China Pharmaceutical University, Nanjing, China.
Chem Biol Interact. 2010 Apr 29;185(2):94-100. doi: 10.1016/j.cbi.2010.03.013. Epub 2010 Mar 12.
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 CCl(4)-induced L02 cells viability loss, alanine transaminase (ALT) leakage and morphological changes. C-PC also showed the following positive effects: prevent the CCl(4)-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 CCl(4)-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 CCl(4)-induced MDA formation and GSH depletion; prevent SOD and glutathione peroxidase (GSH-Px) activity; and prevent the elevation of transforming growth factor-beta1 (TGF-beta1) and hepatocyte growth factor (HGF) mRNAs. Both the in vitro and in vivo results suggested that C-PC was useful in protecting against CCl(4)-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 CCl(4). In addition, C-PC may be able to block inflammatory infiltration through its anti-inflammatory activities by inhibiting TGF-beta1 and HGF expression.
本研究旨在探讨 C-藻蓝蛋白(C-PC)对四氯化碳诱导的体外和体内肝细胞损伤的肝保护活性。在体外研究中,使用人肝细胞系 L02。C-PC 显示出逆转 CCl(4)诱导的 L02 细胞活力丧失、丙氨酸转氨酶(ALT)漏出和形态变化的能力。C-PC 还显示出以下积极作用:预防 CCl(4)诱导的细胞内活性氧(ROS)和丙二醛(MDA)过度产生;预防超氧化物歧化酶(SOD)活性的变化;并降低谷胱甘肽(GSH)水平。在体内,C-PC 显示出降低 CCl(4)诱导的小鼠肝损伤血清 ALT 和天冬氨酸转氨酶(AST)水平的能力。组织学观察结果支持血清酶测定的结果。C-PC 还显示出以下对小鼠肝脏的作用:预防 CCl(4)诱导的 MDA 形成和 GSH 耗竭;预防 SOD 和谷胱甘肽过氧化物酶(GSH-Px)活性;并预防转化生长因子-β1(TGF-β1)和肝细胞生长因子(HGF)mRNA 的升高。体外和体内结果均表明,C-PC 可有效预防 CCl(4)诱导的肝细胞损伤。其机制之一可能是通过 C-PC 的清除能力,保护肝细胞免受 CCl(4)诱导的自由基损伤。此外,C-PC 可能通过抑制 TGF-β1 和 HGF 的表达来阻断炎症浸润,从而发挥抗炎作用。