H-89和Wortmannin对霍乱毒素促进受损视网膜节细胞存活作用的影响

Effects of H-89 and Wortmannin on the Promoting Effects of CTx on the Survival of Injured Retinal Ganglion Cells

[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 survival promoting mechanism of cholera toxin (CTx) on injured retinal ganglion cells (RGCs). [Methods] Fluorescent retrograde labeling method was used to observe the effects of H-89 or wortmannin on the survival promoting effects of CTx on injured RGCs by intrav-itreal injection. [Results]After two weeks , the mean density of surviving RGCs was (220 ±45) /mm2 in the control group. The density of surviving RGCs was(413 ±90)/mm2 in the group treated with CTx (CTx group). In the group treated with H-89 and CTx (CTx + H group), the density of RGCs was (256 ±61)/mm2 ,and in the group treated with wortmannin and CTx (CTx+W group), the density of RGCs was (296 ±39)/mm2. Both H-89 and wortmannin could partly block the promoting effects of CTx on survival of injured RGCs. [Conclusion]The regeneration promoting effects of CTx on injured RGCs might be realized by PKA-CREB and PI3-K-Akt accesses.