辛伐他汀通过上调Bcl-2表达和下调Bax表达来抑制脓毒症诱导的内皮细胞凋亡。
Simvastatin inhibits apoptosis of endothelial cells induced by sepsis through upregulating the expression of Bcl-2 and downregulating Bax.
作者信息
Fu Hui, Wang Qiao-Sheng, Luo Qiong, Tan Si, Su Hua, Tang Shi-Lin, Zhao Zheng-Liang, Huang Li-Ping
机构信息
Department of Critical Care Medicine, First Affiliated Hospital of University of South China, Hengyang 421001, China.
Department of Infection, Third Hospital of Hengyang City, Hengyang 421001, China.
出版信息
World J Emerg Med. 2014;5(4):291-7. doi: 10.5847/wjem.j.issn.1920-8642.2014.04.009.
BACKGROUND
Many studies have showed that apoptosis of endothelial cells plays a curial role in the progress of sepsis. But the role of simvastatin in apoptosis of endothelial cells induced by sepsis is not clear. The present study aimed to investigate the role of simvastatin in apoptosis of endothelial cells induced by sepsis and its mechanism.
METHODS
Human umbilical vein endothelial cells (HUVECs) were randomly divided into three groups: control group, sepsis serum intervention group (sepsis group) and simvastatin+sepsis serum intervention group (simvastatin group). After 24-hour incubation with corresponding culture medium, the relative growth rate of HUVECS in different groups was detected by MTT assay; the apoptosis of HUVECs was detected by Hoechst33258 assay and flow cytometry; and the expression of the Bcl-2 and Bax genes of HUVECs was detected by PCR.
RESULTS
Compared with the sepsis group, HUVECs in the simvastatin group had a higher relative growth rate. Apoptotic HUVECs decreased significantly in the simvastatin group in comparison with the sepsis group. Expression of the Bcl-2 gene in HUVECs decreased obviously, but the expression of the Bax gene increased obviously after 24-hour incubation with sepsis serum; however, the expression of the Bcl-2 and Bax genes was just the opposite in the simvastatin group.
CONCLUSIONS
Our study suggests that simvastatin can inhibit apoptosis of endothelial cells induced by sepsis through upregulating the expression of Bcl-2 and downregulating Bax. It may be one of the mechanisms for simvastatin to treat sepsis.
背景
许多研究表明，内皮细胞凋亡在脓毒症进展中起关键作用。但辛伐他汀在脓毒症诱导的内皮细胞凋亡中的作用尚不清楚。本研究旨在探讨辛伐他汀在脓毒症诱导的内皮细胞凋亡中的作用及其机制。
方法
人脐静脉内皮细胞（HUVECs）随机分为三组：对照组、脓毒症血清干预组（脓毒症组）和辛伐他汀+脓毒症血清干预组（辛伐他汀组）。用相应培养基孵育24小时后，采用MTT法检测不同组HUVECs的相对生长率；采用Hoechst33258法和流式细胞术检测HUVECs的凋亡情况；采用PCR法检测HUVECs中Bcl-2和Bax基因的表达。
结果
与脓毒症组相比，辛伐他汀组HUVECs的相对生长率较高。与脓毒症组相比，辛伐他汀组凋亡的HUVECs明显减少。用脓毒症血清孵育24小时后，HUVECs中Bcl-2基因表达明显降低，而Bax基因表达明显升高；然而，辛伐他汀组中Bcl-2和Bax基因的表达情况则相反。
结论
我们的研究表明，辛伐他汀可通过上调Bcl-2表达和下调Bax来抑制脓毒症诱导的内皮细胞凋亡。这可能是辛伐他汀治疗脓毒症的机制之一。
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