内质网应激在老年大鼠耳蜗细胞凋亡中的作用

目的探讨内质网应激在老年大鼠耳蜗细胞凋亡中的作用,从而进一步探索老年性聋的发病机制。方法Wistar大鼠24只,其中12只为对照组(3～4月龄),12只为自然衰老组(22～24月龄);比色法测定内耳组织中超氧化物歧化酶(superoxide dismutase,SOD),丙二醛(malondialchehyche,MDA)水平;ABR检测听力学改变;免疫组化及western blot检测GRP78/BiP和Caspase-12蛋白的表达。结果老年大鼠听力下降;内耳组织SOD活性降低,MDA升高,与对照组相比差异有统计学意义(P<0.05);耳蜗切片中及western blot结果可见GRP78的表达与对照组相比差异无统计学意义(P<0.05);caspase-12的表达明显高于对照组,差异有统计学意义(P<0.05)。结论内质网凋亡途径是老年大鼠老年性聋的发生机制之一。

Endoplasmic reticulum stress-related apoptosis in the cochlea of aged rats

OBJECTIVE To explore the involve- ment of endoplasmic reticulum stress-related apoptosis in the cochlea of aged rats.METHODS Colorimetry was used to measure the level of superoxide dismutase (SOD)and malondialdehyde(MDA)extracted from inner ear tissue.Hearing threshold was detected with auditory brainstem response(ABR).In addition,expression of GRP78/BiP and Caspase-12 were detected by immunohistochemistry and Western blot.Comparison was conducted between the aged group and the control group.RESULTS The levels of SOD and MDA in aged group were significant different compared with that in control group(P<0.05).The expression of Caspase-12 was statistically increased in the aged group(P<0.05). In contrast,GRP78/BiP did not show obvious change. CONCLUSION Presbycusis is due to apoptosis occurr- ing in the inner ear and endoplasmic reticulum stress- related apoptosis route was thought to be involved.