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Effect of ulinastatin on hepatic ischemia-reperfusion injury in rats

Journal of Pharmaceutical Analysis 2009年第4期21卷 246-248,266页

作者： Mao Ma1,Zhen-hua Ma2,Xiao-lin Wang1 1.Department of Geriatric Surgery,the First Affiliated Hospital,Medical School of Xi’an Jiaotong University,Xi’an 710061 2.Department of Hepatobiliary Surgery,the First Affiliated Hospital,Medical School of Xi’an Jiaotong University,Xi’an 710061,China Department of Geriatric Surgery First Affiliated Hospital Medical School of Xi'an Jiaotong University Xi'an 710061 China Department of Hepatobiliary Surgery First Affiliated Hospital Medical School of Xi'an Jiaotong University Xi'an 710061 China

Objective To investigate the effect of ulinastatin(UTI)on hepatic ischemia-reperfusion injury in rats.Methods Totally 24 adult Sprague-Dawley rats were randomly divided into 3 groups:sham-operated control group(SO group),ischemia-reperfusion group(I/R group)and ulinastatin group(UTI group).Liver in I/R group underwent 1 h of reperfusion after 30 min of ischemia.In UTI group,UTI(2×104 U/kg)was administered to rats 30 min before modeling.The levels of alanine aminotransferase,aspartate aminotransferase and tumor necrosis factor-alpha(TNF-α)in serum were measured and the levels of nitric oxide and malondialdehyde in liver were determined.The histological changes of liver were observed.Results The levels of alanine aminotransferase,aspartate aminotransferase and TNF-α in serum were significantly increased in I/R group compared with those in UTI group(Poxyradical,and ameliorate microcirculatory dysfunction in rats with hepatic ischemia-reperfusion injury.

关键词： liver ischemia-reperfusion injury ulinastatin tumor necrosis factor-alpha oxyradical microcirculatory dysfunction

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Design,synthesis and the mechanism of anti-atherosclerosis of The novel Tetramethylpyrazine derivatives

Design,synthesis and the mechanism of anti-atherosclerosis o...

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华东六省一市生物化学与分子生物学会2008年学术交流会

作者： Cui Lei~(1)) Ding Qian~(1)) Wang Shou-xun~(1)) Liu Xin yong~(2)*) (~(1))Weifang Medical College,Weifang 261053,~(2))School of Pharmaceutical Sciences, Shandong University Ji-nan 25000)

Tetramethylpyrazine(TMP),the active ingredients of Chinese traditional medicine Chuanxiong with effect promoting blood flow,has been widely used in clinical for treatment of atherosclerosis.However,pharmacokinetics study show that TMP has low bioavailability,rapid metabolism and short half-life(T=2.89 h).The accumulated toxicity often appeared in the patients for keep an effective plasma concentration by the frequent administration. Structure-activity relationship studies indicated that pyrazine ring in the molecule of TMP might largely be the determinant of its pharmacodynamies,while the 4 substituted groups might primarily govern its pharmaookinetics and toxicity.Therefore,it is significance to design and synthesize the new TMP derivatives with high potency and high bioavailability. The endothelial cells injury is not only the initiating factor of atherosclerosis,but also has an important role in the development of atherosclerosis-related diseases.So the protection of vascular endothelial cells injury is a necessary means for the treatment of atherosclerosis.It’s generally believed that the free radicals production and calcium overload of endothelial cells is positively related to the cell injury.In order to obtain the agents which have the effects on eliminating free radicals and reducing intraoellular calcium load,we designed,synthesized some TMP derivatives such as double esters,Sehiff bases,lactam,in which active groups and pharmacophores were introduced to the methyl groups of TMP.Anti-atherosclerotic activities and mechanisms of these new compounds were further studied and found some compounds exhibit better pharmacological activities than TMP by the tests of eliminating free radicals and reducing intracellular calcium load.The results provide good information for further investigation and development of the new generation of TMP drugs.

关键词： Tetramethylpyrazine（TMP） TMP derivatives atherosclerosis endothelial cells oxyradical calcium overload

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