Protective effect of C-phycocyanin against carbon tetrachloride-induced hepatocyte damage in vitro and in vivo |
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| Authors: | Yu Ou Shan Zheng Lin Lin Qizhou Jiang Xuegan Yang |
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| Institution: | 1. School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China;2. Department of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, Texas 77555-0615, USA;1. Graduate Program of Clinical Haematology Sciences, Department of Clinical Microscopy, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok 10330, Thailand;2. Center for Research and Development in Molecular Haematology Sciences, Department of Clinical Microscopy, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok 10330, Thailand;1. Immunotoxicology Division, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow, India;2. Department of Biochemistry, Jamia Hamdard (Hamdard University), New Delhi, India;3. Department of Neurology, University of New Mexico, Building NRF, Room: 1131a, Albuquerque 87131, USA;1. Department of Aquatic Products Technology, Faculty of Fisheries and Marine Sciences, Bogor Agricultural University, Jl. Agatis Kampus IPB Darmaga. Bogor 16680, Indonesia;2. Department of Biochemistry, Faculty of Mathematic and Natural Sciences, Bogor Agricultural University, Jl. Agatis Kampus IPB Darmaga. Bogor 16680, Indonesia;1. School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China;2. Department of Integrative Biology & Pharmacology, The University of Texas Health Science Center, Houston, USA |
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| Abstract: | This study focused on the hepatoprotective activity of C-phycocyanin (C-PC) against carbon tetrachloride-induced hepatocyte damage in vitro and in vivo. In in vitro study, human hepatocyte cell line L02 was used. C-PC showed its capability to reverse CCl4-induced L02 cells viability loss, alanine transaminase (ALT) leakage and morphological changes. C-PC also showed the following positive effects: prevent the CCl4-induced overproduction of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA); prevent changes in superoxide dismutase (SOD) activity; and reduce glutathione (GSH) level. In vivo, C-PC showed its capability to decrease serum ALT and aspartate transaminase (AST) levels in CCl4-induced liver damage in mice. The histological observations supported the results obtained from serum enzymes assays. C-PC also showed the following effects in mice liver: prevent the CCl4-induced MDA formation and GSH depletion; prevent SOD and glutathione peroxidase (GSH-Px) activity; and prevent the elevation of transforming growth factor-beta1 (TGF-β1) and hepatocyte growth factor (HGF) mRNAs. Both the in vitro and in vivo results suggested that C-PC was useful in protecting against CCl4-induced hepatocyte damage. One of the mechanisms is believed to be through C-PCs scavenging ability to protect the hepatocytes from free radicals damage induced by CCl4. In addition, C-PC may be able to block inflammatory infiltration through its anti-inflammatory activities by inhibiting TGF-β1 and HGF expression. |
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