【摘要】 目的 :研究碱性成纤维细胞生长因子 (basicfibroblastgrowthfactor ,bFGF)拮抗大鼠心肌细胞缺氧 /复氧(hypoxia/reoxygenation ,H/R)损伤的机制。 方法 :H/R处理的大鼠心肌细胞的孵育液中 ,对照组不加任何处理因素 ,其它各组分别加bFGF(10 μg·L-1)、bFGF与丝裂素活化蛋白激酶 (mitogen activatedproteinkinase,MAPK)抑制剂PD980 5 9(5 0 μmol·L-1)、蛋白激酶C(proteinkinaseC ,PKC)抑制剂H7(40 μmol·L-1)、一氧化氮合酶 (nitricoxidesynthase ,NOS)抑制剂左旋硝基精氨酸甲酯 (NG nitro L argininemethylester,L NAME ,5 0 μmol·L-1)。孵育完毕 ,测定细胞活力、ATP含量及孵育液中乳酸脱氢酶 (lactatedehydrogenase,LDH)含量。 结果 :H/R组心肌细胞活力较对照组降低 32 % (P <0 .0 1) ,细胞ATP含量减少 5 8% (P <0 .0 1) ,孵育液中LDH活性增加 5 .8倍 (P <0 .0 1) ;bFGF组心肌细胞活力较H/R组增高 17% (P <0 .0 1) ,细胞ATP含量增加 45 % (P <0 .0 1) ,孵育液中LDH活性降低 31% (P <0 .0 1) ,细胞PKC、MAPK活性分别增加 32 % (P <0 .0 1)和 10 % (P <0 .0 5 )。PD980 5 9、H7、PD980 5 9+H7及L NAME各组心肌细胞活力较bFGF组分别降低 13%、17%、2 4%和 2 7% (均P <0 .0 1) ,细胞ATP含量分别减少 2更多还原

【Abstract】 Objective: To investigate the mechanism of antagonist effect of basic fibroblast growth factor(bFGF) on rat myocytes injury induced by hypoxia/reoxygenation (H/R). Methods: bFGF (10 μg·L -1 ) , bFGF and mitogen activated protein kinase(MAPK) inhibitor PD98059 (50 μmol·L -1 ), protein kinase C(PKC) inhibitor H 7 (40 μmol·L -1 ), nitric oxide synthase(NOS) inhibitor N G nitro L arginine methyl ester( L NAME, 50 μmol·L -1 ) were added respectively to the medium of H/R treated rat myocytes. After incubation, myocytes viability, ATP content and lactate dehydrogenase(LDH) activity in the medium were determined. Results: Myocytes viability and ATP content were 32% and 58% lower, respectively, and LDH activity in the medium was 5.8 times higher in H/R group than that in control group. Compared with H/R group, myocytes viability, ATP content, PKC and MAPK activity in bFGF group increased by 17%, 45%, 32% ( P <0.01) and 10% ( P <0.05), respectively, and LDH activity decreased by 31% ( P <0.01). Compared with bFGF group, myocytes viability in PD98059, H 7, PD98059 + H 7 and L NAME groups reduced by 13%, 17%,24% and 27% ( P <0.01), respectively. Myocyte ATP content was lowered by 20%, 28%, 37% and 25% ( P <0.01), respectively, and LDH activity in the medium elevated by 49%, 46%, 55% and 40% ( P <0.01), respectively. Conclusion: The antagonist effect of bFGF on rat myocytes injury induced by H/R was mediated by activation of intracellular PKC, MAPK and NOS/NO system. (J Beijing Med Univ, 2000,32:134 137)更多还原