Gallic acid treats dust-induced NAFLD in rats by improving the liver’s anti-oxidant capacity and inhibiting ROS/NFκβ/TNFα inflammatory pathway

سال انتشار: 1400
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 259

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شناسه ملی سند علمی:

JR_IJBMS-24-2_015

تاریخ نمایه سازی: 19 دی 1399

چکیده مقاله:

Objective(s): The burden of disease and death related to environmental pollution is becoming a major public health challenge, especially in developing countries. This study was designed to investigate the effect of dust exposure on liver function and its structure in rats. Gallic acid (GA) as a potent anti-oxidant was also used to treat NAFLD in rats exposed to dust. Materials and Methods: Twenty-four rats were randomly assigned into 3 groups: CA, Dust+N/S (after stopping dust exposure, rats received normal saline as vehicle, 1 ml, orally for 14 consecutive days), and Dust+GA (after stopping dust exposure, rats received GA at 100 mg/kg, orally for 14 consecutive days). Rats were exposed to CA/ dust for 6 weeks on alternate days. At the end of experiments, rats were anesthetized, their blood samples and liver sections were taken to perform molecular, biomedical and histopathological evaluations.Results: Dust exposure induced NAFLD features in rats. It increased the serum levels of liver enzymes, LDL, TG, cholesterol, MDA, and mRNA expression of NFκβ, TNFα, IL-6, HO1, and miRs [122 and 34a], while decreasing serum levels of HDL and liver TAC. Treatment with GA improved liver enzymes, serum levels of miRs, TG, expression of NFκβ, TNFα, IL-6, Nrf2, and HO1 and liver MDA and TAC levels, while it could not improve HDL, LDL, and cholesterol.Conclusion: This study showed dust exposure induced NAFLD in Wistar rats through inducing oxidative stress. Oxidative stress through activating the inflammatory pathways caused NAFLD features. Gallic acid treatment by inhibiting oxidative stress effectively protected liver function against dust induced inflammation.

کلیدواژه ها:

Dust Gallic acid NAFLD Nrf2 Rat TNF ، α

نویسندگان

Hafseh Fanaei

Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Seyyed Ali Mard

Persian Gulf’s Physiology Research Center (PRC), Department of Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Alireza Sarkaki

Persian Gulf’s Physiology Research Center (PRC), Department of Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Gholamreza Godarzi

Air Pollution and Respiratory Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Environmental Technologies Research Center (ETRC), Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Layasadat Khorsandi

Cellular and Molecular Research Center, Department of Anatomical Science, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

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