18β-GA对Wistar大鼠和SHR脑动脉舒缩活动及其连接蛋白表达的影响

发布时间：2018-05-27 11:39

本文选题：脑动脉 + 自发性高血压大鼠　；参考：《石河子大学》2014年硕士论文

【摘要】：目的：探讨18β-甘草次酸(18β-glycyrrhetinic acid,18β-GA)对脑动脉血管舒缩反应中的作用及缝隙连接蛋白在脑血管上分布的差异。为以后临床治疗高血压相关性脑血管疾病提供一些新思路。方法：应用压力肌动图技术，观察血管收缩剂PE和KCl和血管舒张剂SNP对大鼠脑中动脉段舒缩活动的作用；应用缝隙连接阻断剂18β-GA后，对血管舒缩反应的影响。应用Western blot技术，检测Wistar大鼠和SHR脑动脉缝隙连接蛋白的表达变化。结果：(1) KCl对SHR和Wistar大鼠的脑中动脉可引起浓度依赖性收缩反应；18β-GA（100μmol/L）孵育后，SHR和Wistar大鼠脑中动脉收缩幅度均降低，在SHR脑中动脉段，80mmol/L的KCl收缩率由95%±9%降低到63%±8%（P 0.05，n=6），在Wistar大鼠脑中动脉段，80mmol/L的KCl收缩率由100%±8%降低到64%±6%（P 0.05，n=6）。18β-GA干预后，KCl引起SHR脑血管段收缩的EC50为23.99mmol/L和32.62mmol/L，KCl引起Wistar大鼠脑血管段收缩的EC50为36.96mmol/L和34.90mmol/L（P㧐0.05，n=6）。 PE对SHR和Wistar大鼠的脑中动脉均引起浓度依赖性收缩反应；18β-GA（100μmol/L）孵育后，在SHR脑中动脉段，100μmol/L的PE收缩率收缩率由237%±30%降低至91%±3%（P 0.01，n=6）；在Wistar大鼠脑中动脉段，100μmol/L的PE收缩率由100%±11%降低至40%±8%（P 0.01，n=6）18β-GA干预后，PE引起SHR脑血管段收缩的EC50为11.29μmol/L和0.86μmol/L，PE引起Wistar大鼠脑血管段收缩的EC50为0.46μmol/L和5.60μmol/L（P㧐0.05，n=6）。 SNP对SHR和Wistar大鼠的脑中动脉可引起浓度依赖性的舒张反应；18β-GA（100μmol/L）孵育后，SHR和Wistar大鼠脑中动脉舒张幅度均降低，在SHR脑中动脉段，300μmol/L的SNP舒张率由91%±13%降低到57%±8%（P 0.05，n=6），在Wistar大鼠脑中动脉段，300μmol/L的SNP舒张率由100%±7%降低到61%±10%（P 0.05，n=6）。18β-GA干预后， SNP引起SHR脑血管段舒张的EC50为2.12μmol/L和6.24μmol/L（P㧐0.05，n=6）；SNP引起Wistar大鼠脑血管段舒张的EC50为2.56μmol/L和1.51μmol/L（P㧐0.05，n=6）。 (2) SHR与Wistar大鼠脑动脉相比，SHR脑血管中的Cx43和Cx45蛋白表达明显增强（P 0.05，n=6）； Cx40蛋白表达明显降低（P 0.05，n=6）。结论：SHR和Wistar大鼠的微小动脉舒缩活动存在差异；缝隙连接阻断剂可以抑制血管活性物质对脑血管的作用；高血压形成后，脑血管通过改变不同缝隙连接的表达，，调整血管活性物质对血管功能的影响。
[Abstract]:Objective: To investigate the role of 18 beta glycyrrhetinic acid (18 beta -glycyrrhetinic acid, 18 beta -GA) in cerebral arterial vasomotor response and the difference in the distribution of gap connexin on the cerebral vessels. The effect of KCl and vasodilator SNP on the systolic and diastolic activity of the middle cerebral artery in rats; the effect of the gap junction blocker 18 beta -GA on the vasomotor response. Western blot technique was used to detect the changes in the expression of gap connexin in the Wistar rat and SHR cerebral arteries.
Results: (1) KCl could cause a concentration dependent contraction response to the middle cerebral arteries of SHR and Wistar rats. After incubation of 18 beta -GA (100 mu mol/L), the contractile amplitude of middle cerebral artery in SHR and Wistar rats decreased. The contraction rate of 80mmol/L KCl decreased from 95% + 9% to 63% + 8% (P 0.05, n=6) in the middle of SHR brain artery. The contraction rate of Cl decreased from 100% + 8% to 64% + 6% (P 0.05, n=6).18 beta -GA. The EC50 of SHR cerebral vascular segments was 23.99mmol/L and 32.62mmol/L, and KCl induced the contraction of the cerebral vascular segments in Wistar rats.
PE induced a concentration dependent contraction response to the middle cerebral arteries of SHR and Wistar rats. After incubation of 18 beta -GA (100 mu mol/L), the contraction rate of PE contraction rate of 100 mu mol/L decreased from 237% + 30% to 91% + 3% (P 0.01, n=6) in the middle of the cerebral artery segment of the brain. The contraction rate of 100 micron mol/L was reduced from 100% + 11% to 40% 8% (40%) 8% in the middle cerebral artery segment of Wistar rats. After 18 beta -GA, the EC50 of SHR cerebral vascular segments caused by PE was 11.29 mol/L and 0.86 micron mol/L, and PE caused the contraction of cerebral vascular segments in Wistar rats to 0.46 mu mol/L and 5.60 micron mol/L (P? 0.05).
SNP can cause a concentration dependent diastolic response to the middle cerebral arteries of SHR and Wistar rats. After incubation of 18 beta -GA (100 mu mol/L), the diastolic amplitude of the middle cerebral artery in SHR and Wistar rats decreased. The diastolic rate of SNP in the middle of the SHR brain was reduced from 91% + 13% to 57% + 8% (P 0.05, n=6). The rate of tension was reduced from 100% + 7% to 61% + 10% (P 0.05, n=6).18 beta -GA. The EC50 in the SHR cerebral vascular segment caused by SNP was 2.12 Mu and 6.24 u mol/L (P? 0.05, n=6), and the relaxation of the cerebral vascular segment of the rat was 2.56 and 1.51 mu (0.05,).
(2) the expression of Cx43 and Cx45 protein in SHR cerebral arteries was significantly enhanced (P 0.05, n=6) and Cx40 protein expression decreased significantly (P 0.05, n=6) in the cerebral arteries of SHR rats (P 0.05, n=6). Conclusion: there were differences in microarterial systolic and contractile activities between SHR and Wistar rats; gap junctional blockers could inhibit the effect of vasoactive substances on cerebral vessels; high blood pressure After the formation of pressure, the effect of vasoactive substances on vascular function was adjusted by changing the expression of different gap junctions.
【学位授予单位】：石河子大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R743

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