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Year : 2017  |  Volume : 49  |  Issue : 4  |  Page : 282-289

Resveratrol prevents liver fibrosis via two possible pathways: Modulation of alpha fetoprotein transcriptional levels and normalization of protein kinase C responses

1 Department of Pharmacology, Division of Medical, National Research Center, Giza, Cairo, Egypt; Department of Microbiology and Immunology, College of Medicine, UIC, IL, USA
2 Department of Pharmacology, Division of Medical, National Research Center, Giza, Cairo, Egypt
3 Department of Pathology, Faculty of Veterinary Medicine, Cairo University, Giza, Cairo, Egypt
4 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Giza, Cairo, Egypt

Correspondence Address:
Alyaa Farouk Hessin
Department of Pharmacology, Division of Medical, National Research Center, 33 Bohoth St., 12622, Dokki, Giza

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijp.IJP_299_16

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OBJECTIVE: Liver fibrosis is a global health problem that causes approximately 1.4 million deaths per year. It is associated with inflammation, oxidative stress, necrosis and ends with cirrhosis, liver cancer, or liver failure. Therefore, the present study was constructed to investigate the protective effect of resveratrol (RVT) on liver fibrosis, focusing on the possible involvement of alpha 1-fetoprotein and protein kinase C signaling. MATERIALS AND METHODS: Rats received thioacetamide (TAA) (200 mg/kg, intraperitoneal) twice weekly, for 4 successive weeks to induce liver fibrosis. RVT (30 mg/kg, per os) and vehicle were administered orally for 1 month before and another month during TAA intoxication. Body weights and mortality rate were assessed during the experiment. Liver functions and protein concentration were determined in serum, while liver tissues were analyzed for oxidative and fibrotic biomarkers. Moreover, histological examinations were performed to liver biopsies. RESULTS: RVT prevented the debility of TAA; liver functions including alanine aminotransferase, aspartate aminotransferase, bilirubin, and albumin were also protected. RVT prevented TAA oxidative stress, and normal liver contents of malondialdehyde and reduced glutathione were markedly preserved. In addition, RVT abolished the stimulant effect of TAA to fibrosis markers and conserved normal liver contents of nuclear factor kappa B, hydroxyproline, and alpha fetoprotein. Histological examinations indicated normal liver architecture in RVT-administered rats as compared to their TAA-administered peers. CONCLUSION: RVT was able to enhance liver functions, prevent oxidative stress, and eliminate liver fibrosis. Hence, the present data highlight the therapeutic potential of RVT as a protective agent against liver fibrosis.


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