摘要
背景:左卡尼汀(LC)改善恶病质的作用已日渐受到关注。目的:探讨PPARα、PPARγ在LC改善结肠癌小鼠恶病质中的作用。方法:建立结肠癌小鼠恶病质模型,并分为LC组、左卡尼汀棕榈酸酰基转移酶(CPT)抑制剂(ILC)组、阴性对照组(NST),另设立正常对照组(NTB)。实验第19 d处死所有小鼠。测定小鼠体质量、去瘤体质量、摄食量,以全自动生化仪检测血清白蛋白、血糖、胆固醇含量,ELISA法检测血清TNF-α、IL-6含量,实时定量PCR和蛋白质印迹法分别检测肝组织PPARα、PPARγmRNA和蛋白表达。结果:与NST组、ILC组相比,LC组小鼠体质量、去瘤体质量、摄食量、血清白蛋白、血糖均显著升高(P<0.05),血清胆固醇、TNF-α、IL-6含量均显著降低(P<0.05),PPARα、PPARγmRNA和蛋白表达均显著升高(P<0.05)。结论:PPARα、PPARγ可能参与结肠癌小鼠恶病质的发生;LC可能通过PPARα、PPARγ相关肝脏脂质代谢信号通路来改善肿瘤恶病质。
Background： The role of L-carnitine （LC） in ameliorating cachexia has been focused on increasingly in recent years. Aims： To investigate the role of PPARα, PPARy in ameliorating colonic cancer cachexia by LC in mice. Methods： Colonic cancer cachexia model was established in mice. Mice were randomly divided into tumor bearing group treated with LC （ LC group） , tumor bearing group treated with LC palmitoyl-transferase （CFF） inhibitor （ ILC group） , tumor bearing group treated with normal saline （ NST group） , and non-tumor bearing mice were served as normal controls （ NTB group）. On the 19＇h day, all the mice were sacrificed. Body weight, tumor-free body weight, food consumption were measured. Serum levels of albumin, glucose, cholesterol were determined by automatic biochemistry analyzer. ELISA assay was used to detect serum levels of TNF-α and IL-6. mRNA and protein expressions of PPARα, PPARy in liver tissue were determined by real time quantitive PCR and Western blotting, respectively. Results： Compared with NST group and ILC group, body weight, tumor-free body weight, food consumption, serum levels of albumin and glucose in LC group were significantly increased （P 〈 0. 05 ）, serum levels of cholesterol, TNF-α, IL-6 were significantly decreased （ P 〈 0. 05 ）, mRNA and protein expressions of PPARα, PPARy were significantly increased （ P 〈 0.05 ）. Conclusions ： PPARα, PPARy may be involved in the formation of colonic cancer cachexia in mice. The ameliorating of cancer cachexia by LC may be related to the regulating of PPARα-, PPARy-related signaling pathway of hepatic lipid metabolism.
出处
《胃肠病学》
2013年第5期266-270,共5页
Chinese Journal of Gastroenterology
基金
上海市闸北区科委重点科研课题(2012ZD04)资助
