永生化肝细胞微囊化移植治疗大鼠肝豆状核变性

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摘要目的：观察微囊化 HepG2 细胞腹腔移植治疗肝豆状核变性（HLD）模型大鼠的疗效。方法：3 月龄 Wistar 雄性大鼠 120 只随机分为HLD模型组、裸 HepG2 细胞腹腔移植组和微囊化 HepG2 细胞移植组，采用铜负荷饮食法制作大鼠 HLD 模型。根据移植后标本采集时间分设 3 d、7 d、14 d、21 d、28 d 5个时间点，每时间点 8 只大鼠; 另取 8 只大鼠设为空白对照组。测定血清ALT、AST、白蛋白水平及血清铜、肝铜含量。结果：模型组、裸 HepG2 细胞腹腔移植组、微囊化 HepG2 细胞移植组大鼠各时间点 ALT、AST、血清铜、肝铜水平均较空白对照组升高（P<0.05），合成白蛋白水平明显下降（除外微囊化 HepG2 细胞移植组28 d与空白组比较差异无统计学意义）。在大部分时间点裸HepG2细胞腹腔移植组、微囊化HepG2细胞移植组大鼠 ALT、AST、血清铜、肝铜值水平较模型组下降（P<0.05），而白蛋白水平则较模型组增加（P<0.05）。7~14 d后微囊化 HepG2 细胞移植组大鼠 ALT、AST、血清铜、肝铜水平较裸 HepG2 细胞腹腔移植组明显下降（P<0.05），而白蛋白则于 14 d后高于裸 HepG2细胞腹腔移植组。结论：HepG2 细胞微囊化腹腔移植可明显减轻 HLD 大鼠的肝损害，减少肝铜沉积，加速血清铜的代谢，可成为一种细胞移植治疗 HLD 的新方法。［中国当代儿科杂志，2010，12(12)：959-962］

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	林海龙
	陈洁
	黄乐听
	陈益平

关键词 ：永生化肝细胞, 移植, 微囊化, 肝豆状核变性, 大鼠

Abstract：OBJECTIVE: To evaluate the efficacy of intraperitoneal transplantation of microencapsulated HepG2 cells in rats with hepatolenticular degeneration (HLD). METHODS: HLD was induced by copper-overloaded diet with forage containing 1 g/kg copper sulfate and water with 0.185% copper sulfate for 12 weeks in rats. One hundred and twenty three-month-old male Wistar rats were randomly intraperitoneal injected with normal saline (NS), microencapsulated HepG2 cells or non-microencapsulated HepG2 cells 9 weeks after copper-overloaded diet. Blood or liver samples were obtained at five time points: 3, 7, 14, 21 and 28 days after transplantation (n=8). The other 8 rats receiving normal diet were used as the control group. Serum levels of ALT, AST, albumin and Cu and liver Cu contents were measured. RESULTS: Serum ALT, AST and Cu levels and liver Cu contents in the NS-treated HLD, microencapsulated HepG2 cells and non-microencapsulated HepG2 cells transplantation groups increased significantly at all time points, in contrast, serum albumin levels decreased significantly in the NS-treated HLD and non-microencapsulated HepG2 cells transplantation groups compared with those in the control group at all time points (P<0.05), but serum albumin levels in the microencapsulated HepG2 cells transplantation restored to the level of the control group 28 days after transplantation. Serum ALT, AST and Cu levels and liver Cu contents in the microencapsulated HepG2 cells and non-microencapsulated HepG2 cells transplantation groups were significantly lower, in contrast, albumin levels were higher than those in the NS-treated HLD group on almost time points (P<0.05). Serum levels of ALT, AST and Cu and liver Cu contents in the microencapsulated HepG2 cells transplantation group decreased 7 or 14 days after transplantation, while serum albumin levels increased significantly 14 days after transplantation compared with those in the non-microencapsulated HepG2 cells transplantation group (P<0.05). CONCLUSIONS: Intraperitoneal transplantation of microencapsulated HepG2 cells can relieve hepatic damage, reduce serum and liver Cu levels, and improve copper metabolism, therefore it is promising for the treatment of HLD.［Chin J Contemp Pediatr, 2010, 12 (12):959-962］

Key words： HepG2 cell Transplantation Microencapsulation Hepatolenticular degeneration Rats

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R-33

引用本文:

林海龙,陈洁,黄乐听等. 永生化肝细胞微囊化移植治疗大鼠肝豆状核变性[J]. 中国当代儿科杂志, 2010, 12(12): 959-962.

LIN Hai-Long,CHEN Jie,HUANG Le-Ting et al. Efficacy of microencapsulated HepG2 cells transplantation in rats with hepatolenticular degeneration[J]. CJCP, 2010, 12(12): 959-962.

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http://www.zgddek.com/CN/ 或 http://www.zgddek.com/CN/Y2010/V12/I12/959

	［1］Schilsky ML. Wilson disease:current status and the future. Biochimie［J］, 2009, 91(10): 1278-1281.
	［2］Mei J, Sgroi A, Mai G, Baertschiger R, Gonelle-Gispert C, Serre-Beinier V, et al. Improved survival of fulminant liver failure by transplantation of microencapsulated cryopreserved porcine hepatocytes in mice［J］. Cell Transplant, 2009, 18(1): 101-110.
	［3］Kang IK, Moon JS, Jeon HM, Meng W, Kim YI, Hwang YJ, et al. Morphology and metabolism of Ba-alginate encapsulated hepatocytes with galactosylated poly(allyl amine) and poly(vinyl alcohol) as extracellular matrices［J］. J Mater Sci Mater Med, 2005,16(6): 533-539.
	［4］Pulverer BJ, Kyriakis JM, Avruch J, Nikolakaki E, Woodgett JR. Phosphorylation of c-jun mediated by MAP kinases［J］. Nature, 199l, 353(6345): 670-674.
	［5］Malhi H, Irani AN, Volenherg I, Schilsky ML, Gupta S. Early cell transplantation in LEC rats modeling Wilson's disease eliminates hepatic copper with reversa of liver disease［J］. Gastroenterology, 2002, 122(2): 438-447.
	［6］Orive G, Hernández RM, Rodríguez Gascón A, Calafiore R, Chang TM, de Vos P, et al. History, challenges and perspectives of cell microencapsulation［J］. Trends Biotechnol, 2004, 22(2): 87-92.
	［7］Ahmad TA, Fujioka H, Eguchi S, Yanaga K, Kamohara Y, Furui J, et al. Long-term effect of hepatocyte transplantation on fulminant hepatic failure in rats［J］. Hepatogastroenterology, 2003, 50(50): 467-471.
	［8］Carruba G. Aromatase in nontumoral and malignant human liver tissues and cells［J］. Ann N Y Acad Sci, 2009, 1155:187-193.
	［9］Suzuki KT, Kanno S, Misawa S, Aoki Y. Copper metabolism leading to and following acute hepatitis in LEC rats［J］. Toxicology, 1995, 97(1-3): 81-92.
	［10］Friendman LS, Yarze JC. Zinc in the Treatment of Wilson's disease: how it works［J］. Gastroenterology, 1993, 104(5): 1566-1568.