Basic & Clinical Medicine ›› 2021, Vol. 41 ›› Issue (1): 27-32.

• Original Articles • Previous Articles     Next Articles

Hydroxysafflor yellow A inhibits high glucose-induced renal podocyte injury of mice

XIE Fei1, ZHOU Mei-lan2*   

  1. 1. Department of Internal Medicine,Shaanxi Armed Police Corps Hospital,Xi'an 710054;
    2. Department of Kidney Internal Medicine, the First Affiliated Hospital of the Air Force Medical University,Xi'an 710032, China
  • Received:2019-12-31 Revised:2020-05-10 Online:2021-01-05 Published:2020-12-30
  • Contact: *

Abstract: Objective To investigate the effect of hydroxysafflor yellow A (HYSA) on high glucose (HG)-induced podocyte injury of mice and its mechanism. Methods Cultured podocytes(MCP5) were divided into control group, HG group, HG+HYSA-L group, HG+HYSA-M group and HG+HYSA-H group. Cell viability was detected by CCK-8 method, cell apoptosis was detected by flow cytometry, caspase-3 activity was detected by colorimeter, MDA, SOD and GSH-Px content in cells were detected by kit, the expression of nephrin, fibronectin, α-SMA, VEGF protein and JNK phosphorylation level in cells was detected by Western blot. Results Compared with the control group, the cell survival rate, nephrin protein expression, SOD, GSH-Px content of HG group were significantly reduced, apoptosis rate, caspase-3 activity, MDA content, fibronectin, α-SMA, VEGF protein expression and JNK phosphorylation were all significantly increased (P<0.05); compared with HG group, HYSA reversed the above changes caused by HG with a concentration dependent manner (P<0.05). Conclusions HYSA protects podocytes agains high glucose-induced injury by inhibiting apoptosis, epithelial-mesenchymal transformation and oxidative stress. Its mechanism is potentially related to the inhibition of JNK signal pathway activation and VEGF protein expression.

Key words: diabetic nephropathy, podocyte, apoptosis, oxidative stress, JNK signaling pathway

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