Attenuation of Perfluorooctane Sulfonate-Induced Steatohepatitis by Grape Seed Proanthocyanidin Extract in Mice.

Attenuation of Perfluorooctane Sulfonate-Induced Steatohepatitis by Grape Seed Proanthocyanidin Extract in Mice.
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葡萄籽原花青素提取物减轻小鼠全氟辛烷磺酸诱导的脂肪性肝炎

DOI:
10.1155/2020/8818160
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发表时间:
2020
影响因子:
--
通讯作者:
Zhang D
Zhang D
中科院分区:
生物学3区
文献类型:
--
作者:
Huang T;Zhang Y;Zhang W;Lin T;Chen L;Yang B;Wu L;Yang J;Zhang D

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全氟辛烷磺酸(PFOS)是一种环境持久性污染物,已被发现可引起肝毒性。在目前的研究中,我们研究了葡萄籽原花青素提取物(GSPE)对全氟辛烷磺酸引起的小鼠脂肪性肝炎的保护作用。动物灌胃接触全氟辛烷磺酸(10毫克/千克/天)、GSPE(150毫克/千克/天)或其组合。经过21天的治疗,接触全氟辛烷磺酸的小鼠出现脂肪变性、氧化应激和肝脏炎症。然而,同时给予GSPE恢复了全氟辛烷磺酸暴露小鼠血清肝酶活性下降和组织学异常。此外,补充GSPE降低了全氟辛烷磺酸处理小鼠肝脏中甘油三酯(TG)和总胆固醇(TC)的含量以及脂质代谢相关基因CD 36和脂肪酸结合蛋白4(FABP 4)的表达。此外,GSPE抑制脂质过氧化产物丙二醛的产生,并恢复超氧化物歧化酶的活性在全氟辛烷磺酸暴露小鼠的肝脏。此外,GSPE抑制了全氟辛烷磺酸诱导的肝脏促炎细胞因子白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的过度产生。我们的研究结果表明,GSPE减弱全氟辛烷磺酸引起的脂肪性肝炎小鼠通过调节脂质代谢,氧化应激和炎症反应。
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.
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