中文摘要：

目的：探讨内源性硫化氢（H2S）对血管紧张素Ⅱ（AngⅡ）引起的延髓神经元活性氧（ROS）水平升高的作用及其可能机制。方法：首先培养原代延髓神经元；免疫荧光双标法鉴定神经元及内源性H2S生成酶胱硫醚β-合成酶（CBS）存神经元的表达；同时或单独给予AngⅡ（μmol／L）和丁酸钠（NaBu，一种CBS激动剂；100μmol／L、250μmol／L和500μmol／L），二氢乙啶荧光探针法测定ROS水平；采用总超氧化物歧化酶（SOD）活性检测试剂盒观察总SOD的活性；real-timePCR观察CBS mRNA的表达。结果：（1）原代培养的90％以上的细胞为神经元。AngⅡ（1μmol／L）升高延髓神经元ROS水平；（2）AngⅡ抑制神经元总SOD的活性；（3）荧光双标显示CBS在延髓神经元有表达，AngⅡ可降低CBSmRNA的表达；（4）NaBu（250μmol／L和500μmol／L）显著抑制AngⅡ引起的ROS水平的升高，且呈剂量依赖性效应。而NaBu单独对延髓神经元ROS水平作用不明显。结论：AngⅡ引起的延髓神经元ROS水平升高至少部分是通过降低总SOD的活性和CBS mRNA的表达而实现的；而内源性H2S可能通过相反的作用抑制这一过程。

英文摘要：

AIM： To determine the effect of endogenous hydrogen sulfide （ H2 S） on the production of reactive oxygen species （ROS） in medullary neurons induced by angiotensin Ⅱ （Ang Ⅱ）. METHODS： Primary cultured rat me-dullary neurons were used in the study. Identification of medullary neurnns and the co-expression of cystathionine β-syn-thetase （CBS） were detected by double-labeling immunofluorescence. Medullary neurons were treated with Ang II in the presence or absence of sodium butyrate （NaBu, a CBS agonist; 100 μmol/L, 250 μmol/L and 500 μmol/L）. ROS pro-duction was measured by dihydroethidium staining. The activity of total superoxide dismutase （SOD） was detected by ELISA. The mRNA expression of CBS was determined by real-time PCR. RESULTS ： The medullary neurons in the cultured cells were over 90%. Ang Ⅱ （ 1 μmol/L） significantly increased ROS level in the medullary neurons. Ang Ⅱ inhibi-ted the activity of total SOD in the medullary neurons. CBS was expressed in the medullary neurons. Ang Ⅱ decreased the mRNA expression of CBS. NaBu （250 μmol/L and 500 μmol/L） inhibited ROS production induced by Ang Ⅱ with a dosedependent manner, while NaBu alone had no influence on the ROS level in the medullary neurons. CONCLUSION： Ang ii increases the level of ROS in medullary neurons partly by inhibiting the activity of total SOD and the mRNA expression of CBS. Endogenous H2S inhibits the ROS level increased by Ang Ⅱ in the medullary neurons.