Hepatoprotective effect of vitamin A and E on diclofenac induced hepatotoxicity in male Wistar albino rats

Abstract

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.

The protective effect of vitamin A on Concor induced structural changes of the liver and kidney in adult rats

“…Mitchell et al [22] noticed that patients with liver injury secondary to the use of β-blockers characteristically develop symptoms of hepatocellular damage and hyperbilirubinemia, and that the laboratory abnormalities will be recovered after stopping using β-blockers. Furthermore, Fisher et al [23] reported that the levels of transaminase enzyme improved rapidly after the gradual withdrawal of both Metoprolol succinate and Carvedilol in two patients with β-blocker-induced liver injury. In conclusion, β-blocker therapy is uncommon to be a cause of severe hepatotoxicity as a side effect, though doctors should be familiar with the aforementioned possible consequences, as these drugs are frequently used and prescribed in patients with advanced liver disease.…”

Date palm pollen and silymarin administration protect splenic structure toxicity in female rat induced by diclofenac sodium

“…In addition to the inhibition of cyclo-oxygenase 2, DS is known to produce toxicity in the biological systems through increased generation of reactive oxygen species resulting from the metabolism of DS via oxidative hydroxylation by cytochrome P4505 [ 9 ]. So, DS excretes the toxicity on the biological system via inducing oxidative stress which resulted in the damage of the biological tissues.…”