2. Academic Validation
  3. Gastrodin protects endothelial cells against high glucose-induced injury through up-regulation of PPARβ and alleviation of nitrative stress

Gastrodin protects endothelial cells against high glucose-induced injury through up-regulation of PPARβ and alleviation of nitrative stress

  • Microvasc Res. 2023 Mar 22;148:104531. doi: 10.1016/j.mvr.2023.104531.
Chuang Yang 1,  Hongmei Qiu 1,  Mingqi Lv 2,  Junxia Yang 1,  Ke Wu 1,  Jiajun Huang 1,  Qingsong Jiang 3
Affiliations

Affiliations

  • 1 Department of Pharmacology, Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Key Laboratory of Drug Metabolism, College of Pharmacy, Chongqing Medical University, Chongqing 400016, PR China.
  • 2 Experimental Teaching Management Center, Chongqing Medical University, Chongqing 400016, PR China.
  • 3 Department of Pharmacology, Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Key Laboratory of Drug Metabolism, College of Pharmacy, Chongqing Medical University, Chongqing 400016, PR China. Electronic address: [email protected].
PMID: 36963481 DOI: 10.1016/j.mvr.2023.104531
Abstract

In diabetes mellitus (DM), high glucose can result in endothelial cell injury, and then lead to diabetic vascular complications. Gastrodin, as the mainly components of Chinese traditional herb Tianma (Gastrodia elata Bl.), has been widely used for cardiovascular diseases. However, the known of the effect of gastrodin on endothelial cell injury is still limited. In this study, we aimed to investigate the effect and possible mechanism of gastrodin on high glucose-injured human umbilical vein endothelial cells (HUVEC). High glucose (30 mmol/L) treatment caused HUVEC injury. After gastrodin (0.1, 1, 10 μmol/L) treatment, compared with the high glucose group, the cell proliferation ability increased in a dose-dependent manner. Meanwhile, gastrodin (10 μmol/L) up-regulated the mRNA and protein expressions of PPARβ and eNOS, decreased the expressions of iNOS, also reduced the protein expression of 3-nitrotyrosine, and lowed the level of ONOO-, increased NO content. Both the PPARβ antagonist GSK0660 (1 μmol/L) and the eNOS Inhibitor L-NAME (10 μmol/L) were able to block the above effects of gastrodin. In conclusion, gastrodin protectes vascular endothelial cells from high glucose injury, which may be, at least partly, mediated by up-regulating the expression of PPARβ and negatively regulating nitrative stress.

Keywords

Gastrodin; High glucose; Nitrative stress; PPARβ; Vascular endothelial cells.

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