Journal
MOLECULAR MEDICINE
Volume 28, Issue 1, Pages -Publisher
SPRINGER
DOI: 10.1186/s10020-022-00481-w
Keywords
Glabridin; Diabetic nephropathy; Bioinformatics; Ferroptosis; VEGF signaling pathway
Funding
- 2020 Special Fund for Health Care Development (Inheritance and Development of Traditional Chinese Medicine)-TCM Science and Research Project of Traditional Chinese Medicine Bureau of Guangdong Province [20201361]
- 2019 Huizhou Studio Development of Famous Doctor of Traditional Chinese Medicine Project [312]
- 2018 Special Fund for Health Care Development (Inheritance and Development of Traditional Chinese Medicine)-TCM Talent Training and Development Project-The 3rd Session of Famous Traditional Chinese Medicine Practitioners Inheritance in Guangdong Province ( [5]
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Through network pharmacology, the study revealed the protective effects of Glab on diabetic nephropathy, possibly by suppressing ferroptosis and the VEGF/Akt/ERK pathway.
Background Glabridin (Glab) is a bioactive component of licorice that can ameliorate diabetes, but its role in diabetic nephropathy (DN) has seldom been reported. Herein, we explored the effect and underlying mechanism of Glab on DN. Methods The bioactive component-target network of licorice against DN was by a network pharmacology approach. The protective effect of Glab on the kidney was investigated by a high-fat diet with streptozotocin induced-diabetic rat model. High glucose-induced NRK-52E cells were used for in vitro studies. The effects of Glab on ferroptosis and VEGF/Akt/ERK pathways in DN were investigated in vivo and in vitro using qRT-PCR, WB, and IHC experiments. Results Bioinformatics analysis constructed a network comprising of 10 bioactive components of licorice and 40 targets for DN. 13 matching targets of Glab were mainly involved in the VEGF signaling pathway. Glab treatment ameliorated general states and reduced FBG, HOMA-beta, and HOMA-insulin index of diabetic rats. The renal pathological changes and the impaired renal function (the increased levels of Scr, BUN, UREA, KIM-1, NGAL, and TIMP-1) were also improved by Glab. Moreover, Glab repressed ferroptosis by increasing SOD and GSH activity, and GPX4, SLC7A11, and SLC3A2 expression, and decreasing MDA and iron concentrations, and TFR1 expression, in vivo and in vitro. Mechanically, Glab significantly suppressed VEGF, p-AKT, p-ERK1/2 expression in both diabetic rats and HG-induced NRK-52E cells. Conclusions This study revealed protective effects of Glab on the kidney of diabetic rats, which might exert by suppressing ferroptosis and the VEGF/Akt/ERK pathway.
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