GLP-1 protected the diabetic retinopathy through induction of autophagy in rats
- SU Jie, YANG Fuyu, LI Meng, CHEN Huiru, JIANG Lisheng, WANG Lixiang
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Objective Research the GLP-1 induced autophagy through regulation of mTOR signaling pathways, whether there is a protective role in diabetic retinopathy rats. Methods Conform to the requirements of the diabetic retinopathy rats model, divided into model group, insulin group and GLP-1 group, each group of 6, ALL the groups were measured to realise the fasting blood glucose level in rats after 0 d,4 w, 8 w and 12 w, after 12 w killing the rats, we removed the retinal tissue for HE staining and test the expression of P53, LC3 by immunohistochemical method. Collected blood serum to detect oxidative stress product ROS and MDA content with serum superoxide dismutase(SOD)method. Detected mTOR protein expression with Western blotting method. Results Compared with model group, insulin group and GLP-1 group can obviously reduce fasting blood glucose, the difference was statistically significant, and is no statistically significant difference in the two groups. HE staining showed the retinal ganglion cells of model group disordered arrangement and the cells reduced or missed, but in insulin group and GLP-1 group, retinal ganglion cells arrangement was neat, no significant decline, close to normal. Immunohistochemical display, The LC3 and P53 protein expression respectively(2.34±0.13,0.46±0.03)in GLP-1 group increased significantly compared with other groups, and the differences were statistically significance(P<0.05). Oxidative stress product ROS and MDA content respectively(74.68±4.08,55.60±1.50)in GLP-1 group reduced, compared with other groups, the differences between groups were statistically significant(P<0.05). Compared with other groups, mTOR protein content(0.43±0.04)in GLP-1 group decreased, and the differences between groups were statistically significant(F=105.447, P<0.05). Conclusion Glp-1 may through activation of autophagy by regulating mTOR signaling pathways, then reducing oxidative stress injury of retina, as to protect the retina.