Anti-hepatofibrotic effect of ethyl acetate fraction of Bombax costatum Pellgr.EtVuillet stem bark against CCl4-induced liver fibrosis in mice
محورهای موضوعی : مجله گیاهان دارویی
نوحو محمد
1
(گروه داروسازی و درمان ، دانشکده علوم دارویی ، دانشگاه Ahmadu Bello ، زاریا ، نیجریه.)
یوسف آناکا
2
(گروه داروسازی و درمان ، دانشکده علوم دارویی ، دانشگاه Ahmadu Bello ، زاریا ، نیجریه.)
علیو موسی
3
(گروه شیمی دارویی و دارویی ، دانشگاه Ahmadu Bello Zaria ، نیجریه ؛)
جمیلو یان
4
(گروه داروسازی و درمان ، دانشکده علوم دارویی ، دانشگاه Ahmadu Bello ، زاریا ، نیجریه.)
کلید واژه: Mice, Carbon tetrachloride, Bombax costatum, Ethyl acetate, Fibrosis,
چکیده مقاله :
Background & Aim: Bombax costatum stem bark is traditionally used in treatment of liver diseases but the anti-hepatofibrotic effect of its ethyl acetate fraction has not been scientifically evaluated. This study aimed to evaluate the anti-hepatofibrotic effect of ethyl acetate fraction of B. costatum stem bark (EAB) against carbon tetrachloride (CCl4) induced liver fibrosis in mice.Experimental: Normal control group were administered olive oil while mice in the remaining groups received 0.4 ml/kg of CCl4 twice weekly for 6 weeks. Mice in treatment groups received EAB once daily orally for the next 2 weeks at doses of 31.25, 62.5 and 125 mg/kg body weight, respectively. Mice in standard control group received silymarin (100 mg/kg) daily for the next 2 weeks. Mice in toxic control group were sacrificed 72 hours after the last dose of CCl4 while mice in CCl4 control group were observed for the next 2 weeks for spontaneous resolution of fibrosis. Effect of treatment on tumor necrosis factor-α (TNFα), transforming growth factor-β1 (TGFβ1), malondialdehyde (MDA), reduced glutathione (GSH) levels and liver histopathology were evaluated.Results: CCl4 intoxication caused significant (p < 0.05) elevation in TNFα, TGFβ1 and MDA with associated collagen deposition in the liver. Administration of EAB significantly (p < 0.05) decreased the level of TNFα, TGFβ1 as well as MDA and increased GSH level compared to CCl4 toxic group.Recommended applications/industries: Ethyl acetate fraction of B. costatum possesses anti-hepatofibrotic, anti-inflammatory and in vivo anti-oxidant activities against CCl4 induced liver fibrosis.
Background & Aim: Bombax costatum stem bark is traditionally used in treatment of liver diseases but the anti-hepatofibrotic effect of its ethyl acetate fraction has not been scientifically evaluated. This study aimed to evaluate the anti-hepatofibrotic effect of ethyl acetate fraction of B. costatum stem bark (EAB) against carbon tetrachloride (CCl4) induced liver fibrosis in mice. Experimental: Normal control group were administered olive oil while mice in the remaining groups received 0.4 ml/kg of CCl4 twice weekly for 6 weeks. Mice in treatment groups received EAB once daily orally for the next 2 weeks at doses of 31.25, 62.5 and 125 mg/kg body weight, respectively. Mice in standard control group received silymarin (100 mg/kg) daily for the next 2 weeks. Mice in toxic control group were sacrificed 72 hours after the last dose of CCl4 while mice in CCl4 control group were observed for the next 2 weeks for spontaneous resolution of fibrosis. Effect of treatment on tumor necrosis factor-α (TNFα), transforming growth factor-β1 (TGFβ1), malondialdehyde (MDA), reduced glutathione (GSH) levels and liver histopathology were evaluated. Results: CCl4 intoxication caused significant (p < 0.05) elevation in TNFα, TGFβ1 and MDA with associated collagen deposition in the liver. Administration of EAB significantly (p < 0.05) decreased the level of TNFα, TGFβ1 as well as MDA and increased GSH level compared to CCl4 toxic group. Recommended applications/industries: Ethyl acetate fraction of B. costatum possesses anti-hepatofibrotic, anti-inflammatory and in vivo anti-oxidant activities against CCl4 induced liver fibrosis.
Abebi, H.E. 1974. Catalase. Methods of Enzymatic Analysis. New York Academic Press, New York.
Atawodi, S.E., Adekunle, O.O and Bala, I. 2011. Antioxidant, organ protective and ameliorative properties of methanol extract of Anogeissus leiocarpus stem bark against carbon tetrachloride-induced liver injury. International Journal of Pharmaceutical Science Research, 2(6):1443-1448.
Bataller, R. and Brenner, D.A. 2005. Liver fibrosis. Journal of Clinical Investigation, 115:209–218.
Brenner, D.A. 2009. Molecular pathogenesis of liver fibrosis. Transactions of the American Clinical and Climatological Assocociation, 120:361-368.
Chavez, E., Reyes-Gordillo, K. and Segovia, J. 2008. Resveratrol prevents fibrosis, NF-B activation and TGF-increases induced by chronic CCl4 treatment in rats. Journal of Applied Toxicology, 28(1): 35–43.
Constandinou, C., Henderson, N. and Iredale, J.P. 2005. Modeling liver fibrosis in rodents. Methods in Molecular Medicine, 117:237–250.
Dalziel, J.M. 1985. The Useful Plants of West Tropical Africa. Vol 1. Kew: Royal Botanic Gardens.
Demiroren, K., Dogan, Y., Kocamaz,H., Ozercan, I.H., Ilhan, S., Ustundag, B. and Bahcecioglu, I.H. 2014. Protective effects of L-carnitine, N-acetylcysteine and genistein in an experimental model of liver fibrosis. Clinics and Research in Hepatology and Gastroenterology, 38 (1): 63–72.
Domitrovic, R., Jacobac, H., Tomac, J. And Sain, I. 2009. Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin. Toxicology and Applied Pharmacology, 241: 311–321.
Ellman, G.L. 1959. Tissue sulfhydryl groups. Archives of Biochemistry and Biophysics, 82(1): 70-77.
Gandhi, A.P., Joshi, K.C., Jha, K., Parihar, V.S., Srivastav, D.C., Raghunadh, P. and Tripathi, R.N. 2003. Studies on alternative solvents for the extraction of oil-I soybean. International Journal of Food Science and Technology, 38(3):369-375.
Hernandez-Gea, V. and Friedman, S.L. 2011. Pathogenesis of liver fibrosis. Annual Review of Pathology, 6:425–456.
Kahkonen, M.P., Hopia, A.I.,Vuorela, H.J., Rauha, J.P., Pihlaja, K.,Kujala, T.S. and Heinonen, M. 1999. Antioxidant activity of plant extracts containing phenolic compounds. Journal of Agricultural and Food Chemistry, 47: 3954–3962.
Kling, C.E., Perkins, J.D., Carither, R.L., Donovan, D.M. and Sibulesky, L. 2017. Recent trends in liver transplantationfor alcoholic liver disease in the United States. World Journal of Hepatology, 9(36): 1315-1321.
Mohammed, N., Yaro, A.H. and Nazifi, A.B. 2018. Bombax costatum Pellegr. and Vuillet stem bark extract prevents paracetamol and carbon tetrachloride-induced liver injury in rats. Tropical Journal of Natural Product Research, 2(5): 220-226.
Morsy, M.A., Abdalla, A.M., Mahmoud, A.M., Abdelwahab, S.A. and Mahmoud, M.E. 2012. Protective effects of curcumin, α- lipoic acid, and N-acetylcysteine against carbon tetrachloride induced liver fibrosis in rats,”Journal of Physiology and Biochemistry, 68(1): 29–35.
Nanik, S., Vivian, S., Melva, L., Bantari, W.W. and Raymond, R.T. 2018. Protective effect of Phaleria macrocarpa water extract (Proliverenol) against carbon tetrachloride-induced liver fibrosis in rats: Role of TNF-α and TGF-β1. Journal of Toxicology, 1-7.
Samuele, D.M., Marco, M., Stefania, S., Chiara, R., Laura, A., Luciano, T. and Gianluca, S. 2012. Cellular and molecular mechanisms of hepatic fibrogenesis leading to liver cancer. Translational Gastrointestinal Cancer, 1:88-94.
Yang, Y.M. and Seki, E. 2015. TNFα in liver fibrosis. Current Pathobiology Reports
