Protective Effects of Reduced Beta 2 Glycoprotein I on Liver Injury in Streptozotocin (STZ)-Diabetic Rats by Activation of AMP-Activated Protein Kinase.

Abstract

BackgroundProtective effects of reduced beta 2 glycoprotein I (Rβ2GPI) against vascular injury of diabetes mellitus have been extensively investigated. However, the effects of Rβ2GPI on liver injury in diabetic animals have not been reported.Material/MethodsA diabetic rat model of was produced by systemic injection of streptozotocin (STZ). Rats were divided into a normal control group, a model group, and an Rβ2GPI treatment group (N=6 in each group). After treatments, blood serum and liver tissue were collected to test the protection of Rβ2GPI. AMP-activated protein kinase (AMPK) was detected by immunohistochemistry and Western blotting.ResultsOur results revealed that Rβ2GPI reduced blood glucose, serum creatinine, and urea nitrogen levels, as well as serum inflammation cytokines, including interleukin (IL)-6, tumor necrosis factor (TNF)-a and C-reactive protein in the diabetic rats. Importantly, Rβ2GPI prevented liver injury in the diabetic rats as confirmed by hematoxylin-eosin (H&E) staining, alanine transaminase, aspartate transaminase, and gamma-glutamyl transferase. Reactive oxygen species (ROS) were promoted by diabetic modeling and were attenuated by Rβ2GPI administration. Moreover, Rβ2GPI significantly reduced liver catalase, malondialdehyde, and superoxide dismutase levels in the diabetic rats. Rβ2GPI reduced liver glycolipid storage in STZ diabetic rats. Both immunohistochemistry and Western blotting demonstrated that Rβ2GPI promoted AMPK phosphorylation in the diabetic rats.ConclusionsOur data proved that Rβ2GPI prevented liver injury in diabetic rats, likely through activating the AMPK signaling pathway.