Puerarin Prevents Bisphenol S Induced Lipid Accumulation by Reducing Liver Lipid Synthesis and Promoting Lipid Metabolism in C57BL/6J Mice

Zi-Yao Wu; Li Luo; Ya-Qi Kan; Mei-Lin Qin; Hai-Ting Li; Qing-Zhi He; Huai-Cai Zeng

doi:10.3390/toxics11090736

Puerarin Prevents Bisphenol S Induced Lipid Accumulation by Reducing Liver Lipid Synthesis and Promoting Lipid Metabolism in C57BL/6J Mice

Toxics. 2023 Aug 26;11(9):736. doi: 10.3390/toxics11090736.

Authors

Zi-Yao Wu^{1

2}, Li Luo^{1

2

3}, Ya-Qi Kan^{1

2}, Mei-Lin Qin^{1

2}, Hai-Ting Li^{1

2}, Qing-Zhi He³, Huai-Cai Zeng^{1

2}

Affiliations

¹ Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, School of Public Health, Guilin Medical University, Guilin 541199, China.
² Guangxi Health Commission Key Laboratory of Entire Lifecycle Health and Care, School of Public Health, Guilin Medical University, Guilin 541199, China.
³ College of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin 541199, China.

Abstract

Bisphenol S (BPS) is an environmental pollutant that can accumulate in the human body and cause harm. Puerarin (PUE) is a flavonoid with anti-inflammatory and antioxidant effects. In this study, we used 50 mg/kg/d BPS as a poison and PUE as an intervention for model mice for 42 d. BPS exposure significantly increased the levels of the impairment of the mice's liver function, T-CHO, TG, LDL-C, ALT, and AST in the BPS group were significantly increased (p < 0.05). Additionally, BPS exposure caused inflammatory cell infiltration in the mice liver tissue and enhanced oxidative stress response, the level of MDA was significantly increased (p < 0.05). The expression of CD36 and pparγ was stimulated after BPS exposure. Moreover, the expression of cpt1a and cpt1b, which promote fatty acid oxidation, was downregulated. After PUE intervention, the levels of genes and proteins involved in lipid synthesis (PPARγ, SREBP1C, and FASN) and metabolism (Cpt1a, Cpt1b, and PPARα) in mice returned to those of the control group, or much higher than those in the BPS group. Therefore, we hypothesized that BPS causes lipid accumulation in the liver by promoting lipid synthesis and reducing lipid metabolism, whereas PUE reduces lipid synthesis and promotes lipid metabolism. Conclusively, our results imply that long-term exposure to BPS in mice affects liver lipid metabolism and that PUE intervention could maintain the liver function of mice at normal metabolic levels.

Keywords: bisphenol S; lipid accumulation; lipid metabolism; puerarin.

Grants and funding

The project was supported by grants from the National Natural Science Foundation of China (NO. 82160629), the Science and Technology Department of Guangxi Zhuang Autonomous (NO. 2021JJA140831), Innovation Project of Guangxi Graduate Education (NO. YCSW2023421, NO. YCSW2021242).