Proceedings of The Physiological Society

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCB197

Poster Communications

Hepatoprotective role of ashwagandha (withania somnifera) root extract against gentamicin induced liver damage in rats

N. Sultana1

1. Physiology, Sir Salimullah Medical College, Dhaka, Dhaka, Bangladesh.

Liver damage can be occurred due to prolong use of some drugs, exposure to some chemicals or infectious agents1. But liver protective drugs are not available. Many hepatoprotective herbal medicines are often used in the treatment of liver damage. Ashwagandha belongs to the family of solanaceae, is the traditional ayurvedic medicine2, has free radical scavenging activity3 and can be used for the prevention of liver damage4. So, the study was undertaken to observe the hepatoprotective role of ashwagandha root extract against gentamicin induced liver damage in rats. This study was conducted from January to December' 2011 in the Department of Physiology, Sir Salimullah Medical College (SSMC), Mitford, Dhaka, Bangladesh. Total 35 apparently healthy Wistar albino male rats, weighing between 150 to 200 grams, age from 90 to 120 days were used. The animals were purchased from animal house of Bangladesh Council of Scientific and Industrial Research (BCSIR), Dhaka. Ethical permission was taken from the Institutional Ethics Committee (IEC) of SSMC, Mitford, Dhaka and also from the Bangladesh Society of Physiologists (BSP). Prior conducting the study, the animals were acclimatized for 14 days at 23±2degree centigrade room temperature under 12 hour dark- light cycle. During this period, they had free access to food and water ad libitum. After 14 days of acclimatization, body weights were measured, again final body weights of rats before anaesthetized on 23rd day were taken. The rats were divided into control (Group A) and experimental (Group B) groups. Control group was again subdivided into baseline control, (Group A1, consisted of 10 rats) and gentamicin treated control group (Group A2, consisted of 10 rats). Again, experimental group (gentamicin treated group after ashwagandha treatment) consisted of 15 rats. All groups of animals received basal diet for 22 consecutive days. In addition to this, gentamicin treated control group also received gentamicin subcutaneously (100mg/kg body weight/day) for the last eight days. Again, experimental group received ashwagandha root extract (500mg/kg body weight/day, orally) for 22 consecutive days and gentamicin subcutaneously (100mg/kg body weight /day) for last eight days. Then all animals were anaesthetized with the help of chloroform and sacrificed on 23rd day. Their blood samples were collected and liver was removed and was washed in ice cold saline. Then it was wiped in tissue paper, weighed by electric balance analyzer. Blood was centrifuged at the rate of 4000 rpm for 5 minutes and supernatant serum was collected. Out of 35 serum samples, four were hemolyzed. So, 31 samples were estimated. Liver function was assessed by estimating serum levels of aspartate amino transferase (AST), alanine amino transferase (ALT) and bilirubin. However, histological findings of liver tissue were observed under microscope to assess their changes. Values were expressed as mean+SD. Statistical analysis were done by one way ANOVA and Bonferroni test as applicable. Mean serum levels of AST and ALT were significantly higher in gentamicin treated control (90.89+4.53 and 99.11+ 5.26 IU/L respectively, p<0.001) and gentamicin treated group after ashwagandha treatment (50.62+2.14 and 54.69+2.93 IU/L respectively, p<0.05) in comparison to those of baseline control group (47.33+3.74 and 50.11+2.47 IU/L respectively). Again, these levels of gentamicin treated group after ashwagandha treatment (50.62+2.14 and 54.69+2.93 IU/L respectively) were significantly (p<0.001) lower than those of gentamicin treated control group. Serum level of bilirubin was significantly higher in gentamicin treated control group (2.40+1.03 mg/dl, p<0.001) and gentamicin treated group after ashwagandha treatment (1.45+0.49 mg/dl, p<0.01) in comparison to that of baseline control (0.64+0.12 mg/dl ). Again, this level of gentamicin treated group after ashwagandha treatment was significantly (p<0.01) lower than that of gentamicin treated control group. Histological examination of liver revealed abnormal findings in 100% of rats in gentamicin treated rats. Again, 84.62% of rats in gentamicin treated group after ashwagandha treatment showed almost normal structure in liver. This data suggests that higher doses of gentamicin produce hepatocellular damage, which can be prevented by taking ashwagandha, due to its antioxidant property5. Some active components of aswagandha have anti-inflammatory property6 thus may be responsible for this hapetoprotectine role 7.

Where applicable, experiments conform with Society ethical requirements