Bei Jiang
Shandong University
15 Papers
82 Citations
Bei Jiang is an academic researcher from Shandong University. The author has contributed to research in topics: Apoptosis & Nephrotoxicity. The author has an hindex of 8, co-authored 15 publications.
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Papers
Grape seed proanthocyanidin extract protects from cisplatin- induced nephrotoxicity by inhibiting endoplasmic reticulum stress- induced apoptosis
TL;DR: GSPE can protect the renal function from CP-induced nephrotoxicity and can attenuate the endoplasmic reticulum (ER) stress-induced apoptosis via regulation of the caspase-12 pathway.
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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Resveratrol attenuates early diabetic nephropathy by down-regulating glutathione s-transferases Mu in diabetic rats.
Bei Jiang,Ling Guo,Baoying Li,Junhui Zhen,Jian Song,Tao Peng,Xiangdong Yang,Zhao Hu,Hai-Qing Gao +8 more
TL;DR: In vitro, resveratrol inhibited the proliferation of mesangial cells caused by high glucose and down-regulated GSTM and Nrf2 expressions in a dose-dependent manner, suggesting that resver atrol help prevent the progression of DN.
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Grape seed proanthocyanidins ameliorate diabetic nephropathy via modulation of levels of AGE, RAGE and CTGF.
TL;DR: GSPE can decrease proteinuria, attenuating the progression of nephropathy in diabetic rats, andRenoprotective effects of GSPE are correlated with suppression on AGEs/RAGE axis, downregulating expression of CTGF.
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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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