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JNK信号通路通过上调NGAL抑制脂多糖介导的HK-2细胞凋亡。

JNK Signaling Pathway Suppresses LPS-Mediated Apoptosis of HK-2 Cells by Upregulating NGAL.

作者信息

Han Mei, Pan Yuxia, Gao Mengying, Zhang Junli, Wang Fan

机构信息

Department of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Department of Hemopathy, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

出版信息

Int J Inflam. 2020 Apr 24;2020:3980507. doi: 10.1155/2020/3980507. eCollection 2020.

Abstract

OBJECTIVE

To explore the role of the c-Jun N-terminal kinase (JNK) signaling pathway in upregulated NGAL expression and its antiapoptotic mechanism in lipopolysaccharide (LPS)-mediated renal tubular epithelial cell injury.

METHODS

In vitro, HK-2 cells were divided into five groups (Con, LPS 1 h, LPS 3 h, LPS 6 h, and LPS 12 h groups) based on the time of LPS (10 M) treatment. NGAL and caspase-3 gene expression levels were detected by RT-PCR to assess dynamic changes. HK-2 cells were pretreated with SP600125 (20 M) for 2 hours, followed by LPS (10 M) stimulation for 3 hours. NGAL and caspase-3 gene expression levels were then determined.

RESULTS

NGAL mRNA was increased significantly within 6 hours, and caspase-3 mRNA was increased within 3 hours after treatment ( < 0.05). Correlation analysis showed a high correlation between their expression ( = 0.448, < 0.05). After pretreatment with SP600125, mRNA expression of NGAL in the LPS group was inhibited, while that of caspase-3 was increased significantly. The NGAL mRNA expression level in the SB + LPS group was decreased significantly compared with that in the LPS group, but it was slightly higher than that in the SP group (∼1.5 times of that in the Con group). However, caspase-3 mRNA expression was increased significantly in the SB + LPS group ( < 0.001) (3.5 times of that in the Con group). It also showed a significant increase compared with SP and LPS groups ( < 0.001 vs. SB group; < 0.05 vs. LPS group). We also found that NGAL and caspase 3 proteins were increased significantly in LPS and SP + LPS groups, but SP600125 decreased the NGAL level by almost 35% and increased the caspase 3 level by 50% in the SP + LPS group compared with the LPS group ( < 0.05).

CONCLUSIONS

The JNK signaling pathway inhibits LPS-mediated apoptosis of renal tubular epithelial cells by upregulating NGAL.

摘要

目的

探讨c-Jun氨基末端激酶(JNK)信号通路在脂多糖(LPS)介导的肾小管上皮细胞损伤中上调中性粒细胞明胶酶相关脂质运载蛋白(NGAL)表达的作用及其抗凋亡机制。

方法

在体外,根据LPS(10μg/mL)处理时间将人肾小管上皮细胞系HK-2细胞分为五组(对照组、LPS处理1小时组、LPS处理3小时组、LPS处理6小时组和LPS处理12小时组)。采用逆转录聚合酶链反应(RT-PCR)检测NGAL和半胱天冬酶-3(caspase-3)基因表达水平,以评估其动态变化。HK-2细胞先用SP600125(20μmol/L)预处理2小时,然后用LPS(10μg/mL)刺激3小时。随后测定NGAL和caspase-3基因表达水平。

结果

处理后6小时内NGAL mRNA显著增加,处理后3小时内caspase-3 mRNA增加(P<0.05)。相关性分析显示它们的表达之间具有高度相关性(r=0.448,P<0.05)。用SP600125预处理后,LPS组中NGAL的mRNA表达受到抑制,而caspase-3的mRNA表达显著增加。与LPS组相比,SB+LPS组中NGAL mRNA表达水平显著降低,但略高于SP组(约为对照组的1.5倍)。然而,SB+LPS组中caspase-3 mRNA表达显著增加(P<0.001)(为对照组的3.5倍)。与SP组和LPS组相比也显示出显著增加(与SB组相比P<0.001;与LPS组相比P<0.05)。我们还发现LPS组和SP+LPS组中NGAL和caspase 3蛋白显著增加,但与LPS组相比,SP600125使SP+LPS组中NGAL水平降低了近35%,使caspase 3水平升高了50%(P<0.05)。

结论

JNK信号通路通过上调NGAL抑制LPS介导的肾小管上皮细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0390/7196152/a91a442dc1e8/IJI2020-3980507.001.jpg

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