Search

Your search keyword '"Yao, Hui"' showing total 9 results
Start Over Author "Yao, Hui" Search Limiters Full Text Journal biomed research international
9 results on '"Yao, Hui"'

5. Inhibitor of DNA Binding 1 Is Induced during Kidney Ischemia-Reperfusion and Is Critical for the Induction of Hypoxia-Inducible Factor-1α

Author

Yin-Yin Xie, Yaowen Xu, Yao-Hui Gao, Yan-Fang Zou, Pingyan Shen, Dan Wen, Xiaobei Feng, Qian Zhao, Hao Shi, Wen Zhang, Yong-Xi Chen, and Jing Xu

Subjects
0301 basic medicine, Inhibitor of Differentiation Protein 1, Pathology, medicine.medical_specialty, Article Subject, Gene Expression, lcsh:Medicine, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Western blot, RNA interference, Transcription (biology), Gene expression, medicine, Gene silencing, Animals, Humans, Gene Silencing, RNA, Messenger, Kidney Tubules, Distal, General Immunology and Microbiology, medicine.diagnostic_test, Renal ischemia, Chemistry, lcsh:R, Acute kidney injury, Epithelial Cells, General Medicine, Acute Kidney Injury, medicine.disease, Hypoxia-Inducible Factor 1, alpha Subunit, Molecular biology, Cell Hypoxia, Rats, Disease Models, Animal, 030104 developmental biology, Hypoxia-inducible factors, Reperfusion Injury, Research Article
Abstract

In this study, rat models of acute kidney injury (AKI) induced by renal ischemia-reperfusion (I/R) and HK-2 cell models of hypoxia-reoxygenation (H/R) were established to investigate the expression of inhibitor of DNA binding 1 (ID1) in AKI, and the regulation relationship between ID1 and hypoxia-inducible factor 1 alpha (HIF-1α). Through western blot, quantitative real-time PCR, immunohistochemistry, and other experiment methods, the induction of ID1 after renal I/R in vivo was observed, which was expressed mainly in renal tubular epithelial cells (TECs). ID1 expression was upregulated in in vitro H/R models at both the protein and mRNA levels. Via RNAi, it was found that ID1 induction was inhibited with silencing of HIF-1α. Moreover, the suppression of ID1 mRNA expression could lead to decreased expression and transcription of HIF-1αduring hypoxia and reoxygenation. In addition, it was demonstrated that both ID1 and HIF-1αcan regulate the transcription of twist. This study demonstrated that ID1 is induced in renal TECs during I/R and can regulate the transcription and expression of HIF-1α.

Published
2016

9. Galangin Suppresses Renal Inflammation via the Inhibition of NF- κ B, PI3K/AKT and NLRP3 in Uric Acid Treated NRK-52E Tubular Epithelial Cells.

Author

Lu H, Yao H, Zou R, Chen X, and Xu H

Subjects
Animals, Cell Line drug effects, Cyclooxygenase 2 metabolism, Cytokines metabolism, Dinoprostone metabolism, Epithelial Cells metabolism, Flavonoids therapeutic use, Inflammasomes metabolism, Inflammation pathology, Interleukin-18 metabolism, Interleukin-1beta metabolism, Nitric Oxide metabolism, Nitric Oxide Synthase drug effects, Phosphotransferases (Alcohol Group Acceptor) drug effects, Rats, Signal Transduction drug effects, Tumor Necrosis Factor-alpha metabolism, Epithelial Cells drug effects, Flavonoids pharmacology, NF-kappa B metabolism, NLR Family, Pyrin Domain-Containing 3 Protein metabolism, Nephritis drug therapy, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, Uric Acid metabolism
Abstract

Renal inflammation can result in renal injury. Uric acid (UA) is the final product of purine metabolism in humans and because of the lack of urate oxidase, UA may accumulate in tissues, including kidney, causing inflammation. Galangin was isolated from a traditional Chinese medicine plant and possesses several beneficial effects, working as an anti-oxidant, anti-mutagenic, anti-tumor, anti-inflammatory, anti-microbial, and anti-viral agent. Therefore, this study aimed at investigating the molecular mechanism of galangin in the attenuation of UA induced renal inflammation in normal rat kidney epithelial cells NRK-52E. Our findings suggested that galangin treatment efficiently protected NRK-52E cells against UA induced renal inflammation by decreasing tumor necrosis factor (TNF)- α , interleukin (IL)-1 β , IL-18, prostaglandin E2 (PGE2), and nitric oxide (NO) release, and it inhibited nitric oxide synthase (iNOS), prostaglandin endoperoxide synthase 2 (PTGS2), TNF- α , IL-1 β , and IL-18 mRNA expression. In addition, galangin was not exerting any cytotoxicity at the concentrations that were effective against inflammation as assessed by CCK8 assay. Moreover, western blotting showed that galangin treatment effectively inhibited nuclear factor-kappa B (NF- κ B), phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) and nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3) signaling pathway activation. Taken together, these findings suggested that galangin plays a pivotal role in renal inflammation by suppressing inflammatory responses, which might be closely associated with the inhibition of NLRP3 inflammasome, NF- κ B and PI3K/AKT signaling pathway activation.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results