摘要
目的:检测锌离子诱导的HSP72在大鼠视网膜的表达及HSP72对视网膜缺血再灌注损伤所致细胞病理性凋亡的抑制作用。方法:生理盐水前房加压灌注制作视网膜缺血再灌注(RIR)损伤模型,以腹腔注射硫酸锌诱导HSP72表达作为实验组,以腹腔注射HSP表达抑制剂———槲皮素作为实验对照组,以不作任何处理的大鼠为正常对照组。于不同时间段对视网膜HSP72免疫组化染色,Tunel染色、计数凋亡细胞,比较各组差异。结果:实验组在注射硫酸锌后10 h即见视网膜节细胞层有HSP72阳性表达,16 h达高峰,注射后7 d仍呈弱阳性表达,HSP72主要在神经节细胞(RGC)胞浆表达;正常对照组及实验对照组均呈阴性表达。Tunel染色显示,RIR后12 h即有病理性细胞凋亡现象,24 h明显增多,实验组凋亡细胞计数少于对照组且有统计学意义(P<0.05)。结论:(1)腹腔注射锌离子可诱导大鼠视网膜HSP72表达,注射槲皮素可抑制此作用,HSP72主要在RGC胞浆表达;(2)RIR能导致视网膜病理性细胞凋亡,HSP72具有对抗凋亡的作用。
Objective： To examine the expression of HSP72 induced by zinc in rat retina and its inhibition to apoptosis induced by retina ischemic-reperfusion（RIR） injury. Methods： Retina ischemic-reperfusion was induced in rat by acute elevated intraocular pressure through normal saline intracameral perfusion. The HSP72 was induced by zinc sulfate intraperitoneal injection, and the rats in control group were injected zinc sulfate and HSP expression inhibitor-Quercetin. The expression of HSP72 was observed by immuno-histochemistry method. Apoptosis was examined by TUNEL. The number of apoptosis ceils was counted and compared in the two groups. Results： The positive staining of HSP72 in rat retinas of group Zn was observed at the 10th hour after being injected zinc sulfate, and reached the peak at the 16th hour; until the 7th day,weak positive staining could still be observed. HSP72 expressed mostly in cytoplasm of retinal ganglion cell（RGC）. In normal control group and group Q ＋ Zn, the staining of HSP72 was negative. The TUNEL staining showed there was apoptosis at the 12th hour post RIR and most obvious at the 24th hour in both groups. The number of apoptosis cells in group Zn ＋ IR was significant less than in group Q ＋ Zn ＋ IR（ P 〈 0.05）. Conclusions： （ 1 ） Zinc injected intraperitoneally can induce the expression of HSP72 in rat retina, which can be inhibited by quercetin. HSP72 expresses mostly in RGC cytoplasm; （2）RIR can induce neurocyte apoptosis and HSP72 can inhibit the apoptosis.
出处
《山东大学耳鼻喉眼学报》
CAS
2006年第2期167-172,共6页
Journal of Otolaryngology and Ophthalmology of Shandong University
基金
山东省科技厅基金资助项目(2005GG4402055)
