1. Attenuation of Perfluorooctane Sulfonate-Induced Steatohepatitis by Grape Seed Proanthocyanidin Extract in Mice
- Author
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Dalei Zhang, Tao Huang, Bei Yang, Lei Wu, Wenjuan Zhang, Yurong Zhang, Jianhua Yang, Luoting Chen, and Tingting Lin
- Subjects
CD36 Antigens ,Male ,0301 basic medicine ,CD36 ,010501 environmental sciences ,medicine.disease_cause ,01 natural sciences ,Mice ,chemistry.chemical_compound ,Malondialdehyde ,Fluorocarbons ,biology ,Chemistry ,General Medicine ,Cholesterol ,Alkanesulfonic Acids ,Liver ,Medicine ,Research Article ,medicine.medical_specialty ,Article Subject ,Fatty Acid-Binding Proteins ,General Biochemistry, Genetics and Molecular Biology ,Proinflammatory cytokine ,Superoxide dismutase ,03 medical and health sciences ,Internal medicine ,medicine ,Animals ,Proanthocyanidins ,Triglycerides ,0105 earth and related environmental sciences ,Inflammation ,General Immunology and Microbiology ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,Lipid metabolism ,Hydrogen Peroxide ,Lipid Metabolism ,medicine.disease ,Fatty Liver ,Oxidative Stress ,030104 developmental biology ,Endocrinology ,biology.protein ,Lipid Peroxidation ,Steatosis ,Steatohepatitis ,Oxidative stress - Abstract
Perfluorooctane sulfonate (PFOS), an environmentally persistent pollutant, has been revealed to elicit hepatic toxicity. In the current study, we investigated the protective role of grape seed proanthocyanidin extract (GSPE) against PFOS-caused steatohepatitis in mice. Animals were exposed intragastrically to PFOS (10 mg/kg/day), GSPE (150 mg/kg/day), or their combination. After 21 days of treatment, mice exposed to PFOS exhibited steatosis, oxidative stress, and inflammation in the liver. Nevertheless, simultaneous administration of GSPE resumed the declined serum hepatic enzyme activities and histological abnormalities in PFOS-exposed mice. Furthermore, GSPE supplementation reduced the contents of triglyceride (TG) and total cholesterol (TC) and expression of lipid metabolism-associated genes CD36 and fatty acid-binding protein 4 (FABP4) in the liver of mice treated with PFOS. Moreover, GSPE suppressed the generation of lipid peroxidative product malondialdehyde and restored the activity of superoxide dismutase in the liver of PFOS-exposed mice. In addition, GSPE repressed the PFOS-induced hepatic overproduction of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Our results demonstrate that GSPE attenuates PFOS-caused steatohepatitis in mice by regulating lipid metabolism, oxidative stress, and inflammatory response.
- Published
- 2020