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11.
AIM:To observe the influence of captopril on intracellular free calcium concentration ([Ca2+] i) and the involved ion channels mechanisms in cardiac myocytes of the neonatal rat undergone anoxia-reoxygenation injury.METHODS:The anoxia-reoxygenation model in cultured neonatal rat ventricular myocytes was established.Groups were divided into ① normal;② anoxia-reoxygenation;③anoxia-preconditioning (5 min anoxia+5 min reoxygenation);④ captopril preconditioning.Flou-3 /AM loading and flow cytometry technique were used to observe the [Ca2+]i,and whole-cell patch clamp technique was used to record the L-type calcium current and Na+/Ca2+ exchange current.RESULTS:① Compared to normal group,[Ca2+]i in anoxia -reoxygenation group was increased significantly (789.42±9.05 vs 414.08±37.40,P<0.01),L-type calcium current density was decreased (P<0.01),the current-voltage curve was moved up,the inactivation curve was moved left and Na+/Ca2+ exchange current was increased in anoxia-deoxygenating.② Compared to anoxia-reoxygenation group,anoxia and captopril preconditioning resulted in a significant decrease in [Ca2+]i (593.84±5.06,507.08±31.89 vs 789.42±9.05,P<0.01),and a significant increase in L-type calcium current density (P<0.01),the current-voltage curve was moved down,the inactivation curve was moved right and Na+/Ca2+ exchange current was decreased ③ Compared to normal oxygen condition,the anoxia and captopril precondition resulted in a lightly increase in [Ca2+]i (507.08±31.89 vs 414.08±37.40,P<0.05) and Na+/Ca2+ exchange current.④ Compared to anoxia-preconditioning group,captopril-preconditioning resulted in no significant difference in all the markers mentioned above.CONCLUSIONS:The anoxia-reoxygenation injury in cardiac myocytes results in [Ca2+]i abnormal increase and calcium overload by increasing Na+/Ca2+ exchange current.Late preconditioning in cardiac myocytes is triggered by transient and repeated anoxia and captopril,which slightly increases Na+/Ca2+ exchange current and [Ca2+]i and restraines the abnormal increasing of Na+/Ca2+ exchange current and calcium overload induced by subsequenced anoxia-reoxygenation injury,so it plays an delayed protective role in cardiac myocytes.L-typed calcium passage is not involved in calcium overloaded and late preconditioning of calcium in myocytes during reperfusion. 相似文献
12.
AIM: To investigate the antagonistic action of Captopril (Cap) on the activation and injury of human umbilical vascular endothelial cells (HUVECs) induced by lipopolysaccharide(LPS) and the possible mechanisms. METHODS: After 18 h exposure of the cultured HUVECs to LPS (1 mg/L), or LPS (1 mg/L) plus Cap at the concentration of 10-7mol/L, 10-5mol/L and 10-3mol/L, the expression of vWF protein in the conditioned media was tested by enzyme-linked immunosorbent assay (ELISA), the expression of ICAM-1 protein in HUVECs was determined by indirect immunofluorescence technique with flow cytometry as well. In addition, the expression of TNFα mRNA was determined by in situ hybridization. RESULTS: The results of ELISA and indirect immunofluorescence technique showed that exposure to LPS at a concentration of 1 mg/L led to a significant increase in the vWF and ICAM-1 expression in HUVECs as compared to the control (P<0. 05), whereas they were somewhat decreased when exposed to Cap at three increasing concentrations mentioned above, especially in the Cap (10-3mol/L) plus LPS group (P<0.05). Cap inhibited vWF secretion and ICAM-1 expression of HUVECs caused by LPS in a concentration-dependent manner. In situ hybridization revealed that the expression of TNFα mRNA was inhibited by Cap both in a concentration of 10-3mol/L, and in a lower concentration of 10-5mol/L. CONCLUSION: Cap antagonizes the activation and injury of HUVECs induced by LPS, which may be related to the decrease in TNFα mRNA expression. 相似文献
13.
卡托普利/壳聚糖-明胶网络多聚物缓释微球制备工艺的研究 总被引:1,自引:0,他引:1
利用壳聚糖、明胶为载体材料,乳化交联法制备卡托普利/壳聚糖明胶网络多聚物缓释微球(Cap/CGNPMs), 以部分因子设计试验优化微球的制备处方和工艺。结果表明,壳聚糖分子量(700000 Da)、药物与载体材料投料比(1∶4)、交联剂组成(甲醛+三聚磷酸钠)、交联度(1∶0 .75)、添加0 75%微晶纤维素为制备Cap/CGNPMs 的较理想条件。按较理想处方和工艺制得的Cap/CGN PMs粒径分布范围为220~280μm,包封率46. 23±4 .51%,载药量9. 95±0 .77% , 方法重现性好,体外释药试验证明,Cap/CGNPMs具有良好的缓释延效作用。 相似文献
14.
WU Sheng-ying PAN Chun-shui LIU Xiu-hua JIANG Wei QI Yong-fen TANG Chao-shu LI Ju-xiang 《园艺学报》2004,20(11):1961-1965
AIM: To explore the effects of angiotensin II on aortic calcification in the rat. METHODS: Arterial calcification of Sprague-Dawley rats was induced by vitamin D3 plus nicotine. Calcification was confirmed by Von Kossa staining, measurement of calcium content, [45Ca2+]accumulation and alkaline phosphatase (ALP) activity of vascular tissue. RESULTS: The results showed that calcium content, [45Ca2+]accumulation and ALP activity in calcified arteries increased significantly compared with those of control. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in calcified aorta were also increased as compared with control. Captopril (inhibitor of ACE) and losartan (Ang Ⅱ receptor inhibitor) decreased significantly the content of calcium, [45Ca2+] uptake and ALP activity in calcified aorta. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in aortic tissue were down-regulated by captopril. The amount of angiotensinogen mRNA and the content of Ang Ⅱ in the calcified aorta were also decreased by losartan. CONCLUSION: The captopril and losartan significantly alleviate the vascular calcification. 相似文献