本文關(guān)鍵詞：1-磷酸鞘氨醇對心肌細胞離子通道作用的實驗研究　出處：《吉林大學》2008年碩士論文　論文類型：學位論文

  更多相關(guān)文章： 1-磷酸鞘氨醇 膜片鉗 L-型鈣電流 延遲整流鉀電流 心肌細胞培養(yǎng)

【摘要】： 目的:通過全細胞膜片鉗技術(shù)、單通道膜片鉗技術(shù)、臺盼藍染色技術(shù)觀察S1P對豚鼠心室肌細胞L型鈣電流(IL-Ca)、延遲整流鉀電流(IK)及氧化損傷后心肌細胞凋亡的影響,進一步探討其心肌保護作用的機理。 方法:應用全細胞膜片鉗技術(shù),觀察不同劑量S1P對豚鼠心室肌細胞L型鈣電流(IL-Ca)電流幅值的影響。應用單通道膜片鉗技術(shù),觀察S1P對豚鼠心室肌細胞延遲整流鉀電流(IK)開放時間、關(guān)閉時間、開放概率的影響。通過臺盼藍染色技術(shù)觀察不同劑量S1P對H2O2氧化損傷后心肌細胞凋亡的影響。 結(jié)果:不同劑量S1P對豚鼠心室肌細胞L型鈣電流(IL-Ca)均無作用;S1P可使豚鼠心室肌細胞延遲整流鉀電流(IK)的開放時間縮短,關(guān)閉時間延長,開放概率降低,與對照組相比較,P0.05,差異顯著;S1P劑量依賴性的抑制氧化損傷后的心肌細胞凋亡,大、中劑量組與模型組比較,P0.001,差異顯著。 結(jié)論: S1P可以使豚鼠心室肌細胞延遲整流鉀電流(IK)的開放時間縮短,關(guān)閉時間延長,開放概率降低,抑制整個細胞延遲整流鉀電流(IK)外流,S1P可以抑制氧化損傷后的心肌細胞凋亡,上述結(jié)果均說明是S1P對急性心梗后缺血缺氧的心肌有一定的保護作用。
[Abstract]:Objective: to observe the effect of S1P on L-type calcium current (L-type calcium current) in guinea pig ventricular myocytes by whole-cell patch clamp technique, single-channel patch clamp technique and trypan blue staining. The effects of delayed rectifier potassium current (IKK) and oxidative injury on cardiomyocyte apoptosis and the mechanism of myocardial protection were discussed. Methods: the effects of different doses of S1P on the amplitude of L-type calcium current and IL-Ca1 in guinea pig ventricular myocytes were observed by whole-cell patch clamp technique. To observe the opening time and closing time of S1P to delayed rectifier potassium current in guinea pig ventricular myocytes. Effects of different doses of S _ 1P on apoptosis of cardiomyocytes after oxidative injury of H _ 2O _ 2 were observed by trypan blue staining. Results: different doses of S1P had no effect on L-type calcium current and IL-Ca1 in guinea pig ventricular myocytes. S1P could shorten the opening time, prolong the closing time and decrease the open probability of delayed rectifier potassium current in guinea pig ventricular myocytes, which was significantly different from that of control group (P 0.05). S1P dose-dependently inhibited the apoptosis of cardiomyocytes after oxidative injury, and the difference was significant between the middle dose group and the model group (P 0.001). Conclusion: S1P can shorten the opening time, prolong the closing time and decrease the open probability of delayed rectifier potassium current in guinea pig ventricular myocytes. Inhibiting the whole cell delayed rectifier potassium current (IKK) efflux (S1P) can inhibit the apoptosis of cardiomyocytes after oxidative injury. These results suggest that S1P has a protective effect on myocardial ischemia and hypoxia after acute myocardial infarction.
【學位授予單位】：吉林大學
【學位級別】：碩士
【學位授予年份】：2008
【分類號】：R331.3

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本文編號：1405317