Aqueous extract of Terminalia arjuna prevents carbon tetrachloride induced hepatic and renal disorders.
BACKGROUND
Carbon tetrachloride (CCl4) is a well-known hepatotoxin and exposure to this chemical is known to induce oxidative stress and causes liver injury by the formation of free radicals. Acute and chronic renal damage are also very common pathophysiologic disturbances caused by CCl4. The present study has been conducted to evaluate the protective role of the aqueous extract of the bark of Termnalia arjuna (TA), an important Indian medicinal plant widely used in the preparation of ayurvedic formulations, on CCl4 induced oxidative stress and resultant dysfunction in the livers and kidneys of mice.


METHODS
Animals were pretreated with the aqueous extract of TA (50 mg/kg body weight) for one week and then challenged with CCl4 (1 ml/kg body weight) in liquid paraffin (1:1, v/v) for 2 days. Serum marker enzymes, namely, glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) were estimated in the sera of all study groups. Antioxidant status in both the liver and kidney tissues were estimated by determining the activities of the antioxidative enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST); as well as by determining the levels of thiobarbutaric acid reactive substances (TBARS) and reduced glutathione (GSH). In addition, free radical scavenging activity of the extract was determined from its DPPH radical quenching ability.


RESULTS
Results showed that CCl4 caused a marked rise in serum levels of GPT and ALP. TBARS level was also increased significantly whereas GSH, SOD, CAT and GST levels were decreased in the liver and kidney tissue homogenates of CCl4 treated mice. Aqueous extract of TA successfully prevented the alterations of these effects in the experimental animals. Data also showed that the extract possessed strong free radical scavenging activity comparable to that of vitamin C.


CONCLUSIONS
Our study demonstrated that the aqueous extract of the bark of TA could protect the liver and kidney tissues against CCl4-induced oxidative stress probably by increasing antioxidative defense activities.
Manna
Prasenjit
P
Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata-700009, India. prasenjitmanna2005@yahoo.co.in
Sinha
Mahua
M
Sil
Parames C
PC
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D056486:Chemical and Drug Induced Liver Injury; D015500:Chloramphenicol O-Acetyltransferase / Q000097:blood; D004305:Dose-Response Relationship, Drug; D005466:Fluorocarbons; D005982:Glutathione Transferase / Q000097:blood; D007674:Kidney Diseases / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects; D008107:Liver Diseases / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008517:Phytotherapy; D024301:Plant Bark; D010936:Plant Extracts / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000097:blood; D029766:Terminalia
D000975:Antioxidants; D005466:Fluorocarbons; D010936:Plant Extracts; C035066:carbon tetrafluoride; D013482:Superoxide Dismutase; D015500:Chloramphenicol O-Acetyltransferase; D005982:Glutathione Transferase