Liu Hongxia, Sun Hui, Liu Chuanyong
Department of Physiology, Shandong University School of Medicine, Jinan 250012, Shandong, PR China.
Chin J Physiol. 2011 Apr 30;54(2):124-32.
The aim of the present study was to investigate the effect of SP600125 (1,9-pyrazoloanthrone), an inhibitor of JNK, on apoptosis of retinal ganglion cells (RGCs) induced by moderate elevation of intraocular pressure (IOP) in male rats. IOP was elevated by suture-pulley compression on eyeballs. Cell apoptosis, expression of phosphorylated JNK (p-JNK) and cleaved caspase-3 in retina were studied by TUNEL staining and immunohistochemistry. The expression of c-Jun in retina was assayed by Western blot. Following IOP elevation (about 45 mmHg) for 6 h, the number of TUNEL, p-JNK and cleaved caspase-3 positive cells and the amount of c-Jun expression in retina were significantly increased. All these changes were reversed by SP600125 treatment. The immune positive cells for TUNEL, p-JNK and cleaved caspase-3 following IOP elevation were localized at the RGC layer. We conclude that moderate elevation of IOP for 6 h induced apoptosis of RGCs, and SP600125 treatment attenuated this process by suppressing c-Jun expression.
本研究旨在探讨JNK抑制剂SP600125（1,9-吡唑蒽酮）对雄性大鼠眼内压（IOP）适度升高诱导的视网膜神经节细胞（RGCs）凋亡的影响。通过缝线-滑轮压迫眼球升高IOP。采用TUNEL染色和免疫组化研究视网膜细胞凋亡、磷酸化JNK（p-JNK）和裂解的caspase-3的表达。通过蛋白质印迹法检测视网膜中c-Jun的表达。IOP升高（约45 mmHg）6小时后，视网膜中TUNEL、p-JNK和裂解的caspase-3阳性细胞数量以及c-Jun表达量显著增加。SP600125处理可逆转所有这些变化。IOP升高后TUNEL、p-JNK和裂解的caspase-3的免疫阳性细胞定位于RGC层。我们得出结论，IOP适度升高6小时可诱导RGCs凋亡，SP600125处理通过抑制c-Jun表达减轻了这一过程。
