Zhang Feng, Tong Liquan, Qiao Haiquan, Dong Xuesong, Qiao Guojun, Jiang Hongchi, Sun Xueying
Department of General Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, China.
J Surg Res. 2008 Sep;149(1):101-9. doi: 10.1016/j.jss.2007.12.781. Epub 2008 Jan 30.
Intestinal ischemia reperfusion (II/R) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The purpose of this study was to investigate whether taurine, an anti-oxidative, anti-inflammatory, and anti-apoptotic agent, could attenuate multiple organ injury induced by II/R.
Taurine was intravenously injected to Wistar rats 30 min before II/R; physiological saline and sham operation served as controls. II/R was produced by occlusion of superior mesenteric artery for 60 min. Rats were randomly sacrificed 1.5, 3, 12, and 36 h after II/R; blood samples were collected for assessing alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine (Cr), and tumor necrosis factor-alpha (TNF-alpha), and intestines, livers, kidneys, and lungs were removed for histological examination of scoring injury severity and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling analysis. The amount of lipid peroxides (LPO) was measured in intestinal tissues, and expression of caspase-3 was detected in all of the tissues with Western blot analysis.
II/R resulted in injury to intestines as well as livers, kidneys, and lungs, evidenced by morphological alteration, increased cell apoptosis, and elevated serum levels of ALT, AST, BUN, and Cr. The damage reached peak 3 h after II/R. The intestinal LPO and serum levels of TNF-alpha were increased after II/R. Pre-administration of taurine significantly attenuated multiple organ injury as the histological score, apoptosis index, LPO, and levels of ALT, AST, BUN, Cr, and TNF-alpha were significantly lower compared with saline controls.
Taurine attenuates multiple organ injury induced by II/R. Although the mechanism needs further investigation, taurine inhibits production of intestinal LPO, release of TNF-alpha, cell apoptosis, and expression of caspase-3.
肠缺血再灌注（II/R）是一种与同时发生的多器官功能障碍相关的严重临床病症。本研究的目的是调查牛磺酸，一种具有抗氧化、抗炎和抗凋亡作用的药物，是否能减轻II/R诱导的多器官损伤。
在II/R前30分钟给Wistar大鼠静脉注射牛磺酸；生理盐水和假手术作为对照。通过肠系膜上动脉闭塞60分钟来产生II/R。在II/R后1.5、3、12和36小时随机处死大鼠；采集血样以评估丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、血尿素氮（BUN）、肌酐（Cr）和肿瘤坏死因子-α（TNF-α），并取出肠、肝、肾和肺进行组织学检查以评分损伤严重程度和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记分析。在肠组织中测量脂质过氧化物（LPO）的量，并通过蛋白质印迹分析在所有组织中检测caspase-3的表达。
II/R导致肠以及肝、肾和肺损伤，表现为形态学改变、细胞凋亡增加以及血清ALT、AST、BUN和Cr水平升高。损伤在II/R后3小时达到峰值。II/R后肠LPO和血清TNF-α水平升高。预先给予牛磺酸可显著减轻多器官损伤，因为与生理盐水对照组相比，组织学评分、凋亡指数、LPO以及ALT、AST、BUN、Cr和TNF-α水平均显著降低。
牛磺酸可减轻II/R诱导的多器官损伤。尽管其机制需要进一步研究，但牛磺酸可抑制肠LPO的产生、TNF-α的释放、细胞凋亡以及caspase-3的表达。
