首页> 外文期刊>Molecular medicine reports >Tetrahydroxy stilbene glucoside ameliorates H2O2-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
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Tetrahydroxy stilbene glucoside ameliorates H2O2-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses

机译:通过抑制氧化应激和炎症反应,四羟基甾醇葡萄糖苷可在体外改善H2O2诱导的人脑微血管内皮细胞功能障碍

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摘要

Tetrahydroxy stilbene glucoside (TSG) is one of the main active ingredients of Polygonum multiflorum and performs various types of biological activity, particularly anti-inflammatory and anti-oxidative activities. However, the beneficial effect of TSG in H2O2-induced human brain microvascular endothelial cell (HBMEC) dysfunction has not been fully elucidated. In the present study, H2O2-induced oxidative stress and inflammatory responses, and the pharmacological effect of TSG were investigated. The results demonstrated that H2O2 appeared to exert a cytotoxic effect on HBMECs, as the cell viability was significantly inhibited in H2O2-treated HBMECs. Conversely, TSG did not exert a toxic effect on HBMECs, and TSG inhibited H2O2-induced HBMEC cytotoxicity in a dose-dependent manner. Furthermore, the findings indicated that TSG restricted the oxidative stress caused by H2O2 via inhibition of malondialdehyde and reactive oxygen species, and upregulation of superoxide dismutase and glutathione. H2O2-induced injury was associated with enhancing the levels of inflammatory cytokines, tumor necrosis factor-a, interleukin (IL)-6 and IL-1 beta in the cultured HBMECs, which were attenuated by TSG treatment. Furthermore, the findings demonstrated that TSG inhibited necrosis factor-kappa B protein expression levels, which, as an upstream transcription factor, may regulate inflammatory responses. Thus, TSG protected HBMECs from H2O2-induced dysfunction by inhibiting oxidative stress and inflammatory responses.
机译:四羟基芪葡萄糖苷(TSG)是多谷物多叶植物的主要活性成分之一,进行各种类型的生物活性,特别是抗炎症和抗氧化活性。然而,TSG在H2O2诱导的人脑微血管内皮细胞(HBMEC)功能障碍中的有益作用尚未完全阐明。在本研究中,研究了H 2 O 2诱导的氧化应激和炎症反应,并研究了TSG的药理作用。结果表明,H2O2似乎对HBMEC进行细胞毒性作用,因为在H 2 O 2处理的HBMEC中显着抑制细胞活力。相反,TSG对HBMECs没有发挥毒性作用,并且TSG以剂量依赖性方式抑制H2O2诱导的HBMEC细胞毒性。此外,研究结果表明,TSG通过抑制丙二醛和反应性氧物质的抑制来限制由H 2 O 2引起的氧化应激,以及超氧化物歧化酶和谷胱甘肽的上调。 H2O2诱导的损伤与增强培养的HBMECs中的炎症细胞因子,肿瘤坏死因子-A,白细胞介素(IL)-6和IL-1β的水平有关,其通过TSG处理衰减。此外,研究结果表明,TSG抑制坏死因子-Kappa B蛋白表达水平,其作为上游转录因子,可以调节炎症反应。因此,TSG通过抑制氧化应激和炎症反应来保护来自H 2 O 2诱导的功能障碍的HBMEC。

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