CAJ | 학술논문

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(800 mg·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Western blot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.
목적: 탐토내질망분자반려GRP78재의노화대서이와중적변화,연구노년성롱적발병궤제.방법:Wistar대서24지,수궤분위대조조여모형조,매조12지.대조조매일생리염수1ml피하주사,모형조10%D-반유당경부피하주사(800 mg·kg~(-1)·d~(-1)),시간균위8주.용Morris수미궁검측2조동물공간학습기억능력;비색법측정내이조직막미로중초양화물기화매급병이철적수평;ABR검측은역학개변,면역조직화학、RT-PCR급Western blot검측내질망분자반려GRP78적표체.결과:모형조동물유공간기억장애반수초양화물기화매활성강저,병이철승고,여대조조상비차이유통계학의의(P<0.01);모형조은역학개변여대조조상비차이무통계학의의(P>0.05);모형조동물적내이조직GRP78함량재분자급단백표체수평균명현승고,여대조조상비차이유통계학의의(P<0.01).결론:재D-반유당제비아급성쇠로동물모형적과정중,내이조직양화-항양화평형피파배;내질망분자반려GRP78재의노화대서이와조직중유명현변화,추측기삼여료내이손상적과정.
Objective:To explore the involvement of endoplasmic reticulum molecular chaperone GRP78 in the impairment of inner ear consistented with the mimetic aging model.Method:Twenty-four Wistar rats were randomly divided into two groups. model group was in duced by daily hypodermic injection of 10% D-galactose (800 mg·kg~(-1)·d~(-1)) for 8 weeks and the control group was given saline accordingly. Spatial learning and memory was measured by Morris-Water-Maze. Colorimetry was used to analyze superoxide dismutase (SOD) and malondialdehyde (MDA) extracted from inner ear tissue. Hearing threshold of rats were detected with Auditory brainstem response (ABR).In addition, expression of GRP78 in the inner ear was detected by immunohistochemistry,RT-PCR and Western blot. The control group was studied parallel.Result:The escape latency in the model group injected with D-galactose was markedly longer than that in the control group.accordingly ,the changes of SOD and MDA were more significant in the model group, the difference between two groups was significant(t-test,P<0.01). the variation of ABR in two groups was observed, There was no statistically difference of the hearing in the model group compared with the control group(P>0.05). The expression of GRP78 was significantly different between two groups ,which is increased in the inner ear tissue of model group(P<0.01).Conclusion:The impairment of inner ear tissue partly dued to the oxidative stress in the model, which was induced by D-galactose.and endoplasmic reticulum molecular chaperone was thought to contribute to the impairment mechanism of inner ear in mimetic aging model.