[1]蒋诗敏,张珂嘉,周泰,等.丹参酮ⅡA抑制氧化应激减轻人脐静脉内皮细胞损伤[J].徐州医科大学学报,2021,41(04):235-240.[doi:DOI:10.3969/j.issn.2096-3882.2021.04.001]
 JIANG Shimin,ZHANG Kejia,ZHOU Tai,et al.TanshinoneⅡA alleviates human umbilical vein endothelial cell injury by inhibiting oxidative stress[J].Journal of Xuzhou Medical University,2021,41(04):235-240.[doi:DOI:10.3969/j.issn.2096-3882.2021.04.001]
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丹参酮ⅡA抑制氧化应激减轻人脐静脉内皮细胞损伤()
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《徐州医科大学学报》[ISSN:2096-3882/CN:32-1875/R]

卷:
41
期数:
2021年04期
页码:
235-240
栏目:
出版日期:
2021-04-25

文章信息/Info

Title:
TanshinoneⅡA alleviates human umbilical vein endothelial cell injury by inhibiting oxidative stress
作者:
蒋诗敏12张珂嘉12周泰12周瑶1李俐1*
1.徐州医科大学病理生理学教研室,江苏徐州221004;2.徐州医科大学病理学教研室
Author(s):
JIANG Shimin12 ZHANG Kejia12 ZHOU Tai12 ZHOU Yao1 LI Li1*
1. Department of Pathophysiology, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China;2. Department of Pathology, Xuzhou Medical University
关键词:
丹参酮糖尿病氧化应激细胞凋亡
分类号:
R285
DOI:
DOI:10.3969/j.issn.2096-3882.2021.04.001
文献标志码:
A
摘要:
目的 明确丹参酮ⅡA(Tan ⅡA)是否能够减轻人脐静脉内皮细胞(HUVEC)损伤,以及其作用机制是否与调节氧化应激有关。方 法以高糖诱导的损伤HUVEC作为细胞模型,在体外环境下探讨Tan ⅡA的作用。实验中采用CCK-8细胞活性检测明确细胞活性的变化;Western blot实验探讨P38、p-P38、caspase 3、cleaved caspase 3等蛋白表达的变化;活性氧/超氧阴离子(ROS/O-2)荧光探针检测各组细胞ROS、O-2表达的变化。结果 高糖可诱导HUVEC活性下降,ROS、O-2表达明显增加,p-P38、cleaved caspase 3蛋白表达明显上升。而Tan ⅡA可减轻高糖诱导的HUVEC活性的下降,抑制ROS、O-2升高,抑制P38的磷酸化以及caspase 3的活化。结论 高糖可诱导HUVEC凋亡,而Tan ⅡA通过抑制ROS/P38 MAPK信号通路减轻高糖诱导的HUVEC凋亡。
Abstract:
ObjectiveTo determine the effects of tanshinone ⅡA (Tan ⅡA) on the injury of human umbilical vein endothelial cells (HUVECs), and its relationship with oxidative stress regulation. MethodsHUVECs were cultured in high glucose medium to investigate the role of Tan ⅡA in vitro. The cell viability was measured by CCK-8 assay. The levels of P38, p-P38, caspase 3 and cleaved caspase 3 were investigated by Western blot. Reactive oxygen species/superoxide anion (ROS/O-2) fluorescence probe was used to detect the changes of ROS and O-2 in each group. ResultsHigh glucose treatment induced decreased HUVECs viability, enhanced the expression of ROS and O-2, and increased the levels of p-P38 and cleaved caspase 3. Furthermore, exposure to Tan ⅡA resulted in decreases in HUVEC viability induced by high glucose, inhibited the expressions of ROS and O-2, and blocked P38 phosphorylation and the activation of caspase 3. ConclusionsHigh glucose can cause apoptosis in HUVECs, and Tan ⅡA can relieve HUVECs apoptosis induced by high glucose through inhibiting the ROS/P38 MAPK signaling pathway.

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备注/Memo

备注/Memo:
徐州医科大学学报JXuzhouMedUniv2021,41(4)基金项目:国家自然科学基金青年项目(82004107);徐州医科大学优秀人才科研启动基金(D2019016)*通信作者,E-mail:xzmclili@163.com
更新日期/Last Update: 2021-05-12