Department of Nutrition and Food Hygiene, School of Public Health, Hebei Medical University, Hebei Key Laboratory of Environment and Human Health, Shijiazhuang 050017, China.
Undergraduate of College of Public Health, Hebei Medical University, Shijiazhuang 050017, China.
J Agric Food Chem. 2024 Oct 23;72(42):23465-23477. doi: 10.1021/acs.jafc.4c04438. Epub 2024 Oct 11.
Perfluorooctanesulfonate (PFOS) is a widespread, persistent environmental pollutant that exerts apparent liver toxicity. Flaxseed oil (FO), a dietary oil rich in α-linolenic acid, has been demonstrated to possess a diverse array of health benefits. However, whether FO protects against PFOS-induced liver injury and its underlying mechanisms remain unclear. C57/BL6 mice were orally treated with different concentrations of FO alone or in combination with 10 mg/kg of PFOS for 28 consecutive days. Blood and liver tissues were collected for proteomic, histopathological, biochemical, immunohistochemical, and molecular examinations. Results demonstrated that FO supplementation reduced PFOS-induced liver injury, as evidenced by a decrease in histopathological changes, serum transaminase (ALT and AST) levels, levels of oxidative stress, and inflammatory cytokine (TNF-α, IL-1β, and IL-6) levels. Proteomic analyses showed that differentially expressed proteins were enriched in cholesterol metabolic pathways when comparing the PFOS group to the FO supplementation groups. The expression of cholesterol metabolism-related proteins was also subsequently measured, revealing that FO supplementation decreased the protein expressions of SREBP2, HMGCR, and LDLR while increasing the expression of CYP7A1. This study demonstrates that FO can alleviate PFOS-induced hepatotoxicity by regulating hepatic cholesterol metabolism, indicating that FO may serve as an effective dietary intervention for preventing liver injury caused by PFOS.
全氟辛烷磺酸(PFOS)是一种广泛存在且具有持久性的环境污染物,对肝脏具有明显的毒性。亚麻籽油(FO)是一种富含α-亚麻酸的膳食油,已被证明具有多种健康益处。然而,FO 是否能预防 PFOS 诱导的肝损伤及其潜在机制尚不清楚。C57/BL6 小鼠连续 28 天经口给予不同浓度的 FO 单独或与 10mg/kg PFOS 联合处理。收集血液和肝脏组织进行蛋白质组学、组织病理学、生化、免疫组织化学和分子检测。结果表明,FO 补充可减轻 PFOS 诱导的肝损伤,表现为组织病理学变化、血清转氨酶(ALT 和 AST)水平、氧化应激和炎症细胞因子(TNF-α、IL-1β 和 IL-6)水平降低。蛋白质组学分析表明,与 PFOS 组相比,FO 补充组的胆固醇代谢途径中差异表达蛋白明显富集。随后还测量了胆固醇代谢相关蛋白的表达,发现 FO 补充降低了 SREBP2、HMGCR 和 LDLR 的蛋白表达,同时增加了 CYP7A1 的表达。本研究表明,FO 通过调节肝脏胆固醇代谢减轻 PFOS 诱导的肝毒性,表明 FO 可能作为一种有效的膳食干预措施,用于预防 PFOS 引起的肝损伤。