Abstract
Objective - Diabetic hepatotoxicity involves complex events which include kupffer cell activation, formation of reactive oxygen species, cytokines release (TNF-α, IL-1β), and finally leads to hepatocyte death. “β- Aescin showed anti-inflammatory, anti-oxidant, gastroprotective and anti-oedema properties. The present study investigated the protective effect of β- Aescin in streptozotocin induced diabetic hepatotoxicity.
 Method - Female mice were divided into six groups, the first group served as the control, the second to sixth group received single i.p. dose of 90 mg/kg of STZ, the second group served as the untreated diabetic group, the third, fourth and fifth group received β- aescin intra-peritoneally at the dose of 0.9 mg/kg, 1.8 mg/kg and 3.6 mg/kg body weight respectively. The last sixth group was treated with 10 mg/kg glibenclamide i.p. for 14 days. A significant decrease in the blood glucose level was showed in β-aescin group as compared to the control group.
 Result - A significant increase of blood glucose level was observed in high and mid dose of β- aescin (3.6 mg/kg and 1.8 mg/kg respectively), standard drug (glibenclamide 10 mg/kg) groups as compared to control group. ROS generation was evaluated by using DCF-DA estimation method for the acute toxicity in liver tissue. Streptozotocin group showed more ROS generation in comparison to β- aescin group (3.6 mg/kg). Serum biochemical markers showed a significant decrease in β- aescin treated diabetic mice compared to untreated diabetic mice. Histopathological evaluation showed severe changes in untreated diabetic liver tissue marked by large number of inflammatory cells such as lymphocytes along with hepatic sinusoidal inflammation and hepatocyte necrosis whereas treated diabetic mice with β- aescin showed reduction in hepatotoxicity marked by regeneration changes of hepatocytes and mildly hepatocyte degeneration.
 Conclusion - In the study, β- aescin showed beneficial effects on the efficient properties of the liver and microscopic improvements in diabetic hepatotoxicity.
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