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Decreased TRPM7 alleviates high glucose-induced renal tubular epithelial cell injury by inhibiting the HMGB1/TLR4 signaling pathway

作     者:Wei Feng Zheng-Yong Cao Fu-Min Guan Hong Chen Wei Feng;Zheng-Yong Cao;Fu-Min Guan;Hong Chen

作者机构:Laboratory DepartmentMaternal and Child Health Hospital of Qijiang DistrictChongqing401429China Otolaryngology DepartmentPeople’s Hospital of Qijiang DistrictChongqing401420China Pharmacy DepartmentPeople’s Hospital of Qijiang DistrictChongqing401420China Science and Education DepartmentPeople’s Hospital of Qijiang DistrictChongqing401420China 

出 版 物:《Asian Pacific Journal of Tropical Biomedicine》 (亚太热带生物医学杂志(英文版))

年 卷 期:2023年第13卷第9期

页      面:393-402页

核心收录:

学科分类:1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学] 

主  题:Diabetic nephropathy TRPM7 HMGB1/TLR4 High glucose Renal tubular epithelial cell 

摘      要:Objective:To explore the regulatory mechanism of transient receptor potential melastatin-7(TRPM7)in high glucose-induced renal tubular epithelial cell ***:The expression of TRPM7 in the serum of diabetic nephropathy patients and high glucose-induced HK-2 cells was detected by ***,the TRPM7 interference vector was constructed,and the downstream high mobility group box 1(HMGB1)/Toll-like receptor 4(TLR4)signaling pathway proteins were ***,in addition to interference with TRPM7 expression,overexpression of HMGB1 in high glucose-induced HK-2 cells was *** activity,apoptosis,oxidative stress levels,and inflammation levels were determined by CCK8,TUNEL,Western blotting,immunofluorescence and related ***:TRPM7 expression was upregulated in the serum of diabetic nephropathy patients and high glucose-induced HK-2 *** with TRPM7 reduced cell damage,epithelial-mesenchymal transition,oxidative stress,and inflammatory response in high glucose-induced HK-2 cells via inhibiting the HMGB1/TLR4 signaling ***,the effects induced by TRPM7 silencing were abrogated by HMGB1 ***:Decreased TRPM7 alleviates high glucose-induced renal tubular epithelial cell injury by inhibiting the HMGB1/TLR4 signaling *** animal experiments and clinical trials are warranted to verify its effect.

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