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Downregulation of miR-34a ameliorates inflammatory response and apoptosis induced by renal ischemia-reperfusion by promoting Kruppel-like factor 4 expression.

下调和上调 克鲁佩尔 细胞凋亡 内科学 化学 缺血 癌症研究 医学 细胞生物学 转录因子 生物 生物化学 基因
作者
Yunyu Shi,Yunn‐Hwa Ma,Rui Zhang,R.-S. Li
出处
期刊:DOAJ: Directory of Open Access Journals - DOAJ 卷期号:24 (22): 11683-11689 被引量:5
标识
DOI:10.26355/eurrev_202011_23813
摘要

To explore the influence of micro ribonucleic acid (miR)-34a on renal ischemia-reperfusion by regulating Kruppel-like factor 4 (KLF4).A total of 36 Sprague-Dawley (SD) rats weighing 180-200 g were randomly divided into sham operation group (n=12), model group (n=12), and miR-34a inhibitor group (n=12). Renal ischemia-reperfusion modeling was performed in rats of model group and miR-34a inhibitor group. Those in the sham operation group received the same procedures without ligation. 200 μL of miR-34a inhibitor was pre-injected before modeling in rats of miR-34a inhibitor group. An automatic biochemical analyzer was used to detect serum creatinine and urea nitrogen levels in each group of rats, thus reflecting renal functions. The expressions of B-cell lymphoma 2 (Bcl-2), an apoptotic protein, and KLF4, a transcription factor, were detected via Western blotting. Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) assay was conducted to measure the expression levels of miR-34a and KLF4 in rat renal tissues in each group. Immunohistochemistry was employed to determine the expressions of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10). Additionally, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) staining was utilized to determine the apoptotic rate in rat kidney tissues in each group.Compared with those in the sham operation group, serum creatinine level, urea nitrogen level, expressions of miR-34a, TNF-α and Bcl-2 (p<0.05) increased, while the levels of KLF4 and IL-10 (p<0.05) decreased in the model group. Apoptosis rate was also higher in the model group than the controls. In comparison with the model group, miR-34a inhibitor group had lowered serum creatinine level, urea nitrogen level, expressions of miR-34a, TNF-α and Bcl-2, and apoptotic rate (p<0.05), but raised levels of KLF4 and IL-10 (p<0.05), showing statistically significant differences.Downregulation of miR-34a ameliorates inflammatory response and apoptosis induced by renal ischemia-reperfusion by promoting KLF4 level, thus improving renal functions in rats.

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