Journal of Shandong University (Health Sciences) ›› 2017, Vol. 55 ›› Issue (12): 1-6.doi: 10.6040/j.issn.1671-7554.0.2016.1702

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Mechanism of EGCG protecting high-glucose-induced HK-2 cell apoptosis by suppressing endoplasmic reticulum stress

XIANG Chunhong1, LÜ Li2*, JIANG Bei1, XIAO Xiaoyan1, HU Zhao1   

  1. 1. Department of Nephrology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;
    2. Department of Nephrology, First Affiliated Hospital of Baotou Medical College of Inner Mongolia, Baotou 014010, Inner Mongolia, China
  • Online:2017-12-20 Published:2022-09-27

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Abstract: Objective To investigate the protective effect and mechanism of epigallocatechin 3-gallate(EGCG)on HK-2 cells exposed to high glucose. Methods The HK-2 cells were divided into normal glucose group, mannitol group, high glucose group, and EGCG group. After 24-hour treatment, cell proliferation was measured with CCK8; cell apoptosis was measured with Hoechst33258 and Annexin V staining; the expressions of GRP78 and Caspase-12 were determined with Western blotting. Results Compared with the normal glucose group, the high glucose group showed significantly inhibited cell proliferation and increased apoptosis(P<0.001), while the EGCG(20 μmol/L)group displayed significantly improved cell proliferation, reduced apoptosis rate(P<0.001), and decreased GRP78 and Caspase-12 expressions(P=0.001). Conclusion EGCG may reduce high-glucose-induced HK-2 apoptosis by inhibiting endoplasmic reticulum stress.

Key words: Epigallocatechin 3-gallate, Endoplasmic reticulum stress, HK-2 cells, Apoptosis

CLC Number: 

  • R692.6
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