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山茶花皂苷对体外缺氧复氧诱导的内皮细胞损伤的保护作用。

Protective effects of sasanquasaponin on injury of endothelial cells induced by anoxia and reoxygenation in vitro.

作者信息

Huang Qiren, He Ming, Chen Heping, Shao Lijian, Liu Dan, Luo Yongming, Dai Yucheng

机构信息

Jiangxi Provincial Key Laboratory of Molecular Medicine at the Second Affiliated Hospital, Nanchang University, Nanchang, China.

出版信息

Basic Clin Pharmacol Toxicol. 2007 Nov;101(5):301-8. doi: 10.1111/j.1742-7843.2007.00119.x.

Abstract

The protective effects of sasanquasaponin, an effective compound from Chinese traditional herbs, on ischaemia and reperfusion injury in mouse hearts have been suggested through modulation of intracellular Cl(-) homeostasis. The effects of sasanquasaponin on injury of endothelial cells, however, induced by anoxia and reoxygenation remain unknown. Therefore, the present study attempted to observe the effects of sasanquasaponin on anoxia and reoxygenation injury in endothelial cells and investigate its putative mechanisms. Human umbilical vein endothelial cells (HUVECs) were exposed to normoxia or anoxia and reoxygenation in the absence or presence of sasanquasaponin (10.0, 1.0 and 0.1 micromol/l). Lactate dehydrogenase activity was determined in cultured HUVECs supernatant, and malondialdehyde content, superoxide dismutase and glutathione peroxidase activities were measured in HUVECs by a colorimetric method. Neutrophil adhesion to HUVECs was assayed colorimetrically. The levels of intercellular adhesion molecule-1 and tumour necrosis factor-alpha were detected. The activity of nuclear factor kappa B was determined by flow cytometry. The results show that sasanquasaponin decreased the lactate dehydrogenase activity and malondialdehyde contents, and inhibited the neutrophil adhesion to HUVECs; sasanquasaponin, moreover, inhibited nuclear factor kappa B transnuclear activity, lowered tumour necrosis factor-alpha and intercellular adhesion molecule-1 expression levels. On the other hand, sasanquasaponin increased the mitochondrial superoxide dismutase and glutathione peroxidase activities. It is suggested that sasanquasaponin could protect HUVECs against anoxia and reoxygenation injury, and the protective mechanisms appear to be related to anti-lipoperoxidation and anti-adhesion.

摘要

山茶花皂苷是一种来自中国传统草药的有效化合物,通过调节细胞内氯离子稳态,已被证明对小鼠心脏缺血再灌注损伤具有保护作用。然而,山茶花皂苷对缺氧复氧诱导的内皮细胞损伤的影响尚不清楚。因此,本研究试图观察山茶花皂苷对内皮细胞缺氧复氧损伤的影响,并探讨其可能的机制。将人脐静脉内皮细胞(HUVECs)置于常氧或缺氧复氧环境中,同时分别加入或不加入山茶花皂苷(10.0、1.0和0.1 μmol/L)。测定培养的HUVECs上清液中的乳酸脱氢酶活性,采用比色法测定HUVECs中的丙二醛含量、超氧化物歧化酶和谷胱甘肽过氧化物酶活性。采用比色法检测中性粒细胞与HUVECs的黏附情况。检测细胞间黏附分子-1和肿瘤坏死因子-α的水平。通过流式细胞术测定核因子κB的活性。结果表明,山茶花皂苷降低了乳酸脱氢酶活性和丙二醛含量,抑制了中性粒细胞与HUVECs的黏附;此外,山茶花皂苷还抑制了核因子κB的转核活性,降低了肿瘤坏死因子-α和细胞间黏附分子-1的表达水平。另一方面,山茶花皂苷增加了线粒体超氧化物歧化酶和谷胱甘肽过氧化物酶的活性。提示山茶花皂苷可保护HUVECs免受缺氧复氧损伤,其保护机制可能与抗脂质过氧化和抗黏附有关。

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