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目的:探讨内质网分子伴侣GRP78在拟老化大鼠耳蜗中的变化,研究老年性聋的发病机制。方法:Wistar大鼠24只,随机分为对照组与模型组,每组12只。对照组每日生理盐水1ml皮下注射,模型组10%D-半乳糖颈部皮下注射(800mg·kg-1.d-1),时间均为8周。用Morris水迷宫检测2组动物空间学习记忆能力;比色法测定内耳组织膜迷路中超氧化物岐化酶及丙二醛的水平;ABR检测听力学改变,免疫组织化学、RT-PCR及Westernblot检测内质网分子伴侣GRP78的表达。结果:模型组动物有空间记忆障碍伴随超氧化物岐化酶活性降低,丙二醛升高,与对照组相比差异有统计学意义(P<0.01);模型组听力学改变与对照组相比差异无统计学意义(P>0.05);模型组动物的内耳组织GRP78含量在分子及蛋白表达水平均明显升高,与对照组相比差异有统计学意义(P<0.01)。结论:在D-半乳糖制备亚急性衰老动物模型的过程中,内耳组织氧化-抗氧化平衡被破坏;内质网分子伴侣GRP78在拟老化大鼠耳蜗组织中有明显变化,推测其参与了内耳损伤的过程。
Objective: To investigate the changes of the endoplasmic reticulum molecular chaperone GRP78 in the cochlea of aged rats and the pathogenesis of senile deafness. Methods: Twenty-four Wistar rats were randomly divided into control group and model group, with 12 rats in each group. The control group was subcutaneously injected with 1 ml of normal saline every day, and the model group was subcutaneously injected with 800 mg · kg-1.d-1 10% D-galactose for 8 weeks. Morris water maze test was used to detect the spatial learning and memory abilities in both groups. The levels of superoxide dismutase and malondialdehyde were determined by colorimetry. The changes of ABR test were analyzed by audiometry, immunohistochemistry, RT-PCR and Western blot Endoplasmic Reticulum Molecular Chaperone GRP78 Expression. Results: Compared with the control group, there was a significant difference in spatial memory impairment with the decrease of superoxide dismutase (SOD) activity and malondialdehyde (P <0.01) (P> 0.05). The contents of GRP78 in the inner ear tissue of the model group were significantly higher than those in the control group (P <0.01). CONCLUSION: During the process of preparing sub-acute aging animal model by D-galactose, the balance of oxidation-oxidation in the inner ear tissue is destroyed. The endoplasmic reticulum chaperone GRP78 has a significant change in the cochlear tissue of aged rats, suggesting that it participates in the inner ear Damage process.