五味子乙素对链脲佐菌素诱导的糖尿病大鼠视网膜病变的保护作用及机制研究

目的:探究五味子乙素(SB)对链脲佐菌素(STZ)诱导的糖尿病视网膜病变(DR)的作用及作用机制。方法:腹腔注射STZ复制大鼠DR模型,并连续给予SB 9个月,TUNEL检测细胞凋亡,试剂盒检测氧化应激标记分子的含量,ELISA法检测炎症因子的表达,Western blot检测血管新生因子和Cdc42/p38通路蛋白的表达。结果:STZ可明显升高大鼠血糖浓度,表明造模成功; SB可明显减弱STZ对凋亡小体形成的促进作用; SB还能显著促进DR大鼠抗氧化分子SOD的表达,降低氧化产物MDA和LDH的含量;同时,SB可明显缓解STZ对炎症因子(IL-6、TNF-α和IL-1β)分泌的促进作用;此外,SB还能明显减弱STZ对促血管新生因子VEGF和通路蛋白Cdc42和p-p38表达的促进作用。结论:SB可通过Cdc42/p38通路缓解STZ诱导的大鼠DR。

Study on protective effect and mechanism of schisandrin B on streptozotocin induced-diabetic reinopathy

Objective:To evaluate the protective effect and underlying mechanism of schisandrin B(SB)on streptozotocin(STZ)induced-diabetic reinopathy(DR)in rats.Methods:Following STZ injection,rats received gavage of SB for 9 months subsequently.TUNEL assay was performed for apoptosis.The levels of SOD,MDA and LDH were determined by kits.To calculate the levels of inflammatory cytokines,ELISA assay was carried out.And western blot was performed for protein levels.Results:In STZ induced-DR rats,glucose level was makedly increased.SB inhibited STZ-induced apoptosis as demonstrated by increased apoptotic body.SB significantly increased the level of SOD and decreased the levels of MDA and LDH.Meanwhile,SB notably inhibited STZ induced-inflammation by decreasing IL-6,TNF-αand IL-1β.Furthermore,SB partly abolished STZ′s effects on the expressions of VEGF,Cdc42 and p-p38.Conclusion:SB attenuates STZ induced-DR via Cdc42/p38 signaling pathway.