Effect of Rutin on Liver Function and Morphology in Type 1 Diabetes Mice Induced by Streptozotocin

Objective To investigate the effect of Rutin on the function and morphology of liver in type 1 diabetes mice induced by streptozotocin (STZ). Methods Type 1 diabetic mice model was established with the treatment of STZ by a 5 d intraperitoneal administration to male Kunming mice. Normal group had 12 mice without treatment of STZ, the mice with DM after STZ treated were randomly divided into DM group, low-dose（50 mg/kg） Rutin group and high-dose （100 mg/kg） Rutin group, each group had 12 mice. The mice in normal and DM group were given sodium carboxymethyl cellulose (10 mg/kg). Each mice was given above drugs by intragastric administration for 8 weeks. Postprandial random blood glucose was measured at 4 weeks and 8 weeks and the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), total protein (TP) and albumin (ALB) in serum were detected by automatic biochemical analyzer after 8 weeks. The morphology of liver was observed by HE and Masson staining. The ultrastructure of liver tissue was observed by electron microscope. Results After a continuous small-dose injection of STZ, the success rate of diabetes model mice were up to 98%. The blood glucose of the model group was significantly increased (P<0.01), and the levels of ALT, AST and LDH in serum were significantly higher, and TP and ALB were lower than those in normal group (P<0.05, P<0.01). Compared to the DM group, the levels of blood glucose were lower (P<0.05) at 4 weeks and 8 weeks, the contents of ALT, AST and LDH were significantly decreased, and TP and ALB were improved in both Rutin dose group. High-dose group performed more obvious (P<0.05, P<0.01). Morphological observation showed the tissue morphology of Rutin treatment group were improved obviously, and the effect was more significant in high-dose Rutin group. Conclusion Rutin may improve the liver function and reduce the damage of liver tissue in STZ-induced type 1 diabetic mice.