, tannic and gallic acids, sugar, starch, pectin, lignan, calcium oxalate and various inorganic salts. Hepatitis Viruses A to G Viral infection is by far the most frequent cause of acute hepatitis. Search for the casual virus is however difficult since they can not be cultured on most cell lines in vitro and because regulating factors required for viral expression are found only hi the human hepatocytes which can not be maintained in vitro sufficiently long for experiments. Acute hepatitis is a diffuse necro hiflamniatory diseases of liver as result of primary seven hepatotropic viruses namely Hepatitis A (HAV), Hepatitis B (HBV), Hepatitis C (HCV), Hepatitis E (HEV), Hepatitis F (HFV), and Hepatitis G (HGV). Table 1, describes the clinical features of Hepatitis A to G and Table 2, shows the serological markers useful hi the diagnosis of infection caused by these viruses. Present invention relates to Hepatitis non A to G. However, a brief literature of Hepatitis A to G is summarised below hi order to understand the recently described non A to G hepatitis. Hepatitis A virus (HAV) HAV is 27 nm RNA Picorna virus. The virus has been transmitted to marmosets and cultivated in vitro. It is non cytopathic and grows in a variety of epithelial cell lines. The mode of elimination of HAV from liver is unknown, but cytotoxic T cell probably plays a part. A serum antibody (anti HAV) appears as stool becomes negative for virus, reaches a maximum hi several months, and is detectable for many years. IgG anti HAV gives immunity from further infection with HAV. The appearance of anti HAV IgM denotes a recent infection. HAV hepatitis occurs sporadically or hi epidemic form. HAV spreads by faecal-oral route, and 5-14 year is the group most affected. HAV spread is related to overcrowding, poor hygiene and poor sanitation. With an unproved standard of living the HAV prevalence is decreasing worldwide. Chronic HAV carriers have not been identified. The HAV hepatitis is usually mild, particularly in children, where, it is subclinical or passed off as gastroenteritis. The disease is more serious, and prolonged hi adults. Hepatitis B virus (HBV) The virus of HBV is partly double stranded DNA virus (Dane Particle), and consists of surface and core. The core is found in hepatocyte nucleus, and surface particles are made in the cytoplasm. The double stranded DNA genome of HBV has been cloned and sequenced. The surface antigen (HBsAg) of HBV appears hi blood about six weeks after infection, and usually disappears by three months. Persistence of HBsAg for more than six months implies development of a carrier state. Anti HBs appear late, usually about three months after onset and persists. Anti HBsAg levels are rarely high, and 10-15% of patients with acute HBV never develop antibody. Anti HBs accounts for recovery and immunity. HBeAg correlates with ongoing viral synthesis, and with infectivity. It is transiently present during acute attack. Persistence of more than ten weeks strongly suggests development of chronicity. Anti HBe is a marker of relatively low infectivity, and its appearance strongly suggests that patient will completely recover. HBcAg cannot be detected in blood, but its antibody can be measured in blood. IgM and HBc denotes acute viral hepatitis. Low titres of IgG, HBc, with anti HBs denotes a past exposure to HBV. However, high titres of IgG anti HBc without anti HBs indicates the persistence of viral infection. HBV-DNA is the most sensitive index of viral replication. HBV-DNA detected by PCR is a good marker of the level of viremia and correlates with serum transaminase levels, and parallels with presence of HBsAg in serum. HBV is transmitted parenterally, vertically from carrier mother to newborn or by intimate, often sexual contact. The HBsAg carrier rate varies worldwide from 0.1 to 15%, being highest in some isolated communities e.g. Alaskan Eskimos and Australian Aborigines. The clinical course of acute HBV hepatitis may be both icteric/nonicteric. Acute attack usually lasts for about four months. A fulminant course of HBV in first four weeks of illness is related to an enhanced immune response with more rapid clearance of virus. Also, other hepatotropic viruses (Hepatitis A, delta, C, E) may superimpose on symptomless HBV carriers, and may lead to acute or fulminant clinical course. Hepatitis C virus (HCV) HCV is a single stranded, enveloped RNA virus, 50-60 nm in size. Serological tests HCV (anti HCV) have been developed to detect antibodies to viral antigen. A cDNA polymerase chain reaction (PCR) has been developed to diagnose HCV infection. Hepatitis C virus is transmitted primarily through parenteral routes like blood transfusion, haemodialysis, and intravenous drug use. Acute HCV hepatitis has an incubation period of 5-12 weeks and only about 25% of patients are jaundiced, while the majority may be completely asymptomatic. Serum transaminases are only mildly elevated e.g. about 15 times the upper limit of normal. HCV-RNA can be detected 1-2 weeks of infection. In patient having a complete recovery HCV-RNA may be lost, but antibody (anti HCV) may persist for months. Approximately about half of sufferers from post transfusion HCV hepatitis have raised transaminase levels after about one year of infection. Majority of these patients develop chronic hepatitis which may progress to cirrhosis. Hepatitis Delta virus (HDV) HDV is a small (36 nm) RNA particle coated with HBsAg. It is not able to replicate on its own, but is capable of infection when activated by presence of HBV. HDV is a single stranded circular antisense RNA virus, and is highly infectious and can induce hepatitis hi an HBsAg positive host. HBV and HDV infection may be simultaneous (co-infection) or it may infect a chronic HBsAg carrier (super infection). HDV infection is strongly associated with intravenous drug abuse, and can affect all risk groups for HBV infection. HDV infection is worldwide, but particularly present hi Southern Europe, Middle East, South India, and parts of Africa. The appearance of serum anti delta antibodies is the simplest method of diagnosing acute delta infection. Co-infection is characterised by presence of serum IgM anti data hi presence of high titre of IgM anti HBc. Super infection of a HBV carrier with delta virus is marked by presence of serum IgM anti delta, usually at the same tune as early IgG anti delta and both antibodies persists. These patients are usually IgM anti HBc negative. The clinical picture of acute co-infection of HDV hepatitis is usually self limiting. However, with super infection, acute attack may be severe and even fulminant. Hepatitis E virus (HEV) HEV is responsible for sporadic and major epidemics of acute viral hepatitis in countries like India, Pakistan, Mexico, Central and South East Asia, North America, and in travellers returning from these areas. The disease is enterically transmitted usually by sewage contaminated water. HEV has been serially transmitted to monkeys, but has not been propogated in cell culture. HEV is a 32-34 nm RNA virus, member of Calcivirus group. An ELISA for IgG, and IgM anti HEV has been developed to diagnose the infection. HEV clinically resembles HAV. It usually affects young adults with a self limiting course. The mortality is very high in epidemic, and women in the third trimester of pregnancy. Chronicity does not develop. Hepatitis F virus (HFV) A viral agent responsible for Hepatitis was isolated in India and assigned the letter F (HFV). Its pathogenic nature has not been confirmed. It is postulated to be a double stranded DNA virus, transmissible to rhesus monkey by inoculation with stool extracts from infected patients. Hepatitis G virus (HGV) was first identified hi 1994 from plasma of a patient with aetiologically unexplained chronic hepatitis. HGV belongs to the family of flavivindae and is considered a distinct genus. HGV and GBV-C are closely related isolate of the same virus. HGV infections are detected hi approximately 1-2% of the general population and hi upto 30% of the risk group (e.g. drug addicts). HGV can be transmitted parenterally and sexually and from an HGV infected mother to child. Infection with hepatitis G virus lead to viral persistence hi more than 50% of cases. Recovery from HGV infection can occur spontaneously and hi all stages of infection. The detection of HGV infection is performed by a nuclei acid testing of HGV-RNA. Table 2: Serological Markers currently available and utilised in the laboratory diagnosis of Viral hepatitis A to G (Table Remove) HAV = Hepatitis A virus, HBV = Hepatitis B virus; HCV = Hepatitis C virus; HDV = Hepatitis D virus; HEV = Hepatitis E virus, HGV- Hepatitis G virus- HBs = Hepatitis B surface antigen; Hbe = Hepatitis e antigen; Hbc = Hepatitis B core antigen; Anti HBs = Antibody to Hepatitis B surface antigen, Anti HBc = antibody to hepatitis B core antigen; Anti HCV = antibody to Hepatitis C virus, Anti HDV - Antibody to Hepatitis Delta virus, Anti HEV = Antibody to hepatitis E virus, HGV-RT-PCR = Hepatitis G virus reverse transcriptase polymerase chain reaction, + = positive; - = negative Table 2: Serological Markers currently available and utilised in the laboratory diagnosis of Viral hepatitis A to G (Table Remove) HAV = Hepatitis A virus, HBV = Hepatitis B virus; HCV = Hepatitis C virus; HDV = Hepatitis D virus; HEV = Hepatitis E virus, HGV= Hepatitis G virus- HBs = Hepatitis B surface antigen; Hbe = Hepatitis e antigen; Hbc = Hepatitis B core antigen; Anti HBs - Antibody to Hepatitis B surface antigen, Anti HBc = antibody to hepatitis B core antigen; Anti HCV = antibody to Hepatitis C virus, Anti HDV - Antibody to Hepatitis Delta virus, Anti HEV = Antibody to hepatitis E virus, HGV-RT-PCR = Hepatitis G virus reverse transcnptase polymerase chain reaction, + = positive; - = negative Acute sporadic Non A to G hepatitis Rochling et al. (1997) in USA investigated during a period of four years a large panel of patients presenting with clinical and laboratory features consistent with a diagnosis of acute non A, non B hepatitis for the evidence of hepatitis C or hepatitis E infection, and for evidence of severe or prolong liver disease. Antibody to hepatitis C (anti HCV) was detected in 69% patients and antibody to hepatitis E (HEV) hi 3%. However, neither antibody was detected hi 20% patients. Further, HCV-RNA was also not detected in any of the latter group of patients. As compared with patients of acute HCV hepatitis, those with non ABCDE hepatitis had a lower incidence of parentral risk factors, a prolonged jaundice, and more frequent major clinical complications. It was noted that patients with acute non ABCDE hepatitis were less likely to develop chronic hepatitis than those with acute hepatitis C. It was therefore, observed that patients with acute non ABCDE hepatitis are epidemiologically distinct and a separate group from those with acute hepatitis C and have a significantly more severe illness. There have also been a few previous reports suggesting the existence of a syndrome of clinically severe acute non A, non B hepatitis, not attributable to either HCV or HEV infection. Experimental transmission of non A to G hepatitis agent(s) has also been successfully recently attempted hi Macaca Fascicularis by Tassopoulos and Hatzakis (1996) after their observation that the majority of acute community acquired or sporadic non A, non B hepatitis cases in Greece belong to non C, non E, non G. It was observed that a small fraction (15%) of such patients have an accelerated progression to chronic liver disease (cirrhosis). The underlying cause(s) of acute non ABCDE hepatitis remains unclear. Also the clinical course of non ABCDE hepatitis remains to be clearly defined and the incidence of this clinical syndrome appears to be significantly lower than acute hepatitis A, B, C. Moreover, because the diagnosis can only be made after exclusion of multiple other potential causes of acute hepatitis and more extensive diagnostic evaluation for HAV, HBV, HCV, HDV, HEV and HGV. However, it is postulated that there indeed exists a subset of acute viral(s) hepatitis (hepatitis non A-G) which cannot be attributed to any of the known agents at present. The diagnosis of non A to G hepatitis at present is done by exclusion. Detection of antigen/antibody for Hepatitis A, B, C, D, £ and polymerase chain reaction (PCR) for hepatitis B, C and G are required to establish the diagnosis, along wth abnormal liver function test and supported by the clinical features of acute viral hepatitis. SUMMARY OF THE INVENTION The invention provides a novel herbal composition which is useful hi the treatment of acute non A to G viral(s) hepatitis, the said composition consists essentially of extracts from plants namely Phyllanthus amarus, Eclipta alba, Andrographis paniculata and Picrorhiza kurroa. The invention also provides a novel hepatoprotective composition comprising extracts of Phyllanthus amarus, Eclipta alba, Andrographis paniculata, Picrorhiza kurroa and Rheum emodi, used for the treatment of acute viral hepatitis (Hepatitis non A to G virus(s) infection). The invention further provides a novel hepatoprotective composition optionally includes one or more extracts of plants selected from Fumaria officinalis, Tinospora cordifolia, Terminalia chebula, Cichorium intybus Tephrosea purpurea and Boerhaavia diffusa. The invention relates to a novel herbal composition which is useful hi the treatment of acute viral hepatitis infection due to non A to G virus(s). The composition consists essentially of aqueous extractable components of Phyllanthus amarus, Eclipta alba, Andrographis paniculata, Picrorrhiza kurroa and/or Rheum emodi. The invention also provides a novel hepatoprotective composition comprising extracts of Phyllanthus amarus, Eclipta alba, Andrographis paniculata, Picrorhiza kurroa and Rheum emodi. As used herein the expression water extractable components of above plants includes extracts prepared from whole plants or parts thereof. Further, the invention provides a novel composition useful in the clinical treatment of acute viral hepatitis caused by hepatitis non A to G virus(s) infection which comprise of fractions of Phyllanthus amarus, Eclipta alba, Andrographis paniculata, Picrorhiza kurroa and/or Rheum emodi with optional extracts of plants such as Fumaria qfficinalis, Tinospora cordifolia, Terminalia chebula, Cichorium intybus, Tephrosea purpurea and Boerhaavia diffusa, said fractions contain aqueous extractable extractable components of the above plants or parts thereof. Moreover, the invention also relates to a process for the preparation of a novel herbal composition by mixing in any known manner the extracts of Phyllanthus amarus, Eclipta alba, Andrographis paniculata, Picrorhiza kurroa and/or Rheum emodi. The present novel composition is a synergistic mixture showing suprising properties. In addition, the process includes adding optional ingredients such as extracts of plants namely Fumaria officinalis, Tinospora cordifolia, Terminalia chebula, Cichorium intybus, Tephrosea purpurea and Boerhaavia diffusa. The invention, in an embodiment provides a process for preparation of said herbal composition wherein the following ingredients are mixed when the said composition is in the table or syrup form: Ingredients Qty. of crude Herb/ Qty. of crude Herb Tablet for 2 million tablets Revand chini (Rheum emodi 170 mg 13.6 kg Wall.) Bhringraj (Eclipta alba Hassk.) 300 mg 24 kg Bhumyamalaki 300 mg 24 kg (Phyllanthus amarus Linn.) Sarpunkha (Tephrosea 180 mg 14.4 kg purpurea Linn) Kasni (Cichorium intybus 180 mg 14.4 kg Linn.) Punarnava (Boerhaavia 100 mg 8.0 kg diffusia Linn.) Gilo (Tinospora cordifolia 12 mg 5.76 kg Miers) Haritaki (Terminalia 12 mg 5.76 kg chebula Retz) Kahnegh (Andrographis 60 mg 4.8 kg, Paniculata Nees.) Kutki (Picrorrhiza kurroa 60 mg 4.8 kg Royle ex Benth.) Pitpapra (Fumaria 30 mg 2.4 kg officinalis Linn.) purpurea Linn) Kasni (Cichorium intybus 180 mg 36 kg Linn.) Punarnava (Boerhaavia 100 mg 20 kg diffusia Linn.) Gilo (Tinospora cordifolia 72 mg 14.4 kg Miers) Haritaki (Terminalia 72 mg 14.4kg chebula Retzj Kalmegh (Andrographis 60 mg 12 kg. Paniculata Nees.) Kutki (Picrorrhiza kurroa 60 mg 12 kg Royle ex Benth.) Pitpapra (Fumaria 30 mg 6 kg officinalis Linn.) In another embodiment, the invention provides a process wherein the formulation which is hepatoprotective in nature, is produced by mixing the extracts, preferably aqueous extracts of the following ingredients: Common Name Botanical Name Range of extract in mg per dose Bhymyamalaki Phyllanthus amarus Linn 25-250 Bhringraj Eclipta alba Hassk. 25-250 Kalmegh Andrographis paniculate Nees. 25-250 Kutki Picrorhiza kurroa Royle ex Benth 25-250 Revand Chini Rheum emodi Wall 25-250 The invention also provides a process for the preparation of said novel herbal composition wherein the extract of said herbs is converted into any suitable forms such a powder, concentrates, granules or tablets. In yet another embodiment, the invention provides a process for the preparation of the said herbal composition wherein the composition comprises optional ingredients which are extracts, preferably aqueous extracts, obtained from the following plants: Common Name Botanical Name Range of extract in mg per dose Pitpara Fumaria Officinalis Linn 5-50 Gilo Tinospora cordifolia Miers 5-50 Haritaki Terminalia chebula Retz 5-50 Kasni Cichorium intybus Linn 10-50 Sarpaunkha Tephrosea purpurea Linn 10-50 Punarnava Boerhaavia diffusa 10-50 hi still another embodiment, the invention also provides a process wherein the tablet form of the composition is obtained by mixing the following ingredients: Ingredients Qty. of crude Herb/ Qty. of crude Herb Tablet for 2 million tablets Revand chini (Rheum emodi 170 mg 34 kg Wall.) Bhringraj (Eclipta alba Hassk.) 300 mg 60 kg Bhumyamalaki 300 mg 60 kg (Phyllanthus amarus Linn.) Sarpunkha (Tephrosea 180 mg 36 kg DETAILED DESCRIPTION OF THE INVENTION The invention describes (1) a novel herbal composition and a process for the preparation of aqueous extract of plants, its usefulness in (2) treatment of acute viral hepatitis caused by Hepatitis non A to G virus(s) infection. The following description is given merely to illustrate the invention and this should not be construde to limit the scope of the invention. Example 1: Describes the pharmaceutical preparation of plant extract Pharmaceutical preparation of plant extracts The plant extracts which are mixed together to obtain the present novel composition can be obtained by any known manner. All batches of plants used in the preparation the present novel composition were botanically authenticated. The solvent used in the extraction of the plants may be any suitable solvent such as ethanol, methanol, chloroform and water. Preferably, the plants extract can be obtained by any known manner. Most preferably, the whole plants and parts thereof were powdered and extracted with water. The extract was evaporated under reduced pressure below 50°C leaving a residue. For human administration, the residue is mixed with pharmaceutically acceptable neutral excepients and converted into suitable oral dosage form. Alternatively, the method of preparing the novel compositions comprising blending and extracting hi any known ratio of all the plants or plant materials together by any known manner. The hepatoprotective herbs used for the formulation of the present composition contains the extracts, preferably aqueous extracts of the following: Commom Name Botanical Name Range of Extract in mg per dose Bhumyamalaki Phyllanthus amarus 25-250 Bringraj Eclipta alba 25-250 Kalmegh Andrographis paniculata 25-250 Kutki Picrorhiza kurroa 25-250 What is unexpected hi the present invention is that earlier, the above four plant extracts were combined hi the range of 10 to 20 mg individually, the hepatoprotective property of this combination is identified only when the amounts of these ingredients are enhanced to the range of 25 to 250 mg per dose. In other words, the applicants for the first time noticed the hitherto unknown hepatoprotective property of the composition comprising extracts of plants namely Phyllanthus amarus, Eclipta alba, Andrographis paniculata and picrorhiza kurroa when the amounts of these plant extracts are enhanced to the range of 25 to 250 mg per dose. The present invention provides a hepatoprotective hi the liver disease resulting from acute hepatitis non A to G virus(s) infection composition comprising the following plant extracts: Common Name Botanical Name Range of Extract in mg per dose Bhumyamalaki Phyllanthus amarus 25-250 Bringraj Eclipta alba 25-250 Kalmegh Andrographis paniculata 25-250 Kutki Picrorhiza kurroa 25-250 Rheum emodi Rheum emodi Wall 25-250 The above novel compositions also comprising optional ingredients such as extracts, preferably aqueous extracts of the following plants: Common Name Botanical Name Range of Extract in mg per dose Pitpapra Fumaria offlcinalis 5-50 Gilo Tinospora cordifolia 5-50 Haritaki Terminalia chebula 5-50 Kasni Cichoriumiinlybus 10-50 Sarphunka Tephrosea purpurrea 10-50 Punaraava Boerhaavia diffusa 10-50 The present composition is a synergistic composition exhibiting surprising properties such as enhanced hepatoprotective activity in the liver disease caused by Hepatitis non A-G virus(s) infection. The present invention is illustrated with reference to the following examples and such examples should not be construed at any extent to limit the scope of the invention. The most preferred method of preparing the polyherbal composition in tablet form is given below: COMPOSITION Ingredients Qty. of crude Herb/Tablet Qty. of crude Herb for 20 lac tablets Bhringraj (Eclipta alba) Bhumyamalaki (Phyllanthus amarus) Sarpaunkha (Tephrosea purpured) Kasni (Cichorium intybus) Revand Chini (Rheum, emodf) Punaraava (Boerhaavia diffusd) Glio (Tinospora cordifolid) Haritaki (Terminalia chebuld) Kalmegh (Andrographis paniculatd) Kutki (Picrorrhiza kurrod) Pitpapra (Fumaria officinalis) 300 mg 60kg 300 mg 60kg 180mg 36kg 180mg 36kg 170 mg 34kg 100 mg 20kg 72 mg 14.4 kg 72 mg 14.4 kg 60 mg 12kg 60 mg 12kg 30 mg 6kg Total 304.8 kg 1. EXTRACTION The above mentioned herbs were weighed accurately and reduced to moderately coarse powder. The herbs (304.8 kg) were extracted in a steam jacketed boiling pan using 8-9 tunes purified water for 3.0 hours and filtered. The marc was again subjected to extraction as earlier using 6-7 times purified water for three more hours and filtered and both the filtrates were combined together. 2.CONCENTRATION, DRYING AND PULVERISATION OF HERBAL EXTRACT The combined filtrate was concentrated and dried by spray drying method where no excipient is used. Sometimes it is dried by tray drying method also where the combined filtrate is concentrated to a semisolid consistency and was poured on to a thin bed of Starch-Microcrystalline cellulose powder (each 10% of herbal extract) over trays of electric tray drier and dried at 70-80°C. The dried extract was pulverised through micro-pulveriser and sieved through No. 40 sieve. 3. GRANULATION Powdered herbal extract was mixed with inert diluents like Microcrystalline cellulose. Calcium carbonate and granulated using starch-gelatin paste. 4. DRYING AND SIZING OF GRANULES The granules were dried in electric tray drier at 60°C and the entire quantity of granules were passed through No. 16 sieve. 5. COMPRESSION The granules were mixed with lubricants like Starch, Talc and Magnesium stearate and compressed on Rotary Tablet compression machine using circular deep concave punches. Example 2: describes the clinical efficacy of the present composition (with Rheum emodi) in the treatment of acute viral hepatitis caused by Hepatitis non A to G virus(es) infection. MATERIAL AND METHOD Six (6) patients (4 males, 2 females) of a mean age of 20.5 years (range 18 to 45 years) presenting within one week of the onset of clinical symptoms suggestive of classical acute viral hepatitis (AVH) were included in the study. The diagnosis of AVH was established by the clinical symptoms (acute onset of jaundice, gastrointestinal symptoms e.g. abdominal pain, anorexia, vomiting along with tender hepatomegaly). The diagnosis was supplemented by abnormal liver function tests e.g. estimation of Serum Bilirubin, ALT (SGPT), AST (SGOT) and Alkaline phosphatase. The diagnosis of non A to G hepatitis was done by exclusion. Detection of antigen/antibody for Hepatitis A, B, C, D, E by enzyme immune assay (ELISA) and polymerase chain reaction (PCR) for hepatitis B, C and G were done at the time of clinical presentation and subsequent intervals during therapy. In the 6 patients of all the serological markers of hepatitis A, B, C, D, E and G were absent at the time of presentation and subsequent intervals. Further, the other possible causes which might have led to a similar clinical presentation e.g. surgical jaundice, drug induced cholestasis, herpes and cytomegalo virus infection were also excluded in all the 6 patients. A prior consent of all the patients were obtained and they were explained about the treatment protocol. The preparation of polyhedral pharmaceutical preparation in the tablet form for clinical use in the above 6 patients has been described in example 1. Each patient was given 2 tablets of polyhedral pharmaceutical preparation, two tunes a day for a period of 8 weeks. The clinical assessment and the liver function tests was done at two weekly interval, also if required at weekly interval upto 8 week (in patient No. 1). A follow up after stopping therapy was done after 4 weeks. RESULTS All the 6 patients fulfilled the serological criteria for diagnosis of non A to G hepatitis. In all the six acute non A to G virus hepatitis patients a clinical as well as biochemical recovery was noted from second week onward. A complete clinical recovery occurred in all the patients by eight weeks of therapy. No side effect of the therapy was observed in any of the six patients. Table 3 - shows the mean values of liver function tests of non A to G hepatitis at the time of diagnosis and at subsequent period of polyherbal pharmaceutical composition therapy. Table 4 summarises the effects of the polyherbal pharmaceutical composition therapy in patients of non A to G hepatitis. Table 5 to 10 show the details of liver function tests and the hepatitis viruses (A to G) status at the time of presentation (prior to start of therapy) and at subsequent interval of the polyherbal pharmaceutical composition therapy and follow up. Table 3: Summary of Liver function tests (mean values) from patients of acute non A to G virus at initial presentation and after receiving eight weeks Polyherbal pharmaceutical composition therapy (Table Remove) Values 0) show normal ranges Table 4: Demonstrates the effects on physical sign and symptoms of the patients of acute non A to G virus hepatitis receiving polyherbal pharmaceutical composition therapy (6 patients) (Table Remove) Table 5: Patient No. 1: Details of Investigations (Table Remove) Table 6: Patient No. 2: Details of investigations (Table Remove) Table 7: Patient No. 3 : Details of Investigations Table 8: Patient No. 4 : Details of Investigations (Table Remove) The above example suggests that the polyherbal pharmaceutical composition is helpful hi bringing a therapeutic response in patients of acute non A to G hepatitis. We Claim: 1. A synergistic polyherbal composition useful for treating Hepatitis virus infection caused by Hepatitis non-A to G virus, said composition comprising extract of Rheum emodi Wall, in the range of (25-250) mg , Phyllantus amarus Linn, in the range of (25-250) mg, Eclipta alba Hassk. in the range of (25-250) mg, Andrographis paniculate Nees. in the range of (25-250) mg, and Picrorhiza kurroa Royle ex Benth. in the range of (25-250) mg, and optionally Fumaria officinalis in the range of (5-50) mg, Tinospora cordiofolia Miers. in the range of (5-50) mg, Terminalia chebula Retz. in the range of (5-50) mg, Cichorium intybus Linn, in the range of (10-50) mg , Tephrosea purpurea Linn, in the range of (10-50) mg, and Boerhaavia diffusa Linn, in the range of (10-50)mg; the combined extract thus obtained is mixed with pharmaceutically acceptable neutral agents and converted into suitable pharmaceutically acceptable dosage form. 2. A composition as claimed in claim 1, wherein the composition comprises: Ingredients Qty. Revand chini {Rheum emodi Wall) 170 mg Bhringraj {Eclipta alba Hassk 300 mg Bhumyamalaki {Phyllanthus amarus Linn.) 300 mg Sarpanunkha {Tephrosea purpurea Linn.) 180 mg Kasni {Cichorium intybus Linn.) 180 mg Punarnava {Boerhaavia diffusa Linn.) 100 mg Gilo {Tinospora cordifolia Miers) 72 mg Haritaki {Terminalia chebula Retz.) 72 mg Kalmegh {Andrographispeniculate Nees.) 60 mg Kutki {Picrorrhiza kurroa Royle ex Benth. i) 60 mg Pitpapra {Fumaria officinalis Linn.) 30 mg 3. A composition as claimed in claim 1, wherein the composition is a powder, tablet, syrup or granules. 4. A process for preparing a composition as claimed in claim 1, comprising the steps of: a) preparing an extract of Rheum emodi Wall., Phyllanthus amarus Linn., Eclipta alba Hassk., Andrographis paniculate Nees., and Picrorhiza kurroa Royle ex Benth; b) preparing an extract of Fumaria offcinalis, Tinospora cordifolia Miers., Terminalia chebul Retz., Cichorium intybus Linn., Tephrosea purpurea Linn. and Boerhaavia diffusa Linn; c) mixing the extracts of step (a) and step (b); d) concentration, drying of the combined extract obtained in step (c) to obtain a residue and e) mixing of the residue obtained in step (d) with pharmaceutically neutral excepients to get a suitable herbal composition. 5. A process as claimed in claim 4, wherein the extract is a solvent extract. 6. A process as claimed in claim 4, wherein the solvent for extraction is selected from ethanol, methanol, chloroform hexane, ethyl acetate, methyl chloride, carbon tetrachloride, toluene, acetone , water and mixtures thereof. 7. A process as claimed in claim 4, wherein plants or components thereof are extracted in steam jacketed boiling pan first using 8-9 times purified water for 3 hours and again extracted in 6-7 times purified water for more than three hours. 8. A process as claimed in claim 7, wherein filterate obtained after each extraction are combined together. 9. A process as claimed in claim 7, wherein combined filterate is concentrated and optionally dried by spray drying method. 10. A process as claimed in claim 7, wherein the combined filterate is concentrated to semi solid consistency. 11. A process as claimed in claim 7, wherein the combined filterate is dried by pouring it on a thin bed of starch microcrystalline cellulose powder (each of 10% of herbal extract) over trays of electric drier and dried at 70-80°C. 12. A process as claimed in claim 11, wherein the dried extract is pulverized through micro-pulveriser and sieved through .No. 40 sieve. 13. A pharmaceutical composition and process for preparing the same substantially as herein described with reference to the foregoing examples.

Documents:

2141-del-1997-abstract-(12-09-2008).pdf

2141-del-1997-abstract-(15-09-2008).pdf

2141-del-1997-abstract.pdf

2141-del-1997-claims-(12-09-2008).pdf

2141-del-1997-claims-(15-09-2008).pdf

2141-del-1997-claims.pdf

2141-del-1997-correspondence-others-(12-09-2008).pdf

2141-del-1997-correspondence-others-(15-09-2008).pdf

2141-del-1997-correspondence-others.pdf

2141-del-1997-description (complete)-(12-09-2008).pdf

2141-del-1997-description (complete).pdf

2141-del-1997-form-1-(12-09-2008).pdf

2141-del-1997-form-1-(15-09-2008).pdf

2141-del-1997-form-1.pdf

2141-del-1997-form-13-(15-09-2008).pdf

2141-del-1997-form-18.pdf

2141-del-1997-form-2-(12-09-2008).pdf

2141-del-1997-form-2-(15-09-2008).pdf

2141-del-1997-form-2.pdf

2141-del-1997-form-26.pdf

2141-del-1997-form-4.pdf

2141-del-1997-form-5.pdf

2141-del-1997-form-6.pdf

2141-del-1997-gpa-(12-09-2008).pdf