Jie Zhu1, Fangfang Zhu2, Wenfeng Song3, Bin Zhang2, Xie Zhang2, Xiaofeng Jin4, Hong Li5. 1. College of Medicine, Ningbo University, China. 2. Ningbo Medical Centre of LIHuiLi Hospital, China. 3. The First Affiliated Hospital, College Of Medicine, Zhejiang University. 4. College of Medicine, Fudan University. 5. Ningbo Medical Centre of LIHuiLi Hospital, China. Electronic address: 1411101252@nbu.edu.cn.
Abstract
BACKGROUND & AIMS: MicroRNAs (miRNAs) are a class of small endogenous, non-coding RNAs that regulate gene expression at both the transcription and translation levels. Whether miRNAs have taken part in liver ischemia-reperfusion (IR) injury was rarely reported. The purpose of this article is to investigate the potential role of miR-370 in hepatic IR injury. METHODS: Male C57BL/6 mice were divided into 5 groups (sham-operated group, I/R group, IPC group, antagomir-370 group and antagomir-NC), and the expression levels of miR-370 were assessed by quantitative real-time PCR. Serum enzyme analysis and histological examination of liver were used as the index of the effect of miR-370 on hepatic IR injury and following treatment of mice with antagomir-370 or antagomir-NC. The classical pathway factors of NF-κB (TAK1, TAB1, TAB2, IkBα, IKKα, IKKβ, p50, p65) were studied by quantitative real-time PCR and Western blot. RESULTS: The results showed that the IR group's miR-370 expression level was significantly upregulated as compared with the sham-operated group and IPC group. Also inhibition of miR-370 led to the low expression levels of miR-370 and low levels of serum aminotransferase and hepatic histological damage as compared with the IR group. Quantitative real-time PCR showed the levels of TAK1, TAB1, TAB2, IkBα, IKKα, p65 was elevated when improving the miR-370 levels, at the same time, Western blot showed the levels of TAK1, TAB1, TAB2, IkBα, IKKα, IKKβ, p50, p65 were all elevated. CONCLUSION: miR-370 acting via NF-κB might play a crucial role in hepatic IR injury, and inhibition of miR-370 could alleviate the injury to the liver. And miR-370 might positively regulated the NF-κB pathway.
BACKGROUND & AIMS: MicroRNAs (miRNAs) are a class of small endogenous, non-coding RNAs that regulate gene expression at both the transcription and translation levels. Whether miRNAs have taken part in liver ischemia-reperfusion (IR) injury was rarely reported. The purpose of this article is to investigate the potential role of miR-370 in hepatic IR injury. METHODS: Male C57BL/6 mice were divided into 5 groups (sham-operated group, I/R group, IPC group, antagomir-370 group and antagomir-NC), and the expression levels of miR-370 were assessed by quantitative real-time PCR. Serum enzyme analysis and histological examination of liver were used as the index of the effect of miR-370 on hepatic IR injury and following treatment of mice with antagomir-370 or antagomir-NC. The classical pathway factors of NF-κB (TAK1, TAB1, TAB2, IkBα, IKKα, IKKβ, p50, p65) were studied by quantitative real-time PCR and Western blot. RESULTS: The results showed that the IR group's miR-370 expression level was significantly upregulated as compared with the sham-operated group and IPC group. Also inhibition of miR-370 led to the low expression levels of miR-370 and low levels of serum aminotransferase and hepatic histological damage as compared with the IR group. Quantitative real-time PCR showed the levels of TAK1, TAB1, TAB2, IkBα, IKKα, p65 was elevated when improving the miR-370 levels, at the same time, Western blot showed the levels of TAK1, TAB1, TAB2, IkBα, IKKα, IKKβ, p50, p65 were all elevated. CONCLUSION:miR-370 acting via NF-κB might play a crucial role in hepatic IR injury, and inhibition of miR-370 could alleviate the injury to the liver. And miR-370 might positively regulated the NF-κB pathway.