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血红素加氧酶（ｈｅｍｅｏｘｙｇｅｎａｓｅ，ＨＯ）是血红素分解代谢过程中的限速酶，它能使细胞内的血红素降解成胆绿素和一氧化碳（ｃａｒｂｏｎｍｏｎｏｘｉｄｅ，ＣＯ）。近来资料表明内源性一氧化碳对生理和病理状态下的血管张力有重要的调节作用。目前尚不清楚内源性ＨＯ／ＣＯ系统是否参与平滑肌细胞增殖过程的调节。本实验在体外培养的大鼠主动脉平滑肌细胞模型上，用血色素加氧酶抑制剂卟啉锌９（ｚｉｎｃｐｒｏｔｏｐｏｒｐｈｙｒｉｎＩＸ，ＺｎＰＰ９）及酶底物血色素左旋赖氨酸盐（ｈｅｍｅＬｌｙｓｉｎａｔｅ，ＨＬＬ）作用于内皮素处理的平滑肌细胞，同时观察细胞ＨＯ活性、ＣＯ产生和释放以及丝裂素活化蛋白激酶（ＭＡＰＫ）活性的变化，以探讨细胞内源性ＨＯ／ＣＯ系统对细胞增殖的调节作用。结果发现：内皮素明显刺激细胞的３ＨＴｄＲ参入，其ＭＡＰＫ活性亦明显增加，同时伴有ＨＯ活性上调和ＣＯ产生释放增加；同时给予ＥＴ１和ＺｎＰＰ９时，ＨＯ活性和ＣＯ的生成释放明显减少，此时３ＨＴｄＲ参入和ＭＡＰＫ活性比单独ＥＴ１组分别增加３１８％（Ｐ＜００１）和３４６％（Ｐ＜００１）；而同时加入ＥＴ１和ＨＬＬ时，ＨＯ活性和ＣＯ生成释放明显?
Hemeoxygenase (HO) is a rate-limiting enzyme in heme catabolism, which degrades intracellular heme to biliverdin and carbon monoxide (CO). Recent data indicate that endogenous carbon monoxide has an important regulatory role on vascular tone in both physiological and pathological conditions. It is unclear whether endogenous HO / CO system is involved in the regulation of smooth muscle cell proliferation. This experiment in vitro cultured rat aortic smooth muscle cell model, the use of hemopigment oxygenase inhibitor porphyrin zinc 9 (zincprotoporphyrinIX, ZnPP 9) and enzyme substrate heme L-lysine salt (heme L slyinate, HLL) on endothelin-treated smooth muscle cells, and observe the changes of HO activity, CO production and release, and mitogen-activated protein kinase (MAPK) activity in order to investigate the effects of endogenous HO / Regulatory effect of proliferation. The results showed that: Endothelin significantly stimulated cellular 3H-TdR incorporation, the MAPK activity was also significantly increased, accompanied by increased HO activity and CO release increased at the same time given ET 1 and ZnPP 9, HO activity and CO formation Release significantly reduced at this time 3H TdR accession and MAPK activity than ET alone increased 31 8% (P <0 01) and 34 6% (P <0 01), while adding ET 1 and HLL, HO activity and CO release was significantly?