Liu Mei, Xu Wei-hong, Duan Zhong-ping, Chen Yu, Zheng Su-jun, Liu Xu-hua, Zhao Jun, Ding Mei, Lv Zhi-wu
Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2010 Sep;30(9):2165-8.
To observe the effects of neurotrophin 3(NT-3)on interdigestive migrating motor complex (MMC) in rats with D-galactosamine induced acute liver injury.
Twenty-four specific pathogen-free purebred rats were equally randomized into control and acute liver injury groups. The control group was injected with equal volume of normal saline via tail vein. Acute liver injury model of the rats was induced by D-galactosamine injection via the tail vein in the acute liver injury group. And the indexes of interdigestive MMC before and after NT-3 injection were recorded by a polygraph and analyzed in model group. The serum NT-3 concentration was assayed in the two groups.
There were no significant changes of gastrointestinal MMC cycle and jejunal phase I MMC after NT-3 injection. Compared with the acute liver injury rats before NT-3 injection , the antral phases I, III and IV MMC were significantly prolonged [(577.44 ± 248.60)s vs (343.58 ± 227.30) s, (80.94 ± 21.15) s vs (24.76 ± 7.41) s, (405.69 ± 131.34) s vs (191.67 ± 128.15) s, P < 0.05] and the phase II MMC was shortened [ (883.94 ± 488.50) s vs (1519.00 ± 831.14) s, P < 0.05] in the acute liver injury group. The duodenal phases I, III and IV MMC were significantly prolonged [ (557.63 ± 335.14) s vs (309.46 ± 220.22) s,(75.91 ± 15.75) s vs (31.15 ± 13.67) s, (423.38 ± 135.22) s vs (209.77 ± 123.83) s, P < 0.05] and MMC II phase was shortened [ (748.81 ± 579.69) s vs (1535.86 ± 930.50) s, P < 0.05] in the acute liver injury rats. In addition, the jejunal MMC III and MMC IV phase was significantly prolonged [ (86.58 ± 23.40) s vs (31.41 ± 16.09) s,(385.18 ± 110.02) s vs (220.59 ± 159.30) s, P < 0.05] and phase II MMC was shortened [ (876.89 ± 652.01) s vs (1870.89 ± 1010.35) s, P < 0.05 ] in the acute liver injury rats. The serum NT-3 level was significantly higher in model group than in control group.
NT-3 could enhance the gastrointestinal motility in acute liver injury rats.
观察神经营养因子3（NT-3）对D-氨基半乳糖诱导的急性肝损伤大鼠消化间期移行性复合运动（MMC）的影响。
将24只无特定病原体的纯种大鼠随机分为对照组和急性肝损伤组，每组12只。对照组经尾静脉注射等体积的生理盐水，急性肝损伤组经尾静脉注射D-氨基半乳糖诱导大鼠急性肝损伤模型。采用多导记录仪记录模型组大鼠注射NT-3前后的消化间期MMC指标并进行分析，同时检测两组大鼠血清NT-3浓度。
注射NT-3后，胃肠MMC周期和空肠MMCⅠ相无明显变化。急性肝损伤组注射NT-3前与注射后比较，胃窦MMCⅠ、Ⅲ、Ⅳ相明显延长[（577.44±248.60）s比（343.58±227.30）s，（80.94±21.15）s比（24.76±7.41）s，（405.69±131.34）s比（191.67±128.15）s，P<0.05]，MMCⅡ相缩短[（883.94±488.50）s比（1519.00±831.14）s，P<0.05]；十二指肠MMCⅠ、Ⅲ、Ⅳ相明显延长[（557.63±335.14）s比（309.46±220.22）s，（75.91±15.75）s比（31.15±13.67）s，（423.38±135.22）s比（209.77±123.83）s, P<0.05]，MMCⅡ相缩短[（748.81±579.69）s比（1535.86±930.50）s，P<0.05]；空肠MMCⅢ、Ⅳ相明显延长[（86.58±23.40）s比（31.41±16.09）s，（385.18±110.02）s比（220.59±159.30）s，P<0.05]，MMCⅡ相缩短[（876.89±652.01）s比（1870.89±1010.35）s，P<0.05]。模型组血清NT-3水平明显高于对照组。
NT-3可增强急性肝损伤大鼠的胃肠动力。
