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出 处:《中国皮肤性病学杂志》2015年第6期559-561,共3页The Chinese Journal of Dermatovenereology
摘 要:目的探讨肌肽(carnosine)对脂多糖(lipopolysaccharide,LPS)诱导的人皮肤微血管内皮细胞(human dermal microvessel endothelial cells,HDMEC)氧化应激及促炎症反应的影响。方法建立脂多糖(1μg/m L)诱导的人皮肤微血管内皮细胞损伤模型,MTT法检测其细胞活性,荧光法测定细胞内活性氧族物质(ROS),试剂盒检测一氧化氮(NO)、8-羟基脱氧鸟苷(8-OHDG)、3-硝基酪氨酸(3-NT)、白介素(IL)-1β,IL-6、肿瘤坏死因子(TNF-α)含量,超氧化物歧化酶(SOD)及谷胱甘肽过氧化酶(GSH-Px)酶活性。结果肌肽预孵育或与脂多糖处理对人皮肤微血管内皮细胞细胞活力无明显影响,脂多糖增加胞内ROS和胞外上清液NO水平,增加胞内MDA,8-OHDG及3-NT含量,增加促炎症因子IL-1β,IL-6及TNF-α产生,降低SOD和GSH-Px酶活性,而肌肽可以恢复脂多糖所致的上述效应。结论肌肽对脂多糖所致的人皮肤微血管内皮细胞损伤具有保护作用。Objective To investigate the effects of carnosine on lipopolysaccharide (LPS)-induced oxidative stress and inflammation in human dermal microvascular endothelial cells ( HDMEC ). Methods The experimental model of HDMEC injury was induced by LPS (Ixg/mL). HDMEC viability was measured by MTT assay. The levels of intraceUular reactive oxygen species (ROS) were assessed by fluorescence assay. Respective commercial kit Was used to measure the concentrations of NO, 8-OHDG, 3-NT, IL-113, IL-6 and TNF-α, and the activities of SOD and GSH-Px. Results Either carnosine alone or in combination with LPS did not change HDMEC viability. LPS increased the intracellular ROS production, extraceUular NO production, and the concentrations of MDA, 8-OHDG and 3-NT, in addition to the production of the pro-inflammatory cyto- kine (IL-1β, IL-6 and TNF-α). Moreover, LPS decreased SOD and GSH-Px activity. Carnosine overrode LPS-induced changes of oxidative stress and cytokines in HDMEC. Conclusion Carnosine can attenuate LPS-induced damages in HDMEC.
关 键 词:肌肽 脂多糖 人皮肤微血管内皮细胞 氧化应激 促炎症反应
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