中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2014年
2期
231-234
,共4页
rac1 GTP结合蛋白质/代谢%耳蜗%豚鼠%庆大霉素类/毒性
rac1 GTP結閤蛋白質/代謝%耳蝸%豚鼠%慶大黴素類/毒性
rac1 GTP결합단백질/대사%이와%돈서%경대매소류/독성
rac1 GTP-binding protein/metabolism%Cochlea%Guinea pigs%Gentamicins/toxicity
目的：研究庆大霉素所致耳毒性损伤及应用抗氧化剂水杨酸钠保护时Rac1在豚鼠耳蜗中的表达，探讨Rac1在庆大霉素耳毒性机制中的作用。方法健康雄性白色红目豚鼠30只，按随机数字表法分成3组。对照组：腹腔内注射生理盐水，连续7d；庆大霉素组：腹腔内注射硫酸庆大霉素，连续7d；庆大霉素＋水杨酸钠组：腹腔内注射硫酸庆大霉素和水杨酸钠，连续7 d。7 d后处死大鼠，采用石蜡切片免疫组织化学染色技术检测各组豚鼠耳蜗Rac1蛋白的表达与分布情况；提取耳蜗蛋白，采用Western blot检测各组Rac1蛋白表达水平。结果对照组耳蜗螺旋器和螺旋神经节细胞Rac1呈弱阳性表达，主要表达于细胞浆和细胞膜；庆大霉素组耳蜗Rac1表达增强；庆大霉素＋水杨酸钠组呈阳性表达，其表达程度介于对照组和庆大霉素组之间；各组灰度值比较差异有统计学意义（ P ＜0.05）。对照组耳蜗Rac1蛋白有低强度表达；庆大霉素组耳蜗Rac1蛋白表达最强；庆大霉素＋水杨酸钠组耳蜗Rac1蛋白表达程度介于对照组和庆大霉素组之间；各组间蛋白电泳积分光密度值比较差异有统计学意义（ P ＜0.05）。结论 Rac1在正常豚鼠耳蜗螺旋器和螺旋神经节细胞的胞浆及胞膜弱表达，庆大霉素给药后耳蜗中Rac1表达增强，同时给予抗氧化剂水杨酸钠后可使Rac1表达较庆大霉素组减弱。提示Rac1可能在庆大霉素导致耳蜗损伤过程中起作用。
目的：研究慶大黴素所緻耳毒性損傷及應用抗氧化劑水楊痠鈉保護時Rac1在豚鼠耳蝸中的錶達，探討Rac1在慶大黴素耳毒性機製中的作用。方法健康雄性白色紅目豚鼠30隻，按隨機數字錶法分成3組。對照組：腹腔內註射生理鹽水，連續7d；慶大黴素組：腹腔內註射硫痠慶大黴素，連續7d；慶大黴素＋水楊痠鈉組：腹腔內註射硫痠慶大黴素和水楊痠鈉，連續7 d。7 d後處死大鼠，採用石蠟切片免疫組織化學染色技術檢測各組豚鼠耳蝸Rac1蛋白的錶達與分佈情況；提取耳蝸蛋白，採用Western blot檢測各組Rac1蛋白錶達水平。結果對照組耳蝸螺鏇器和螺鏇神經節細胞Rac1呈弱暘性錶達，主要錶達于細胞漿和細胞膜；慶大黴素組耳蝸Rac1錶達增彊；慶大黴素＋水楊痠鈉組呈暘性錶達，其錶達程度介于對照組和慶大黴素組之間；各組灰度值比較差異有統計學意義（ P ＜0.05）。對照組耳蝸Rac1蛋白有低彊度錶達；慶大黴素組耳蝸Rac1蛋白錶達最彊；慶大黴素＋水楊痠鈉組耳蝸Rac1蛋白錶達程度介于對照組和慶大黴素組之間；各組間蛋白電泳積分光密度值比較差異有統計學意義（ P ＜0.05）。結論 Rac1在正常豚鼠耳蝸螺鏇器和螺鏇神經節細胞的胞漿及胞膜弱錶達，慶大黴素給藥後耳蝸中Rac1錶達增彊，同時給予抗氧化劑水楊痠鈉後可使Rac1錶達較慶大黴素組減弱。提示Rac1可能在慶大黴素導緻耳蝸損傷過程中起作用。
목적：연구경대매소소치이독성손상급응용항양화제수양산납보호시Rac1재돈서이와중적표체，탐토Rac1재경대매소이독성궤제중적작용。방법건강웅성백색홍목돈서30지，안수궤수자표법분성3조。대조조：복강내주사생리염수，련속7d；경대매소조：복강내주사류산경대매소，련속7d；경대매소＋수양산납조：복강내주사류산경대매소화수양산납，련속7 d。7 d후처사대서，채용석사절편면역조직화학염색기술검측각조돈서이와Rac1단백적표체여분포정황；제취이와단백，채용Western blot검측각조Rac1단백표체수평。결과대조조이와라선기화라선신경절세포Rac1정약양성표체，주요표체우세포장화세포막；경대매소조이와Rac1표체증강；경대매소＋수양산납조정양성표체，기표체정도개우대조조화경대매소조지간；각조회도치비교차이유통계학의의（ P ＜0.05）。대조조이와Rac1단백유저강도표체；경대매소조이와Rac1단백표체최강；경대매소＋수양산납조이와Rac1단백표체정도개우대조조화경대매소조지간；각조간단백전영적분광밀도치비교차이유통계학의의（ P ＜0.05）。결론 Rac1재정상돈서이와라선기화라선신경절세포적포장급포막약표체，경대매소급약후이와중Rac1표체증강，동시급여항양화제수양산납후가사Rac1표체교경대매소조감약。제시Rac1가능재경대매소도치이와손상과정중기작용。
Objective To investigate the expression of Rac 1 in the guinea pig cochlea of gentamicin-induced ototoxic damage and prevention with antioxidant sodium salicylate , and to explore the roles of Rac 1 in the ototoxic mechanism of aminoglycoside antibi-otics.Methods Thirty healthy male guinea pigs were involved in this study .All the guinea pigs were randomly divided into 3 groups and received intraperitoneal injections according to their arranged group .Group I (control) was treated with normal saline for 7 days. Group II [Gentamicin (GM)] was treated with gentamicin alone for 7 days.Group III [GM+sodium salicylate(SA)] was treated with gentamicin in combination with sodium salicylate for 7 days.Paraffin-embedded cochlear section with immunohistochemical stai-ning was used for evaluation of Rac 1 expression in the cochlea .The protein was extracted from the cochlea tissues , and Rac1 protein levels in the cochlea were detected by Western blot assay .Results Immunohistochemistry showed a slightly positive reaction for Rac 1 staining found in the cochlea of the control group was mainly shown in the cytoplasm and cytomembrane of ganglion and organ of Corti ;a highly positive expression was shown in GM group;and the extent of Rac 1 expression of GM+SA group was between the control and GM groups.Image analysis showed that the differences in Rac1 expression between each two groups were statistically significant ( P <0.05).Western blot assay showed that expression of Rac 1 protein was highest in GM group and decreased in GM +SA group, while the intensity of Rac1 protein expression in GM +SA group was between the control and GM group .Statistics analysis showed that the expression between each two groups had significant difference ( P <0.05 ) .Conclusions A slightly positive reaction for Rac 1 stai-ning was found in the cochlea of guinea pigs , and mainly observed in the cytoplasm and cytomembrane of spiral ganglion and organ of Corti.With the administration of gentamicin , Rac1 protein expression was upregulated in the cochlea .Simultaneous administration of antioxidant sodium salicylate could significantly decrease the expression of Rac 1 protein.These results indicated that Rac1 might play an important role in the processes of gentamicin-induced oxidative damage of cochlea .
