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.
Highlights
Steatohepatitis is a common histological finding that involves a variety of etiologies
To observe the ameliorative role of grape seed proanthocyanidin extract (GSPE) in Perfluorooctane sulfonate (PFOS)-caused hepatic injury, liver function parameters AST, alanine transaminase (ALT), and lactate dehydrogenase (LDH) were detected in mice
The increased liver index and enzyme activities were resumed by combined treatment with GSPE in mice exposed to PFOS (P < 0:05)
Summary
Steatohepatitis is a common histological finding that involves a variety of etiologies. Toxicant-associated steatohepatitis is one of the most frequent causes of steatohepatitis [1]. Perfluorooctane sulfonate (PFOS), a member of a family of perfluoroalkyl substances (PFAS), has widely aroused public attention due to its ubiquitous distribution, environmental persistence, high bioaccumulation, and potential toxicity [2]. PFOS has been detected in populations worldwide [3], and the consumption of contaminated foods and drinking water and inhalation of indoor dust are the predominant exposure pathways of PFOS to nonoccupationally exposed people [4]. Owing to the long half-life of elimination in people (approximately 5 years) [5], PFOS accumulates in the body and poses a threat to human health, for occupationally exposed persons. Tests in rodents have revealed that PFOS exposure caused hepatic steatosis [6,7,8,9]
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