It is reported that Ischemia and reperfusion damage (I/R damage) can lead to retinal ganglion cell (RGC) death and neurodegeneration, which in turn can lead to irreversible vision loss. In this study, we sought to understand the neuroprotective effect of resveratrol, the important activator of sirtuin1 (SIRT1), on RGC survival in I/R damage model and the molecular mechanism that mediate this effect. Our results show that resveratrol could reverse axonal swelling, holes, and the chaos of the nucleus in axons of RGCs caused by I/R. At the same time, resveratrol could also reverse the activation of retinal astrocytes and the loss of RGCs caused by I/R. Resveratrol increased the expression of SIRT1 while decreasing the phosphorylation of N-terminal kinase (JNK). SP600125(JNK inhibitor) decreased the phosphorylation of JNK while increasing the expression of SIRT1, indicating that SIRT1 and JNK can interact with each other. Simultaneous administration of resveratrol and sirtinol (SIRT1 inhibitor) neither increased the expression of SIRT1 nor decreased the phosphorylation of JNK, indicating that resveratrol affects the phosphorylation of JNK by SIRT1. In total, our research shows that resveratrol treatment significantly reduces apoptosis and axonal degeneration of RGCs, and this protection is partly mediated through the SIRT1-JNK pathway.

据报道，缺血和再灌注损伤（I / R损伤）可导致视网膜神经节细胞（RGC）死亡和神经变性，进而可导致不可逆的视力丧失。在这项研究中，我们试图了解白藜芦醇（sirtuin1（SIRT1）的重要激活剂）对I / R损伤模型中RGC存活的神经保护作用，以及介导这种作用的分子机制。我们的研究结果表明，白藜芦醇可以逆转由I / R引起的RGC轴突的轴突肿胀，孔洞和核的混乱。同时，白藜芦醇还可以逆转由I / R引起的视网膜星形胶质细胞的活化和RGC的丢失。白藜芦醇增加SIRT1的表达，同时减少N末端激酶（JNK）的磷酸化。SP600125（JNK抑制剂）可降低JNK的磷酸化，同时增加SIRT1的表达，表明SIRT1和JNK可以相互作用。同时给予白藜芦醇和sirtinol（SIRT1抑制剂）既不增加SIRT1的表达也不减少JNK的磷酸化，表明白藜芦醇影响SIRT1的JNK磷酸化。总的来说，我们的研究表明白藜芦醇治疗可显着减少RGC的凋亡和轴突变性，并且这种保护作用部分是通过SIRT1-JNK途径介导的。表明白藜芦醇会通过SIRT1影响JNK的磷酸化。总的来说，我们的研究表明白藜芦醇治疗可显着减少RGC的凋亡和轴突变性，并且这种保护作用部分是通过SIRT1-JNK途径介导的。表明白藜芦醇会通过SIRT1影响JNK的磷酸化。总的来说，我们的研究表明白藜芦醇治疗可显着减少RGC的凋亡和轴突变性，并且这种保护作用部分是通过SIRT1-JNK途径介导的。