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目的研究PC12细胞在低氧状态下,内源性一氧化碳(CO)的生成及其导致细胞凋亡的作用。方法将PC12细胞分为常氧对照组(C组)、低氧组(H组)和低氧加血红素氧合酶(HO)抑制剂卟啉锌-9组(H+ZnPP组)。检测2h时间点PC12细胞血红素氧合酶的表达及内源性CO水平和细胞凋亡率。结果氧应激状态下,HO-1明显表达,HO-2无表达;H组HO水平与C组、H+ZnPP组比较明显升高(P<0.01),H+ZnPP组的HO水平高于C组(P<0.01);内源性CO水平以及细胞凋亡率与C组、H+ZnPP组比较均明显升高(P<0.01)。结论低氧状态下,PC12细胞表面HO-1高表达,HO-2无明显表达,PC12细胞的凋亡率与内源性CO的水平密切相关,提示HO/内源性CO可能导致细胞凋亡的发生。
Objective To investigate the generation of endogenous carbon monoxide (CO) and its role in apoptosis in PC12 cells under hypoxia. Methods PC12 cells were divided into normoxic control group (C group), hypoxia group (H group) and hypoxia plus heme oxygenase (HO) inhibitor porphyrin zinc -9 group (H + ZnPP group). The expression of heme oxygenase, endogenous CO level and apoptosis rate in PC12 cells were detected at 2h. Results The HO-1 expression was not observed in HO-1 cells under oxygen stress. The HO level in H group was significantly higher than that in C and H + ZnPP groups (P <0.01) C group (P <0.01). The levels of endogenous CO and apoptosis were significantly increased compared with C and H + ZnPP groups (P <0.01). Conclusions Under hypoxic condition, HO-1 is highly expressed on the surface of PC12 cells but not on HO-2. The apoptosis rate of PC12 cells is closely related to the level of endogenous CO, suggesting that HO / endogenous CO may lead to apoptosis happened.