Gycyrrhizic acid alleviates atherosclerotic lesions in rats with diabetes mellitus
- Yaodong Zhao
- Wei Li
- Daimin Zhang
Affiliations: Department of General Internal Medicine, The Fifth Affiliated Hospital of Zhengzhou University, Zhenzhou, Henan 450052, P.R. China, Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China
- Published online on: September 2, 2021 https://doi.org/10.3892/mmr.2021.12395
Copyright: © Zhao
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Gycyrrhizic acid (GA), an inhibitor of high mobility group box 1 (HMGB1), inhibits inflammatory responses and is involved in the occurrence and development of several inflammation‑related diseases. However, the role of GA in the atherosclerotic lesions caused by diabetes mellitus (DM) remains unknown. In the present study, Sprague Dawley rats were selected to desi=gn a diabetic atherosclerosis (AS) model. Rats from the DM‑AS group were subsequently divided into DM‑AS, DM‑AS + GA (50 mg/kg) and DM‑AS + GA (150 mg/kg) groups. Biochemical analyzers were used to measure levels of blood glucose, fasting insulin, total cholesterol, total triglyceride, low‑density lipoprotein and high‑density lipoprotein. The number of plaques was recorded after collection of thoracic aortas from the rats. The intimal thickness of arterial tissue was detected by hematoxylin and eosin staining. The expression levels of CD68 and α‑smooth muscle actin (α‑SMA) were detected by immunohistochemistry. The expression of tumor necrosis factor‑α, interleukin (IL)‑6 and IL‑1β in the serum of the rats was detected by ELISA. The expression of fatty acid synthetase, sterol regulatory element binding protein 1C, HMGB1 and receptor for advanced glycation end products (RAGE) was detected by western blotting. Reverse transcription quantitative PCR was used to detect the mRNA expression of HMGB1 and RAGE. The results demonstrated that GA treatment could decrease the body weight, blood glucose level and biochemical parameters of AS DM rats in a dose‑dependent manner. In addition, GA decreased the intimal thickness of carotid artery and the formation of plaque in rats with diabetic AS. Furthermore, GA inhibited macrophage activation and decreased α‑SMA expression in vascular smooth muscle cells, and decreased the expression of proteins (FAS and SREBP‑1c) and inflammatory factors. Taken together, the findings from the present study demonstrated that GA may have a therapeutic effect on DM‑associated AS. This study provides a theoretical basis for the treatment of diabetic AS.