Analysis of microRNA Expression after Glutamine Intervention in Acute Renal Ischemia-Reperfusion Injury.

Suhua Li,Shun Wang,Xueqian Chu,Munire Aierken,Xuan Huang,Kalidoss Rajakani

doi:10.1155/2022/2401152

Abstract

Background Ischemia-reperfusion acute kidney injury (I/R AKI) is a severe kidney disease with high mortality and morbidity. This study aimed to explore the protective mechanism of glutamine (GLN) against I/R AKI. MethodsThe I/R AKI rat model was established, and HE staining of kidney tissue and serum creatinine (SCr) and blood urea nitrogen (BUN) detection were performed. The miRNAs were sequenced by high throughput in rat kidney tissue samples. Differentially expressed miRNAs (DEmiRs) between the I/R group and I/R + GLN group were screened, and enrichment analysis for target genes of DEmiRs was performed. Meanwhile, human HK-2 cells were cultured, and an I/R model was established to verify the expression of DEmiRs. Results Compared with the I/R group, the SCr and BUN levels at each time point were lower in the I/R + GLN group. Vacuolar degeneration of renal tubules in the I/R + GLN group was significantly reduced. In the 104 DEmiRs, we selected miR-132-5p, miR-205, and miR-615 as key miRNAs. KEGG analysis showed that the Notch signaling pathway, PI3K-Akt signaling pathway, and cGMP signaling pathway were mainly related to the GLN against I/R. qRT-PCR verified the downregulation of miR-205 in the I/R group, compared to the sham and I/R + GLN group. The I/R model was established with HK-2 cells, and the expression of miR-132-5p and miR-205 was decreased. Conclusion GLN reduced I/R-induced AKI. There were significant differences between miRNAs expression in I/R after GLN treatment. The process of GLN against I/R-induced AKI may be related to the Notch and PI3K-Akt signaling pathway.

Highlights

Acute kidney injury (AKI) is characterized by acute renal function loss and affects 13.3 million people each year [1]
Effect of Glutamine on the Renal Function of Rats after Ischemia Reperfusion. e serum creatinine (SCr) and blood urea nitrogen (BUN) levels were first examined in the three groups of rats (Figures 1(a) and 1(b))
In the I/R + GLN group, SCr and BUN levels were increased from 1 hour to 12 hours, but the increase trend was slower than that in the I/R group

Summary

Introduction

Acute kidney injury (AKI) is characterized by acute renal function loss and affects 13.3 million people each year [1]. Among a variety of factors, renal ischemia-reperfusion injury (I/R) is one of the underlying causes of AKI and an inevitable problem in kidney transplantation [2, 3]. Recent studies have found that glutamine, a drug used as a conventional nutritional therapy for AKI, could protect the kidney by reducing oxidative stress [8, 9]. Is study aimed to explore the protective mechanism of glutamine (GLN) against I/R AKI. E I/R AKI rat model was established, and HE staining of kidney tissue and serum creatinine (SCr) and blood urea nitrogen (BUN) detection were performed. Expressed miRNAs (DEmiRs) between the I/R group and I/R + GLN group were screened, and enrichment analysis for target genes of DEmiRs was performed. Human HK-2 cells were cultured, and an I/R model was established to verify the expression of DEmiRs. Results. GLN reduced I/R-induced AKI. ere were significant differences between miRNAs expression in I/R after GLN treatment. e process of GLN against I/R-induced AKI may be related to the Notch and PI3K-Akt signaling pathway

Methods

Results

Conclusion