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Usman Sabir,1 Hafiz Muhammad Irfan,1 Alamgeer,2 Aman Ullah,3 Yusuf S Althobaiti,4,5 Mulazim Hussain Asim1 1Department of Pharmacology, College of Pharmacy, University of Sargodha, Sargodha, Punjab, Pakistan; 2Punjab University College of Pharmacy, University of the Punjab, Lahore, Punjab, Pakistan; 3College of Pharmaceutical Sciences, Shifa Tameer-e-Millat University, Islamabad, Pakistan; 4Department of Pharmacology and Toxicology, College of Pharmacy, Taif University, Taif, Saudi Arabia; 5Addiction and Neuroscience Research Unit, Taif University, Taif, Saudi ArabiaCorrespondence: Hafiz Muhammad Irfan, Department of Pharmacology, College of Pharmacy, University of Sargodha, Sargodha, 40100, Punjab, Pakistan, Tel +92 3334673193, Email muhammad.irfan@uos.edu.pk Yusuf S Althobaiti, Department of Pharmacology and Toxicology, College of Pharmacy, Taif University, P.O. Box 11099, Taif, 21944, Saudi Arabia, Email ys.althobaiti@tu.edu.saIntroduction: Non-alcoholic fatty liver disease (NAFLD) is intimately linked to hepatic steatosis, inflammation, insulin resistance (IR), oxidative stress (OS), and ballooning. A high fat diet (HFD) is considered a major etiological factor that primarily covers the numerous features of NAFLD.Methods: The present study aimed to evaluate the protective effect of safranal on hepatic steatosis, OS, liver index, IR index, liver function enzymes, plasma lipids, TNF-α, malondialdehyde (MDA), advanced oxidation protein products (AOPPs) and nitrite (NO2–) levels in a NAFLD rat model fed with a HFD for 12 weeks. The ELISA kits were used to measure TNF-α and insulin in serum and plasma, respectively.Results: HFD significantly induced hepatic steatosis, OS, IR, liver, and oxidative enzyme elevation and inflammation in experimental animals. Rats treated with safranal in ascending order of doses 250 and 500 mg/kg orally for 4-weeks showed a reduction in hepatic lipid’s accumulation, liver index, hepatic enzymes, collagen, hepatic oxidonitrative stress markers (like AOPP, MDA and NO2–), and raised the levels of catalase (CAT) and superoxide dismutase (SOD) enzymes. Glutathione system components, namely glutathione (GSH), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) levels were also restored in the safranal-treated groups. The reduction in serum TNF-α and IR provided further support to the anti-NAFLD effect of safranal. Moreover, the histopathological images indicated reverse of NAFLD activity score (NAS) through mild fatty degeneration, ballooning and inflammation in hepatocytes of treated groups.Conclusion: Findings of blood and tissue analysis concluded that safranal can be a good choice in the management and cure of NAFLD.Graphical Abstract: Keywords: non-alcoholic fatty liver disease, inflammation, insulin resistance, glutathione, safranal |
