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MYC通过促进细胞增殖和抑制凋亡参与脂多糖诱导的脓毒症。

MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis.

作者信息

Li Yin, Kong C Hengqi, Feng Lei, Tang Wenliang, Chen Mengwei, Zheng Zhiyuan

机构信息

Emergency Department of Huadong Hospital, Fudan University, Yan'an Xi Road, Shanghai, China.

Cardiovascular Department of Huadong Hospital, Fudan University, Shanghai, China.

出版信息

Cell J. 2020 Jul;22(Suppl 1):68-73. doi: 10.22074/cellj.2020.6961. Epub 2020 Jul 18.

Abstract

OBJECTIVE

This study aimed to explore the potential mechanism of proto-oncogene, BHLH Transcription Factor gene, on sepsis.

MATERIALS AND METHODS

In this experimental study, rat-derived H9C2 cardiomyocyte cells were cultured , followed by lipopolysaccharide (LPS) treatment with different concentration gradients. The cholecystokinin octapeptide (CCK-8) assay, enzyme-linked immunoassay (ELISA) assay, quantitative reverse transcription polymerase chain reaction (qRT-PCR), cell transfection, Western blot and flow cytometry were used to observe the cellular apoptosis and proliferation of cells in both treated LPS groups and normal control group.

RESULTS

The result of CCK-8 assay showed that silencing inhibited cellular proliferation of sepsis in absence or presence of LPS treatment. ELISA assay showed that the expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were decreased in silenced group, but they were increased after LPS treatment. Moreover, Flow cytometry assay showed that silencing contributed to the apoptosis of sepsis cells. Furthermore, the expression of inflammatory factors showed that silencing elevated the expression of inflammation factors.

CONCLUSION

might take part in the process of LPS induced sepsis through suppressing apoptosis and inducing cell proliferation. Moreover, might reduce inflammation during the progression of LPS induced sepsis.

摘要

目的

本研究旨在探讨原癌基因BHLH转录因子基因在脓毒症中的潜在机制。

材料与方法

在本实验研究中,培养大鼠来源的H9C2心肌细胞,然后用不同浓度梯度的脂多糖(LPS)进行处理。采用细胞计数试剂盒-8(CCK-8)检测、酶联免疫吸附测定(ELISA)、定量逆转录聚合酶链反应(qRT-PCR)、细胞转染、蛋白质免疫印迹法和流式细胞术观察LPS处理组和正常对照组细胞的凋亡及增殖情况。

结果

CCK-8检测结果显示,沉默在有无LPS处理的情况下均抑制脓毒症细胞的增殖。ELISA检测显示,沉默组肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的表达降低,但LPS处理后升高。此外,流式细胞术检测显示,沉默促进脓毒症细胞的凋亡。此外,炎症因子表达显示,沉默提高了炎症因子的表达。

结论

可能通过抑制凋亡和诱导细胞增殖参与LPS诱导的脓毒症过程。此外,可能在LPS诱导的脓毒症进展过程中减轻炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3dd/7481895/d89654a54b4f/Cell-J-22-Suppl1-68-g01.jpg

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