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作 者:黄琛[1] 徐戈[2] 王利兵[2] 欧婷[2] 黄美慧[2]
机构地区:[1]广西中医药大学第一附属医院,南宁市东葛路899号530023 [2]广西医科大学第一附属医院,530021
出 处:《广西中医药》2014年第6期62-65,共4页Guangxi Journal of Traditional Chinese Medicine
基 金:广西自然科学基金项目(编号:2010GXNSFB013074)
摘 要:目的:探讨茶多酚对缺氧诱导的大鼠肺动脉高压及右心室肥厚的干预作用。方法:24只SD大鼠随机均分为正常对照组、缺氧组和茶多酚组。缺氧前茶多酚组大鼠每日予茶多酚[200 mg/(kg·d)]灌胃,正常对照组和缺氧组大鼠给予等体积生理盐水灌胃,随后茶多酚组和缺氧组大鼠置于常压低氧舱内间断缺氧4周(8 h/d,6 d/w)。4周后比较各组的平均肺动脉压(m PAP)、右心室肥厚指数(RVHI)及肺小动脉管壁厚度,比较肺动脉平滑肌细胞(PASMCs)凋亡情况。结果:缺氧组大鼠的m PAP、RVHI及肺小动脉管壁厚度均比正常对照组显著升高(均P<0.01),且PASMCs凋亡明显减少(P<0.01);茶多酚组m PAP及RVHI与缺氧组相比均明显降低(P<0.05或P<0.01),肺小动脉管壁增厚程度减轻,而PASMCs凋亡明显增加(P<0.05)。结论:茶多酚能降低肺动脉高压大鼠的肺动脉压,促进肺动脉平滑肌细胞凋亡,改善右心室肥厚,具有抗肺动脉高压的作用。Objective:To investigate the intervention of Tea polyphenols on Hypoxia-induced pulmonary hyper- tension in rat pulmonary artery pressure and right ventricular hypertrophy. Methods: 24 SD rats were randomly di- vided into three groups : Normal control group(C), Hypoxia group(H) and TP group. In the pre-hypoxia period, the TP group were given tea polyphenols at a dose of 200 mg/(kg· d) via intragastric administration each day. The C and the H group were given equal volume of normal saline by the same route of administration. Then the TP and H group were kept in hypobaric oxygen chamber atmospheric with intermittent hypoxia for 4 weeks (8 h/d, 6 d/w). 4 weeks later, mPAP, RVHI, wall thickness of small pulmonary artery, as well as apoptosis of PASMCs were compared. Results: Compared with C group,mPAP, RVHI and wall thickness of small pulmonary artery were significantly in- creased in H group (all P 〈0.01), decreased in smooth muscle cell apoptosis (P〈0.01). Compared with H group, mPAP,RVHI,were significantly decreased (P〈0.05 or P〈0.01). Compared with H group, the degree of pulmonary arterial wall thickening mitigated, the apoptosis of PASMCs was increased (P〈0.05). Conclusion: Tea polyphenols can reduce pulmonary artery pressure of pulmonary hypertension in rats, and promote apoptosis of pulmonary artery smooth muscle cells and improve fight ventricular hypertrophy. It has the function of anti- pulmonary artery hyper- tension.
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