Background: Asparagus racemosus is a climber shrub used in Indian medicine for centuries. It has been used as galactogogue and nerve tonic in folk medicine. The recent research on A. racemosus has revealed its disease fighting properties such as anti-bacterial, immunomodulatory, cardio protective, anti-stress, etc. Phytochemicals present in the plants are associated with their therapeutic capabilities. Hence, phytochemical screening of a therapeutic plant is essential. Materials and Methods: A preliminary qualitative screening of phytoconstituents present in the ethanol and aqueous extract of the plant was done. high-performance thin layer chromatography (HPTLC) was used to create a phytochemical fingerprint of the plant extract. Further, a series of antioxidant assays, i.e., 2,2-diphenyl-1picrylhydrazyl (DDPH) radical, Nitric oxide (NO) radical, Superoxide (SO) radical and 2,2'-azinobis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) radical scavenging assays were done. Results: The phytochemical screening and the HPTLC fingerprint showed the presence of phenolic compounds, flavonoids, glycosides, triterpenoids, saponins etc. They also showed free radical scavenging property and hence can be used as potential primary antioxidant. Conclusion: A preliminary screening created a phytochemical profile of A. racemosus extracts. These phytoconstituents may be linked to the various known therapeutic applications of the plant. This may aid in further extensive studies for identifying and isolating compounds with potential therapeutic value in A. racemosus.

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This study was done to show the changes in the liver following diclofenac treatment and to study the hepatoprotective effects of Vitamin E and A in diclofenac treated rats. Rats were divided into four groups of six rats each. Group-1: Control rats (n= 6), Group-2: Rats (n= 6) treated with diclofenac at dose of 50 mg/kg IM for 7 days, Group-3: Rats (n= 6) treated with Vitamin A at dose of 400 IU/kg orally followed by diclofenac at 50 mg/kg IM 2 h later for 7 days, and Group 4: Rats (n= 6) treated with Vitamin E at dose of 200 IU/kg orally followed by diclofenac at 50 mg/kg IM 2 h later for 7 days. Later it was analysed with standard biomarkers, and it was histologically interpreted. The results showed that there was an rapid increase in the levels of liver function test in diclofenac treated group, which was significantly decreased after pre-treatment with vitamin E than vitamin A. The liver acinus showed centriacinar necrosis of hepatocytes after 7 days of diclofenac treatment, which was prevented by administration of Vitamin E and A. Drug-induced liver injury possesses a major clinical problem and has become a leading cause of acute liver failure and transplantation. Overstressed liver compromises its detoxification role which may expose it to a variety of diseases and disorders. Diclofenac sodium is a phenylacetic acid derivative, a widely used nonsteroidal anti-inflammatory drug (NSAID) for the treatment of inflammatory conditions such as osteoarthritis, rheumatoid arthritis, polymyositis, dermatomyositis, dental pain and spondyloarthritis. Although the exact mechanism by which diclofenac injuries in liver is not understood, some studies explain the toxicity by affecting cytochrome P 450 leading to the production of active metabolites. Hepatoprotective effects of Vitamin E were better compared to Vitamin A following treatment with NSAIDS. Hence, it may be necessary to administer Vitamin E in patients treated with diclofenac.

Drug induced liver injury possesses a major clinical problem and has become leading cause of acute liver failure and transplantation. Overstressed liver compromises its detoxification role which may expose it to a variety of diseases and disorders. The present study was to determine whether pre- administration of various doses of vitamin E would have protective effect against diclofenac induced hepatotoxicity in wistar male rats. Twenty-four albino male rats weighing 180-200g were divided equally into four groups. In control group rats were administrated with physiological saline 2ml/kg b.wt /intramuscularly. Another group with 50mg/kg b.wt/ intramuscularly/seven days diclofenac was used for inducing toxicity. In experimental groups rats were administrated with different doses of vitamin E along with diclofenac sodium [200 and 400 IU orally and 50mg/kg b.wt/ intramuscularly/seven days]. Showed that there was a rapid increase in the levels of liver function test in diclofenac treated group, which was significantly decreased after pre-treatment with high dose than low dose of vitamin E. The liver acinus showed Centro acinar necrosis of hepatocytes after 7 days of diclofenac treatment, which was prevented by administration of Vitamin E. Drug-induced liver injury possesses a major clinical problem and has become a leading cause of acute liver failure and transplantation. Overstressed liver compromises its detoxification role which may expose it to a variety of diseases and disorders. Diclofenac sodium is a phenylacetic acid derivative, a widely used nonsteroidal anti-inflammatory drug (NSAID) for the treatment of inflammatory conditions such as osteoarthritis, rheumatoid arthritis, polymyositis, dermatomyositis, dental pain, spondyloarthritis, acute migraine, gout attacks and pain management in gall and renal stones. Although the exact mechanism by with diclofenac injuries liver is not understood, some studies explain the toxicity by affecting cytochrome P 450 leading to the production of active metabolites. Administration of different dose of diclofenac sodium induces severe adverse effects in liver and kidney.