黄芩苷对肺动脉高压大鼠模型的治疗作用及可能的机制 |
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引用本文: | 髙 钊,曹 波,张 力,王韬渊,杨 超,张华,陈 虹. 黄芩苷对肺动脉高压大鼠模型的治疗作用及可能的机制[J]. 心脏杂志, 2013, 25(4): 389-392 |
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作者姓名: | 髙 钊 曹 波 张 力 王韬渊 杨 超 张华 陈 虹 |
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作者单位: | (1.桂林医学院研究生院,广西 桂林 541004;2.武警陕西省总队医院心脏中心,陕西 西安 710054;3.武警后勤学院生药与药剂教研室,天津 300162) |
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摘 要: | 目的:观察黄芩苷对野百合碱诱导的大鼠肺动脉高压模型的治疗作用和肺动脉平滑肌细胞凋亡的影响。方法:将48只大鼠随机分为正常对照组、模型组、辛伐他汀阳性对照组(辛伐他汀组)、3个黄芩苷剂量组(20 mg/kg、40 mg/kg、80 mg/kg,简称低、中、高黄岑苷组),每组8只。通过皮下注射野百合碱诱导建立大鼠肺动脉高压模型,辛伐他汀组给予2 mg/kg灌胃,药物治疗组分别给予黄芩苷20、40、80 mg/kg灌胃。观察黄芩苷对肺动脉压、右室肥大指数的影响。将肺组织切片HE染色后,观察肺动脉的形态学变化。用免疫组化染色法检测肺血管平滑肌细胞中Bcl-2、Bax表达的变化。结果:与模型组比较,高、中黄芩苷可显著降低野百合碱所致大鼠的平均肺动脉压(P<0.01),高黄芩苷可降低其右室肥大指数(P<005);高、中黄岑苷可显著降低模型大鼠肺动脉中膜厚度比(P<0.01)和中膜面积比(P<0.01);高、中黄芩苷可增加Bax的表达率(P<0.01),降低Bcl-2的表达率(P<0.01)。结论:一定剂量的黄芩苷可有效降低野百合碱诱导的模型大鼠的肺动脉压,逆转肺动脉重构。黄芩苷可能是通过抑制肺动脉中膜平滑肌细胞增殖、促进其凋亡而发挥作用的。
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关 键 词: | 黄芩苷 肺动脉高压 野百合碱 大鼠 |
收稿时间: | 2013-01-24 |
Effect and mechanism of baicalin in rats with pulmonary hypertension |
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Abstract: | AIM:To observe the effect of baicalin on rats with pulmonary hypertension induced by monocrotaline (MCT) and on pulmonary artery smooth muscle cell apoptosis. METHODS: Forty eight rats were randomly divided into control group, model group, positive drug group (simvastatin group), and baicalin groups according to three dosages (20 mg/kg, 40 mg/kg, 80 mg/kg, i.e., low, medium, high baicalin group), eight per group. Rats with pulmonary hypertension were induced by MCT, simvastatin group was given simvastatin 2 mg/kg by gavage, and baicalin groups were given baicalin (20, 40, 80 mg/kg) by gavage. The effect of baicalin on pulmonary artery pressure and the index of right ventricular hypertrophy were observed. Pulmonary artery morphology was examined by HE staining and Bcl 2 and Bax changes of pulmonary vascular smooth muscle cells were detected by immunohistochemistry. RESULTS: Compared with those in the model group, high and medium baicalin reduced MCT induced pulmonary arterial pressure (P<001), high baicalin reduced indexes of right ventricular hypertrophy (P<005), high and medium baicalin reduced the media tunica thickness and area percentage of pulmonary artery wall (P<001), and high and medium baicalin increased the positive staining rate of Bax and reduced the positive staining rate of Bcl 2 (P<001) in a concentration dependent manner. CONCLUSION: Baicalin inhibits MCT induced pulmonary hypertension and reverses reconstruction of pulmonary artery in rats, probably by inhibiting proliferation of pulmonary artery smooth muscle cells and inducing their apoptosis. |
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