The effect and mechanism of H2S protecting neurons against ischemia-reperfusion injury
- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF NEUROMEDICINE
- Issue:
- 6
- DOI:
- 10.3760/cma.j.issn.1671-8925.2007.06.002
- Key Word:
- H2S;ERK1/2;P90RSK;细胞信号转导;神经元缺血再灌注
Abstract： 目的 研究H2S对缺血再灌注损伤后神经元存活信号转导通路ERK1/2/P90RSK的影响. 方法 将培养7 d的海马神经元随机分为5组:正常培养组(C组)、缺血再灌注组(I/R组)、缺血再灌注+NaHS组(NaHS组)、缺血再灌注+NaHS+U-0126(ERK抑制剂)组(U组)、缺血再灌注+NaHS+Rapamycin(RS6K抑制剂)组(R组).C组神经元按正常培养方法培养.NaHS组神经元在神经元进行缺血再灌注时加入NaHS使其终浓度为150 μmol/L.U组和R组在加入150 μmol/L NaHS的同时分别加入U-0126 10 μmol/L或Rapamycin 10 nmol/L.各组行细胞存活力、神经元凋亡、cAMP、磷酸化ERK1/2(PERK1/2)和磷酸化P90RSK(PP90RSK)蛋白表达的检测. 结果 NaHS显著增加了cAMP的浓度(与I/R组比较,P＜0.01)、PERK1/2蛋白(与I/R组比较,P＜0.05)和PP90RSK蛋白(与I/R组比较,P＜0.05)表达,同时增加了神经元存活率(与I/R组比较,P＜0.05)、降低了神经元凋亡率(与I/R组比较,P＜0.05);U-0126抑制了PERK1/2蛋白(与NaHS组比较,P＜0.05)和pp90RK蛋白(与NaHS组比较,P＜0.05)表达同时使神经元存活率降低(与NaHS组比较,P＜0.05)、神经元凋亡率升高(与NaHS组比较,P＜0.05);Rapamycin抑制了PP90RSK蛋白(与NaHS组比较,P＜0.05)表达同时使神经元存活率降低(与NaHS组比较,P＜0.05)、神经元凋亡率升高(与NaHS组比较,19＜0.05)而不影响PERK1/2的表达(与NaHS组比较,P＞0.05). 结论 H2S通过cAMP激活了ERK1/2/P90RSK信号通路,在海马神经元缺血再灌注时抑制了神经元的凋亡,保护了神经元.
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