首页> 外文期刊>Journal of diabetes research. >Protective Effects of Resveratrol on TNF-alpha-Induced Endothelial Cytotoxicity in Baboon Femoral Arterial Endothelial Cells
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Protective Effects of Resveratrol on TNF-alpha-Induced Endothelial Cytotoxicity in Baboon Femoral Arterial Endothelial Cells

机译:白藜芦醇对TNF-α诱导的狒狒股动脉内皮细胞内皮细胞毒性的保护作用

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Endothelial injury induced by inflammatory factors plays a critical role in the pathogenesis of cardiovascular disease. Endothelial cell (EC) apoptosis, proliferation, migration, and cellular adhesion molecule (CAM) expression contribute to the development of atherosclerosis. We investigated the effects of resveratrol (0.1-100 muM) on the proliferation, migration, and CAM expression of primary cultures of baboon arterial endothelial cells (BAECs). In addition, we tested its effects under normal conditions as well as under inflammatory conditions induced by tumour necrosis faclor-a (TNF-a) administered either by cotreatment, pretrealment, or posttreatment. Immunocytochemistry, MTT, wound-healing, and flow cytometry assays were performed. The resveratrol treatment significantly enhanced BAEC proliferation and attenuated TNF-a-induced impairment of proliferation at the optimal doses of 1-50 muM. Resveratrol at a high dose (100 muM.) and TNF-a impaired BAEC migration, while low doses of resveratrol (1-50 muM) attenuated TNF-a-induced impairment of BAEC migration. Moreover, resveratrol inhibited TNF-a-induced ICAM-1 and VCAM-1 expression. Taken together, our results suggest that the resveratrol protects BAECs after inflammatory stimulation as well as ameliorates inflammatory effects at low concentrations. Consequently, resveratrol should be considered as a candidate drug for the prevention and treatment of inflammatory vascular diseases.
机译:炎性因子引起的内皮损伤在心血管疾病的发病机理中起关键作用。内皮细胞(EC)的凋亡,增殖,迁移和细胞粘附分子(CAM)的表达有助于动脉粥样硬化的发展。我们调查了白藜芦醇(0.1-100μM)对狒狒动脉内皮细胞(BAEC)原代培养物的增殖,迁移和CAM表达的影响。另外,我们测试了在正常条件下以及在通过联合治疗,治疗前或治疗后施用的肿瘤坏死因子-a(TNF-a)诱导的炎症条件下的作用。进行了免疫细胞化学,MTT,伤口愈合和流式细胞术测定。在1-50μM的最佳剂量下,白藜芦醇治疗显着增强了BAEC的增殖,并减轻了TNF-α诱导的增殖损害。高剂量白藜芦醇(100μM。)和TNF-a损害了BAEC迁移,而低剂量白藜芦醇(1-50μM)减弱了TNF-a诱导的BAEC迁移损伤。此外,白藜芦醇抑制TNF-α诱导的ICAM-1和VCAM-1表达。两者合计,我们的结果表明,白藜芦醇可在炎症刺激后保护BAEC,并在低浓度时改善炎症作用。因此,白藜芦醇应被视为预防和治疗炎症性血管疾病的候选药物。

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