Ginsenoside Rg1 promoted the wound healing in diabetic foot ulcers via miR-489–3p/Sirt1 axis
Autor: | Ming-Sheng Zhang, Hua-An Cai, Liang Huang, Ruo-Yi Liao, Xing Huang, Feng-Dan Hu |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Ginsenosides
Angiogenesis Gene Expression Neovascularization Physiologic Apoptosis RM1-950 Umbilical vein Rats Sprague-Dawley Sirtuin 1 Downregulation and upregulation Cell Movement miR-489–3p Human Umbilical Vein Endothelial Cells Animals Humans Medicine MTT assay Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Pharmacology Wound Healing Sirt1 Ginsenoside Rg1 business.industry medicine.disease Diabetic foot Diabetic Foot MicroRNAs Cancer research Diabetic foot ulcers Molecular Medicine Therapeutics. Pharmacology business Wound healing Phytotherapy |
Zdroj: | Journal of Pharmacological Sciences, Vol 147, Iss 3, Pp 271-283 (2021) |
ISSN: | 1347-8613 |
Popis: | Purpose Diabetic foot ulcers (DFUs) are common complications of high severity for diabetes. Ginsenoside Rg1 (Rg1) has the potential for diabetes and cardiovascular diseases therapy. This research aimed at exploring the regulation of Rg1 on DFUs treatment and the underlying mechanism. Methods Human umbilical vein endothelial cells (HUVECs) incubated with high-glucose culture medium were established for induction of diabetes model. The MTT assay, Annexin V/PI assay and oxidative stress detection were carried out on high-glucose-induced HUVECs. Dual-luciferase reporter assay was performed to prove the interaction of miR-489–3p and Sirt1. DFUs model was established to determine the efficiency of Rg1 and miR-489–3p in wound closure of DFUs in vivo. Results Rg1 promoted cell proliferation, migration and angiogenesis, and reduced cell apoptosis in high-glucose-induced HUVECs. Knockdown of miR-489–3p alleviated the high-glucose-induced damage to HUVECs, while overexpression of miR-489–3p attenuated the protection effects of Rg1. Overexpression Sirt1 promoted wound healing in DFUs and Sirt1 was a direct target of miR-489–3p. In addition, animal experiments demonstrated that Rg1 promoted wound closure by regulating miR-489–3p/Sirt1 axis. Conclusions Rg1 alleviated the DFUs by increasing Sirt1 expression via miR-489–3p downregulation and promoting activation of PI3K/AKT/eNOS signaling. |
Databáze: | OpenAIRE |
Externí odkaz: |