本文選題：腦動(dòng)脈 + 自發(fā)性高血壓大鼠��； 參考：《石河子大學(xué)》2014年碩士論文

【摘要】：目的：探討18β-甘草次酸(18β-glycyrrhetinic acid,18β-GA)對(duì)腦動(dòng)脈血管舒縮反應(yīng)中的作用及縫隙連接蛋白在腦血管上分布的差異。為以后臨床治療高血壓相關(guān)性腦血管疾病提供一些新思路。方法：應(yīng)用壓力肌動(dòng)圖技術(shù)，觀察血管收縮劑PE和KCl和血管舒張劑SNP對(duì)大鼠腦中動(dòng)脈段舒縮活動(dòng)的作用；應(yīng)用縫隙連接阻斷劑18β-GA后，對(duì)血管舒縮反應(yīng)的影響。應(yīng)用Western blot技術(shù)，檢測(cè)Wistar大鼠和SHR腦動(dòng)脈縫隙連接蛋白的表達(dá)變化。 結(jié)果：(1) KCl對(duì)SHR和Wistar大鼠的腦中動(dòng)脈可引起濃度依賴性收縮反應(yīng)；18β-GA（100μmol/L）孵育后，SHR和Wistar大鼠腦中動(dòng)脈收縮幅度均降低，在SHR腦中動(dòng)脈段，80mmol/L的KCl收縮率由95%±9%降低到63%±8%（P 0.05，n=6），在Wistar大鼠腦中動(dòng)脈段，80mmol/L的KCl收縮率由100%±8%降低到64%±6%（P 0.05，n=6）。18β-GA干預(yù)后，KCl引起SHR腦血管段收縮的EC50為23.99mmol/L和32.62mmol/L，KCl引起Wistar大鼠腦血管段收縮的EC50為36.96mmol/L和34.90mmol/L（P㧐0.05，n=6）。 PE對(duì)SHR和Wistar大鼠的腦中動(dòng)脈均引起濃度依賴性收縮反應(yīng)；18β-GA（100μmol/L）孵育后，在SHR腦中動(dòng)脈段，100μmol/L的PE收縮率收縮率由237%±30%降低至91%±3%（P 0.01，n=6）；在Wistar大鼠腦中動(dòng)脈段，100μmol/L的PE收縮率由100%±11%降低至40%±8%（P 0.01，n=6）18β-GA干預(yù)后，PE引起SHR腦血管段收縮的EC50為11.29μmol/L和0.86μmol/L，PE引起Wistar大鼠腦血管段收縮的EC50為0.46μmol/L和5.60μmol/L（P㧐0.05，n=6）。 SNP對(duì)SHR和Wistar大鼠的腦中動(dòng)脈可引起濃度依賴性的舒張反應(yīng)；18β-GA（100μmol/L）孵育后，SHR和Wistar大鼠腦中動(dòng)脈舒張幅度均降低，在SHR腦中動(dòng)脈段，300μmol/L的SNP舒張率由91%±13%降低到57%±8%（P 0.05，n=6），在Wistar大鼠腦中動(dòng)脈段，300μmol/L的SNP舒張率由100%±7%降低到61%±10%（P 0.05，n=6）。18β-GA干預(yù)后， SNP引起SHR腦血管段舒張的EC50為2.12μmol/L和6.24μmol/L（P㧐0.05，n=6）；SNP引起Wistar大鼠腦血管段舒張的EC50為2.56μmol/L和1.51μmol/L（P㧐0.05，n=6）。 (2) SHR與Wistar大鼠腦動(dòng)脈相比，SHR腦血管中的Cx43和Cx45蛋白表達(dá)明顯增強(qiáng)（P 0.05，n=6）； Cx40蛋白表達(dá)明顯降低（P 0.05，n=6）。結(jié)論：SHR和Wistar大鼠的微小動(dòng)脈舒縮活動(dòng)存在差異；縫隙連接阻斷劑可以抑制血管活性物質(zhì)對(duì)腦血管的作用；高血壓形成后，腦血管通過改變不同縫隙連接的表達(dá)，，調(diào)整血管活性物質(zhì)對(duì)血管功能的影響。
[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.
【學(xué)位授予單位】：石河子大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R743

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