Binbin Chen
Shandong University
5 Papers
80 Citations
Binbin Chen is an academic researcher from Shandong University. The author has contributed to research in topics: Nephrotoxicity & Apoptosis. The author has an hindex of 4, co-authored 4 publications.
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Papers
Epigallocatechin-3-gallate protects against cisplatin-induced nephrotoxicity by inhibiting endoplasmic reticulum stress-induced apoptosis
TL;DR: EGCG decreased biochemical factors and immunohistochemical damage induced by CP, and expression of phosphorylated-extracellular signal-regulated kinase (p-ERK), glucose-regulated protein 78 (GRP78), caspase-12, and apoptosis of kidney were decreased by EGCG via inhibition of endoplasmic reticulum (ER) stress-induced apoptosis.
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•Journal Article
Epigallocatechin-3-gallate protects against cisplatin nephrotoxicity by inhibiting the apoptosis in mouse.
TL;DR: It is suggested that EGCG can ameliorate CP-induced apoptosis in the kidney by regulating death receptor Fas conducted extrinsic pathway, and the expression of Bax and Bcl-2.
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Grape seed proanthocyanidins protect against streptozotocin‑induced diabetic nephropathy by attenuating endoplasmic reticulum stress‑induced apoptosis.
TL;DR: The results indicated that GSPE can protect renal function and attenuate endoplasmic reticulum stress-induced apoptosis via the Caspase-12 pathway in STZ-induced DN.
Original Article Epigallocatechin-3-gallate protects against cisplatin nephrotoxicity by inhibiting the apoptosis in mouse
Peimei Zou,Jian Song,Bei Jiang,Fei Pei,Binbin Chen,Xiangdong Yang,Guangyi Liu,Zhao Hu +7 more
- 01 Jan 2014
TL;DR: In this article, Epigallocatechin-3-gallate (EGCG) treatment significantly ameliorated the histopathological changes and increased serum creatinine and blood urea nitrogen (BUN) induced by Cisplatin.
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Lack of Faecalibacterium prausnitzii and Bifidobacterium is associated with a higher risk of metabolic associated fatty liver disease in young-onset type 2 diabetes
TL;DR: In this paper , the authors investigated the relationship between the number of gut flora and metabolic-associated fatty liver disease (MAFLD) in young-onset type 2 diabetes mellitus (T2DM) patients and found that Faecalibacterium prausnitzii and Bifidobacterium were independent protective factors for MAFLD.