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[目的]探讨霍乱毒素(CTx)促进受损视网膜节细胞(RGCs)存活的作用机制。[方法]采用荧光逆行示踪标记术,研究蛋白激酶A(PKA)抑制剂H-89和PI3-K特异抑制剂wortmannin玻璃体内注射对CTx促进成年地鼠受损RGCs存活的影响。[结果]动物存活2周后,对照组存活节细胞数为:(220±45)/mm2,CTx组存活节细胞数为:(413±90)/mm2,CTx+H组存活节细胞数为:(256±61)/mm2,CTx+W组存活节细胞数为:(296±39)/mm2;H-89和wortmannin均可部分抑制CTx对受损RGCs的促存活作用。[结论]CTx可能是通过PKA-CREB和PI3-K-Akt通路实现对受损RGCs的促存活作用。
[Objective] To investigate the mechanism of cholera toxin (CTx) promoting the survival of damaged RGCs. [Methods] Fluorescent retrograde tracer labeling was used to study the effect of intravitreal injection of protein kinase A (PKA) inhibitor H-89 and PI3-K specific inhibitor wortmannin on the survival of injured RGCs in adult hamsters. [Results] After two weeks of survival, the number of viable cells in control group was (220 ± 45) / mm2, the number of viable cells in CTx group was (413 ± 90) / mm2, the number of viable cells in CTx + H group was : (256 ± 61) / mm2, the number of viable cells in CTx + W group was (296 ± 39) / mm2. Both H-89 and wortmannin could partially inhibit the pro-survival effect of CTx on damaged RGCs. [Conclusion] CTx may promote the survival of injured RGCs through PKA-CREB and PI3-K-Akt pathway.