Junhui Zhen
Shandong University
14 Papers
30 Citations
Junhui Zhen is an academic researcher from Shandong University. The author has contributed to research in topics: Creatinine & Kidney. The author has an hindex of 7, co-authored 14 publications.
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Papers
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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Expression of human T cell immunoglobulin domain and mucin-3 (TIM-3) on kidney tissue from systemic lupus erythematosus (SLE) patients
TL;DR: The results showed that there was the expression of TIM-3 in renal tissue from the patients with SLE, but rarely expression in cases without SLE and high immuno-reactivity of tim-3 was found to be significantly correlated with serological grade (p < 0.001).
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Protective effect of calcitriol on podocytes in spontaneously hypertensive rat
Weiwei Shi,Ling Guo,Guangyi Liu,Tao Peng,Hongyu Li,Tingting Xie,Dengren Li,Junhui Zhen,Yan Wang,Huimin Yang,Xiangdong Yang +10 more
TL;DR: The present results indicated that there was injury of podocytes in hypertensive nephropathy, which can be ameliorated by calcitriol in SHR, but there was no significant anti‐hypertensive effect.
13
Expression of human T cell immunoglobulin domain and mucin-3 on kidney tissue from immunoglobulin A nephropathy patients
TL;DR: The results showed that there was the expression of Tim-3 in renal tissue from the patients with IgAn, but rarely expression in cases without IgAN, and Expression ofTim-3 was associated with the diseases’ activity.
13
Mycophenolate mofetil ameliorates diabetic nephropathy through epithelial mesenchymal transition in rats
TL;DR: Data suggested that MMF may have a protective role in diabetic nephropathy, and that the underlying mechanism may be partially dependent upon the suppression of the epithelial mesenchymal transition.