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目的 观察聚天冬氨酸 (PAA)对庆大霉素 (GM)所致耳蜗组织磷脂沉积的拮抗作用 ,进一步探讨PAA对庆大霉素耳毒性拮抗作用机制。方法 采用高效液相色谱分析法 (HPLC)测定不同给药组、不同给药时间后豚鼠耳蜗组织各类磷脂的含量 ;记录听性脑干诱发应答 (ABR) ,用透射电镜观察耳蜗Corti器毛细胞溶酶体形态改变。结果 给药 5d后耳蜗组织磷酸肌醇 (PI) (19.7μg± 6 .6μg)、一磷酸肌醇 (PIP) (12 1μg± 2 1μg)、给药 10d后PIP(12 6 μg± 8μg)含量较其他 3组明显升高 (P <0 .0 1) ;超微结构Ⅰ组耳蜗Corti′s器外毛细胞表皮板下溶酶体改变给药 10d较给药 5d更明显 ,可见较多溶酶体聚集 ,体积略增大 ;Ⅰ组ABR阈值改变随用药时间延长而升高。结论 PAA对GM干扰耳蜗组织磷脂代谢有抑制作用 ,从而拮抗了GM所致溶酶体磷脂沉积病态及耳蜗毒性的发生。
Objective To investigate the antagonistic effect of polyaspartic acid (PAA) on the phospholipid deposition induced by gentamicin (GM) in cochlear tissues and to explore the mechanism of PAA antagonizing gentamicin ototoxicity. Methods The content of phospholipids in guinea pig cochleas of different administration groups and different administration time were determined by high performance liquid chromatography (HPLC). The auditory brainstem response (ABR) was recorded. The Corti hairs were observed with transmission electron microscope Cell lysosome morphology changes. Results After 5 days of administration, the levels of PI (19.7 μg ± 6. 6 μg), PIP (12 1 μg ± 2 1 μg) and PIP (12 6 μg ± 8 μg) Compared with the other three groups was significantly higher (P <0.01); ultrastructure I group cochlear cochlear outer hair cell epidermal platelet lysosome change administration 10d than 5d after administration more obvious, can be seen more soluble Enzymatic aggregation, the volume slightly increased; Ⅰ ABR threshold changes with drug treatment time increases. Conclusion PAA can inhibit the phospholipid metabolism of cochlear in GM and thus antagonize the pathogenesis of GM-induced lysosomal phospholipid deposition and cochlear toxicity.