Fanaei Hafseh, Mard Seyyed Ali, Sarkaki Alireza, Goudarzi Gholamreza, Khorsandi Layasadat
Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Air Pollution and Respiratory Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Avicenna J Phytomed. 2021 Sep-Oct;11(5):527-540. doi: 10.22038/AJP.2021.17835.
The burden of diseases and death related to environmental pollution is becoming a major public health challenge. This study was designed to evaluate the deleterious effects of a combination of dust exposure and high-fat diet on liver function. Gallic acid as a potent antioxidant was used to prevent/alleviate non-alcoholic fatty liver disease (NAFLD) in rats exposed to dust and HFD.
24 rats were randomly divided into 3 experimental groups: HFD+Clean air, HFD+N/S+Dust and HFD+gallic acid+Dust. Animals were exposed to CA/ dust for six weeks on alternate days. At the end of the experiments, rats were anesthetized and samples were taken to perform molecular, biomedical, and histopathological evaluations.
Dust exposure induced NAFLD features in rats under HFD. Dust exposure and HFD disrupted liver enzymes and lipid profile. Dust exposure and HFD increased liver MDA level, mRNA expression of , , , , and miRs122, and 34a. Dust+HFD also decreased liver total antioxidant capacity level. Pretreatment with GA improved almost studied variables in the HFD+GA+Dust group.
The present study showed that HFD given for 6 weeks and dust exposure induced NAFLD in Wistar rats through inducing oxidative stress. Oxidative stress through activating the inflammatory pathways caused NAFLD features. GA pretreatment by inhibiting oxidative stress, effectively protected liver functions against HFD+Dust induced inflammation.
与环境污染相关的疾病负担和死亡正成为一项重大的公共卫生挑战。本研究旨在评估粉尘暴露与高脂饮食联合对肝功能的有害影响。使用没食子酸作为一种有效的抗氧化剂来预防/减轻暴露于粉尘和高脂饮食的大鼠的非酒精性脂肪性肝病(NAFLD)。
将24只大鼠随机分为3个实验组:高脂饮食+清洁空气组、高脂饮食+生理盐水+粉尘组和高脂饮食+没食子酸+粉尘组。动物每隔一天暴露于清洁空气/粉尘中6周。在实验结束时,将大鼠麻醉并采集样本以进行分子、生物医学和组织病理学评估。
在高脂饮食条件下,粉尘暴露诱导大鼠出现NAFLD特征。粉尘暴露和高脂饮食扰乱了肝酶和血脂水平。粉尘暴露和高脂饮食增加了肝脏丙二醛水平、 、 、 、 和miR122以及miR34a的mRNA表达。粉尘+高脂饮食还降低了肝脏总抗氧化能力水平。用没食子酸预处理改善了高脂饮食+没食子酸+粉尘组中几乎所有研究的变量。
本研究表明,6周的高脂饮食和粉尘暴露通过诱导氧化应激在Wistar大鼠中诱发了NAFLD。氧化应激通过激活炎症途径导致了NAFLD特征。没食子酸预处理通过抑制氧化应激,有效保护肝功能免受高脂饮食+粉尘诱导的炎症影响。