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Effect of oxytocin on gastric ischemia-reperfusion injury in rats

ZHANG Wenwen, ZHANG Jianfu, ZHANG Yongmei, XU Ming

《医学前沿（英文）》 2007年第1卷第4期页码 433-437 doi: 10.1007/s11684-007-0085-4

摘要： The effect of peripherally administered oxytocin (OT) on gastric ischemia-reperfusion injury (GI-RI) and its possible mechanism were investigated. The Sprague-Dawley (SD) rats were randomly divided into different treatment groups ( = 6). The animal GI-RI model was established by clamping the celiac artery for 30 min to induce ischemia and then released to allow reperfusion for 1 h, and the degree of GI-RI was assessed by scoring the gastric mucosal damage index (GMDI), the gastric fluid output, gastric fluid output, gastric acidity were measured and the surgical preparations of vagotomy and sympathectomy were used to investigate the possible mechanism of OT on GI-RI. The results were as follows. Compared with the control group (NS plus GI-R only, GMDI 121.33±10.40, = 6), the intra peritoneal (ip) administration of oxytocin (20, 100 μg/0.5 mL) obviously attenuated GI-RI (<0.05), GMDI were 82.33±14.26, 53.5±5.58 respectively ( = 6); the gastric fluid output and the gastric acidity (evaluated by pH) of the control group were (430.17±87.36) μL, 1.55±0.25 ( = 6), and those of the OT group were (102.45±48.00) μL, 2.65±0.40 ( = 6) res pectively; differences had statistical significance (<0.01). The effect of oxytocin was reversed by atosiban, a selective oxytocin receptor antagonist. The GMDI of the group given atosiban 10 min before OT was 138.17±24.06 ( = 6), which had no significant difference with the control group. Oxytocin further attenuated GI-RI after vagotomy and sympathectomy (GMDI 6.83±8.89, 29.67±5.54, = 6), compared with the GI-R group and the oxytocin group (<0.01). These results indicated that the oxytocin could significantly protect gastric mucosal against injury induced by ischemia-reperfusion, and the oxytocin receptor was involved. This effect of oxytocin may be mediated through the vagus and sympathetic nerve, and then lead to the reduction of gastric juice output and the depression of gastric acidity.

关键词： control significant difference surgical statistical significance Sprague-Dawley

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Effects of RNA interference targeting angiotensin 1a receptor on blood pressure and cardiac hypertrophy of rats with renovascular hypertension

ZHANG Jingqun, SUN Honglei, MA Yexin, WANG Daowen

《医学前沿（英文）》 2008年第2卷第1期页码 19-24 doi: 10.1007/s11684-008-0005-2

摘要： The aim of this study is to investigate the effects of RNA interference (RNAi) targeting angiotensin 1a receptor (AT1a) on blood pressure and cardiac hypertrophy of rats with renovascular hypertension. Two RNAi plasmids, pAT1a-shRNA1 and pAT1a-shRNA2 each carrying a U6 promoter and an AT1a-specific shRNA-coding template sequence corresponding to the sites 928–946, 978–996 of the mRNA transcript, and a control plasmid pCon carrying a nonspecific shRNA-coding sequence were constructed. Thirty Sprague – Dawley rats with renovascular hypertension (2-kidney 1-clip) were randomly divided into 5 equal groups: Control group (without any intervention), pAT1a-shRNA1, pAT1a-shRNA2, pCon groups (with injection of the corresponding plasmid 4 mg/kg respectively into the tail vein), and valsartan group (30 mg/kg·d by gavage). Three weeks after drug administration, pAT1a-shRNA1, pAT1a-shRNA2 and valsartan respectively resulted in decrease of the tail blood pressure by (15.1 ± 5.4), (16.4 ± 8.4) and (30.6 ± 18.2) mmHg. However, the tail blood pressure increased further by about 25 mmHg in both of pCon and control groups. The carotid artery pressures of pAT1a-shRNA1, pAT1a-shRNA2 and valsartan groups were all significantly lower than those of the control and pCon groups. The ratio of left ventricle weight to body weight (LV/BW) of the rats in pAT1a-shRNA1, pAT1a-shRNA2, and valsartan groups decreased significantly than in the control group ( < 0.01), similar to those of the normal SD rats( > 0.05). Histopathological examination showed that the myocardiocytes were significantly hypertrophic and the basal membrane of the aorta was significantly thickened in the control group and such changes were alleviated in the pAT1a-shRNA1, pAT1a-shRNA2 and valsartan groups. Compared with the control group, pAT1a-shRNA1 and pAT1a-shRNA2 groups had lowered expression of AT1 receptor (in the myocardium and the thoracic aorta (all < 0.01); however, there were no significant differences in expression levels of AT1 receptor in valsartan and the control groups ( > 0.05). We conclude that RNAi targeting AT1a receptor inhibits the development of renovascular hypertension and the accompanying cardiac hypertrophy. RNAi technology may become a new strategy of gene therapy for hypertension.

关键词： therapy Sprague administration cardiac hypertrophy valsartan