科研成果详情

题名Diosmin mitigates high glucose-induced endoplasmic reticulum stress through PI3K/AKT pathway in HK-2 cells
作者
发表日期2022-04-27
发表期刊BMC COMPLEMENTARY MEDICINE AND THERAPIES   影响因子和分区
语种英语
原始文献类型Article
关键词Diabetic nephropathy Diosmin High glucose Endoplasmic reticulum stress Phosphatidylinositol 3-kinase protein kinase-B pathway
其他关键词UNFOLDED PROTEIN RESPONSE ; TUBULAR EPITHELIAL-CELLS ; DIABETIC-NEPHROPATHY ; OXIDATIVE STRESS ; RAT MODEL ; APOPTOSIS ; MECHANISMS ; AUTOPHAGY
摘要Background Diosmin has been reported to treat diabetes, but its role in diabetic nephropathy (DN) remains unclear. This research investigated the mechanism by which diosmin alleviated high glucose (HG)-induced HK-2 cell injury. Methods First, we used CCK-8 to detect the effect of 0.1, 1, or 10 mu g/mL diosmin on the viability of HK-2 cells treated with normal glucose or HG. Next, we used flow cytometry, automatic biochemical analyzer, ELISA, immunofluorescence, and colorimetric assay kit to examine the apoptosis, oxidative stress, inflammatory factors, and Caspase-3 expression in HK-2 cells. Thereafter, we used the western blot and qRT-PCR to examine the expression of the endoplasmic reticulum stress-, oxidative stress-, inflammation-, apoptosis-, and autophagy, and PI3K/AKT pathway-related factors. Results Diosmin was non-cytotoxic to normal HK-2 cells and enhanced the HK-2 cell viability suppressed by HG. Meanwhile, diosmin restrained apoptosis, the contents of MDA, pro-inflammatory factors, and Caspase-3 but intensified the contents of SOD and CAT induced by HG. We further confirmed that diosmin blunted oxidative stress-, inflammation-, apoptosis-, and autophagy-related factors expression induced by HG via restraining the CHOP and GRP78 expressions. Further, we also discovered that PTEN level was restrained and the ratios of p-PI3K/PI3K and p-AKT/AKT were enhanced in HK-2 cells induced by HG, which was reversed by co-treatment of HG and diosmin. Conclusions Our study manifested that diosmin alleviated the HG-mediated endoplasmic reticulum stress injury in HK-2 cells via restraining the PI3K/AKT pathway.
出版者BMC
出版地LONDON
ISSN2662-7671
EISSN2662-7671
卷号22期号:1页码:116
DOI10.1186/s12906-022-03597-y
页数10
WOS类目Integrative & Complementary Medicine
WOS研究方向Integrative & Complementary Medicine
WOS记录号WOS:000788308200001
收录类别SCIE ; SCOPUS ; PUBMED
URL查看原文
PubMed ID35477428
SCOPUSEID2-s2.0-85128941646
通讯作者地址[Zheng, Chao]The Second Affiliated Hospital Zhejiang University,School of Medicine,Jiefang Road 88, Shangcheng District, Zhejiang Province,Hangzhou City,310009,China
Scopus学科分类Complementary and Alternative Medicine
引用统计
被引频次[WOS]:0   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/148221
专题温州医科大学
通讯作者Zheng, Chao
作者单位
1.Wenzhou Medical University,Chashan Higher Education Park,Zhejiang Province,Wenzhou City,325035,China;
2.Department of Endocrinology,Second People’s Hospital of Pingyang County,Zhejiang Province,Wenzhou City,325405,China;
3.The Second Affiliated Hospital Zhejiang University,School of Medicine,Jiefang Road 88, Shangcheng District, Zhejiang Province,Hangzhou City,310009,China;
4.Department of Nephrology,The Poeple’ s Hospital of Suichang County,Zhejiang Province,Lishui City,323300,China;
5.Department of Endocrinology and Nephrology,Jiande Hospital of Traditional Chinese Medicine,Zhejiang Province,Hangzhou City,311600,China;
6.Shangyu People’s Hospital of Shaoxing,Zhejiang Province,Shaoxing City,312300,China;
7.Department of Nephrology,Huzhou Central Hospital; Affiliated Central Hospital of Huzhou University; Affiliated Huzhou Hospital; Zhejiang University School of Medicine,Zhejiang Province,Huzhou City,313000,China
第一作者单位温州医科大学
第一作者的第一单位温州医科大学
推荐引用方式
GB/T 7714
Deng, Jiuhong,Zheng, Chao,Hua, Zhou,et al. Diosmin mitigates high glucose-induced endoplasmic reticulum stress through PI3K/AKT pathway in HK-2 cells[J]. BMC COMPLEMENTARY MEDICINE AND THERAPIES,2022,22(1):116.
APA Deng, Jiuhong, Zheng, Chao, Hua, Zhou, Ci, Haideng, Wang, Guiying, & Chen, Lijing. (2022). Diosmin mitigates high glucose-induced endoplasmic reticulum stress through PI3K/AKT pathway in HK-2 cells. BMC COMPLEMENTARY MEDICINE AND THERAPIES, 22(1), 116.
MLA Deng, Jiuhong,et al."Diosmin mitigates high glucose-induced endoplasmic reticulum stress through PI3K/AKT pathway in HK-2 cells".BMC COMPLEMENTARY MEDICINE AND THERAPIES 22.1(2022):116.

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