Studies on the molecular and protective mechanisms of carbon monoxide on the ischemia, intoxication and infection.

已知一氧化碳（CO）保护心肌和血管细胞免受由于缺血-再灌注或炎症引起的损伤。我们发现，C^<2+>依赖性蛋白酶钙蛋白酶通过α-胞衬蛋白水解促进心肌细胞来源的H9 c2细胞因缺氧而坏死性细胞死亡。在此，我们发现缺血诱导坏死性细胞死亡，这可以被CO、细胞外Ca^<2+>剥夺或L-型Ca^<2+>通道阻滞剂抑制。全细胞膜片钳实验支持CO抑制L型Ca^<2+>通道介导的Ca^<2+内流和H9 c2细胞缺血性死亡。

Carbon monoxide (CO) is known to protect myocardial and vascular cells against injuries due to ischemia-reperfusion or inflammation. We showed that a C^<2+>-dependent protease calpain promotes necrotic cell death of cardiomyocyte-derived H9c2 cells due to hypoxia through α-fodrin proteolysis. Here, we show that ischemia induces necrotic cell death, which is inhibited by either CO, extracellular Ca^<2+> deprivation or L-type Ca^<2+> channel blockers. A whole cell patch clamp experiments supports that CO inhibits L-type Ca^<2+> channel mediated influx of Ca^<2+> and the ischemic death of H9c2 cells.