College of Traditional Chinese Medicine, Hunan University of Traditional Chinese Medicine, Changsha, Hunan, China.
Department of Gastroenterology, The Third People's Hospital of Yunnan Province, Kunming, Yunnan, China.
J Biochem Mol Toxicol. 2024 Sep;38(9):e23809. doi: 10.1002/jbt.23809.
Nonalcoholic fatty liver disease (NAFLD) is an alarming ailment that leads to severe liver damage and increases the risk of serious health conditions. The prevalence of NAFLD due to oxidative stress could be mitigated by plant-derived antioxidants. This study aims to investigate the effects of syringic acid (SA) on NAFLD in a high-fat diet (HFD) rat model. Twenty-four rats were randomly divided into four groups (n = 6): normal control, HFD, SA-administered HFD, and positive control SA on a normal diet. Rats in the normal control and positive control groups received a normal diet, and the remaining groups received an HFD for 8 weeks. SA (20 mg/kg b.w.) was orally (gavage) administered for 8 weeks. Lipid profiles were controlled by SA against HFD-fed rats (p < 0.05). SA reduced the serum aspartate aminotransferase and alanine aminotransferase levels by 70%-190%. SA also suppressed pro-inflammatory cytokines and attenuated histopathological and immunohistochemical changes against HFD-fed rats. SA reversed oxidative stress by suppressing the malondialdehyde formation by 82% and replenished the nonenzymatic and enzymatic antioxidant activities (p < 0.05). Gene expressions of nuclear factor-erythroid 2-related factor/heme oxygenase 1 (Nrf2/HO-1) were elevated in SA-treated rats. Ameliorative effects of SA on NAFLD induced by an HFD in rats were prominent through the reversal of oxidative stress and inflammation, regulated by an intrinsic mechanism of defense against oxidative stress, the Nrf2/HO-1 pathway.
非酒精性脂肪性肝病(NAFLD)是一种严重的肝脏损伤疾病,会增加严重健康问题的风险。植物源性抗氧化剂可以减轻氧化应激引起的 NAFLD 患病率。本研究旨在探讨丁香酸(SA)对高脂肪饮食(HFD)大鼠模型中 NAFLD 的影响。将 24 只大鼠随机分为四组(n = 6):正常对照组、HFD 组、SA 处理的 HFD 组和正常饮食下的阳性对照 SA 组。正常对照组和阳性对照组给予正常饮食,其余两组给予 HFD 喂养 8 周。SA(20mg/kg b.w.)经口(灌胃)给予 8 周。SA 控制 HFD 喂养大鼠的血脂谱(p < 0.05)。SA 将血清天冬氨酸转氨酶和丙氨酸转氨酶水平降低了 70%-190%。SA 还抑制了促炎细胞因子,并减轻了 HFD 喂养大鼠的组织病理学和免疫组织化学变化。SA 通过抑制丙二醛形成 82%并补充非酶和酶抗氧化活性来逆转氧化应激(p < 0.05)。SA 处理大鼠的核因子-红细胞 2 相关因子/血红素加氧酶 1(Nrf2/HO-1)基因表达升高。SA 通过逆转氧化应激和炎症对 HFD 诱导的大鼠 NAFLD 具有明显的改善作用,这是通过抗氧化应激的内在防御机制,即 Nrf2/HO-1 途径来调节的。