Therapeutic effect of Tongluo recipe on hepatic injury in streptozotocin-induced diabetic rats and its possible mechanism
10.3724/SP.J.1008.2010.00499
- Author:
Jie SHEN
1
Author Information
1. Department of Endocrinology
- Publication Type:Journal Article
- Keywords:
Diabetes mellitus;
Hepatic injury;
Oxidative stress;
Tongluo recipe;
Ultrastructure
- From:
Academic Journal of Second Military Medical University
2010;31(5):499-503
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the therapeutic effect of Tongluo recipe(TLR) on hepatic injury in streptozotocininduced diabetic rats and the possible mechanism. Methods: Experimental diabetes was induced by intraperitoneal injection of streptozotocin(60 mg/kg) in male Sprague-Dawley rats. The study included 5 groups: normal control(CN) group, diabetes mellitus control (DM) group, low-dose TLR (TL) group, middle-dose TLR (TM) group and high-dose TLR (TH) group, with 10 rats in each group. Diabetic rats in the latter three groups received 0.5 g/(kg·d), 1.0 g/(kg·d), 2.0 g/(kg·d) TLR, respectively throughout the experiment. The fasting glucose, blood lipid, and serum liver function indices were measured. Twelve weeks after treatment, rats were sacrificed and the liver tissues were collected to examine the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA). The ultrastructure of liver tissues was observed through transmission electron microscope. Results: The serum AST, ALT and AKP levels of diabetic rats were increased 12 weeks after intraperitoneal injection of streptozotocin (P<0.01), and electron microscope observation showed characteristic pathological changes of diabetes. TLR treatment (middle and high dose) obviously decreased serum AST, ALT levels(P<0.05)and ameliorated ultrastructure changes of liver tissues: glycogen granules decreased in cytoplasm, mitochondrial cristae became distinct and electron density decreased, appearance of smooth and rough endoplasmic reticulum became nearly normal, and the interstitial collagenofiber decreased. The SOD and CAT activities were significantly decreased and MDA levels were increased in liver tissues of diabetic rats (P<0.01). Twelve weeks of treatment with TLR obviously improved SOD activity (at all three doses, P<0.01) and decreased the levels of MDA (middle and high dose, P< 0.01). Conclusion: Our data suggest that TLR can improve hepatic injury in streptozotocin-induced diabetic rats, probably through increasing activities of antioxidant and depleting lipid peroxidation production.
