4.6 Article

Puerarin attenuates cadmium-induced hepatic lipid metabolism disorder by inhibiting oxidative stress and inflammation in mice

Journal

JOURNAL OF INORGANIC BIOCHEMISTRY
Volume 222, Issue -, Pages -

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jinorgbio.2021.111521

Keywords

Cadmium; Puerarin; Liver; Lipid metabolism; Oxidative stress; Inflammation

Funding

  1. Chengdu Science and Technology Bureau [2018-YFYF-00055-SN]

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In a 9-week study involving 40 mice, Puerarin (PU) was shown to improve liver damage and lipid metabolism disorder induced by Cadmium (Cd). PU reduced lipid accumulation and liver injury, exerted antioxidant and anti-inflammatory effects, and normalized lipid metabolism-related proteins disturbed by Cd exposure.
Cadmium (Cd) is a common environmental pollutant with known toxic effects on the liver. Puerarin (PU), a natural flavonoid, has been shown to exert protective effect in numerous pathological processes. However, whether PU affords protection in Cd-induced liver damage is still equivocal. Therefore, 40 mice were treated with Cd and/or PU by gavage for 9 weeks, then the serum and liver samples were collected to verify this issue. In this study, Cd exposure triggered hepatic lipid metabolism disorders and resultant liver damage as evidenced by Oil Red O staining and total cholesterol (TC) and triglyceride (TG) levels in serum and liver, aspartate transaminase (AST) and alanine transaminase (ALT) levels in serum, and histopathology, which were significantly improved by PU. Moreover, PU also normalized the expression of Cd-disturbed lipid metabolism-related proteins to improve lipid accumulation, contributing to the alleviation of liver injury. Moreover, Cd-decreased anti-oxidative indices superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) as well as glutathione (GSH) in hepatic tissues were significantly attenuated by PU administration, while Cd-elevated hepatic malondialdehyde (MDA) and reactive oxygen species (ROS) levels were markedly down-regulated by PU treatment, demonstrating the antioxidant effect of PU against Cd exposure. In addition, PU supplementation increased the anti-inflammatory potential, and normalized the levels of proinflammatory cytokines during Cd exposure. In conclusion, these observations demonstrate that PU treatment decreases oxidative stress and inflammation response, which may contribute to prevent Cd-induced lipid metabolism disorder and consequent liver damage.

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