Therapeutic Potential of Meloxicam in Ameliorating Sepsis-Induced Renal Injury Through the PI3K/AKT Pathway

被引:1
作者
Hu, Jianyun [1 ]
Qin, Shiyuan [1 ]
Xiang, Yuanbing [2 ]
He, Yan [3 ]
Hu, Haifeng [1 ]
机构
[1] Chengdu Univ, Affiliated Hosp, Urol Dept, Chengdu 610081, Peoples R China
[2] Chengdu Univ, Affiliated Hosp, Dept Nephrol, Chengdu 610081, Peoples R China
[3] Chengdu Univ, Affiliated Hosp, ICU, Chengdu 610081, Peoples R China
关键词
Meloxicam; RenalInjury; Sepsis; Lipopolysaccharide; PI3K; AKT Pathway; ACUTE KIDNEY INJURY; PATHOPHYSIOLOGY; INFLAMMATION;
D O I
10.1166/sam.2023.4487
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
Infectious ureteral stones often lead to sepsis. This study investigated the effect of meloxicam on renal injury caused by sepsis. A sepsis kidney injury model was established using lipopolysaccharide (LPS). HK-2 cells were divided into three groups: control, LPS, and LPS + Mel. The expression of TNF-a, IL-6, Bcl-2, and Bax mRNA and protein were detected using PCR and Western blot. The inflammation of HK-2 cells was observed using IL-1(3 immunofluorescence. Apoptosis was investigated using LDH content, TUNEL staining, and flow cytometry. The viability of HK-2 cells was detected using a CCK-8 assay. The protein expression of the PI3K/AKT pathway was examined to investigate the mechanism of action of Mel. LPS treatment increased TNF-a, IL-6, and Bax expression while decreasing Bcl-2 expression. However, Mel treatment reversed these effects. Mel also decreased the number of TUNEL-positive cells and the apoptotic rate and LDH content in the LPS + Mel group. Additionally, Mel up-regulated the p-PI3K and p-AKT expression, indicating that Mel inhibits IP: 203.8.109.20 On: Wed, 02 Aug 2023 05:50:50 inflammation and apoptosis of HK-2 cells treated with LPS by ativating the PI3K/AKT pathway. In conclusion, Mel could inhibit inflammation and apoptosis of HK-2 cells treated with LPS via activation of PI3K/AKT pathway. Delivered by Ingenta
引用
收藏
页码:717 / 723
页数:7
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