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作 者:汤浩[1] 崔桂英[1] 石丽娟[1] 高青华[1] 曹宇[1]
机构地区:[1]中国医科大学基础医学院生理学教研室,沈阳110001
出 处:《生理学报》2007年第4期534-538,共5页Acta Physiologica Sinica
基 金:This work was supported by the National Natural Science Foundation of China(No.39470246).
摘 要:本文旨在研究川芎嗪(tetramethylpyrazine,TMP)拮抗链霉素耳毒性作用及其对豚鼠耳蜗外毛细胞K^+通道的影响,探讨TMP拮抗链霉素耳毒性的离子通道机制。60只豚鼠随机分为6组,应用听觉脑干反应(auditory brainstem response,ABR)技术检测豚鼠ABR听阈,观测TMP的抗链霉素耳毒作用;并采用全细胞膜片钳技术观察TMP对耳蜗外毛细胞Ca^(2+)敏感K^+电流的影响。结果显示,TMP明显降低链霉素导致的豚鼠ABR听阈升高,提示TMP具有抗链霉素耳毒性作用;TMP能明显增大豚鼠耳蜗外毛细胞Ca^(2+)敏感K^+电流,并呈浓度依赖关系。结果提示,TMP通过增大K^+通道电导而拈抗链霉素耳毒性作用。In order to elucidate the mechanism underlying the attenuation of streptomycin ototoxicity by tetramethylpyrazine (TMP), the present study investigated the effect of TMP on the outward K^+ current in the outer hair cells of guinea pig cochlea. Sixty guinea pigs were divided into 6 groups randomly. Auditory brainstem response (ABR) was used to observe the change in thresholds and to evaluate ototoxicity induced by streptomycin. Whole-cell patch-clamp technique was used to observe the effect of TMP on outward K^+ current in isolated outer hair cells. The results showed that TMP attenuated the threshold shift caused by streptomycin and increased the amplitudes of Ca^2+-sensitive K^+ current [IK(Ca] in the outer hair cells. The present data suggest that TMP displays anti-ototoxicity induced by streptomycin. The augmented amplitudes of IK(Ca) of the outer hair cells induced by TMP may be one of the mechanisms underlying its ototoxicity-attenuating effect.
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