【摘要】：目的:以七氟醚后處理為干預(yù)措施,探討mi RNA-133a及凋亡相關(guān)蛋白在七氟醚心肌保護中的作用。方法:30只C57小鼠隨機分為3組,即對照組(control,TC)、缺血/再灌注組(Ischemia/reperfusion,I/R)、七氟醚后處理組(Sevo+IR)。對照組只進行開胸,不結(jié)扎冠狀動脈后關(guān)胸;缺血/再灌注組結(jié)扎冠狀動脈成功后關(guān)胸,30min后松開結(jié)扎線,復(fù)灌180min。七氟醚后處理組結(jié)扎冠狀動脈成功后關(guān)胸,30min后松開結(jié)扎線,并持續(xù)吸入2.4%七氟醚5min,復(fù)灌180min。心肌梗死的程度由乳酸脫氫酶(LDH)和肌酸激酶(CK)的水平以及心肌梗死面積說明;Western blot法檢測Caspase-9的表達;RT-PCR法分別檢測mi RNA-133a、Bax、Bcl-2及Caspase-9水平的變化。結(jié)果:七氟醚后處理能夠減少缺血/再灌注損傷導(dǎo)致的左心室心梗面積,減少LDH及CK的水平。與缺血/再灌注組對比,七氟醚后處理組中心肌細胞凋亡顯著減少(P0.05)。通過RT-PCR法測得心肌特異性Mi RNA-133a在缺血/再灌注時水平顯著下降,經(jīng)七氟醚后處理水平上升(P0.05);同時,七氟醚后處理下調(diào)凋亡相關(guān)蛋白Bax及Caspase-9的m RNA表達,上調(diào)Bcl-2的m RNA表達(P0.05)。Western blot也證實與缺血/再灌注組相比,七氟醚后處理組使Caspase-9的蛋白表達顯著下降(P0.05)。結(jié)論:七氟醚后處理能夠上調(diào)Micro RNA-133a的表達,減少細胞凋亡。Micro RNA-133a的抗細胞凋亡的靶點可能為Caspase-9。Micro RNA-133a參與七氟醚后處理的心肌保護作用,在其過程中扮演了重要的角色。
[Abstract]:Aim: to investigate the role of mi RNA-133a and apoptosis-related protein in the myocardial protection of sevoflurane by sevoflurane post-treatment. Methods Thirty C57 mice were randomly divided into three groups: control group, ischemia / reperfusion group and sevoflurane post-treatment group (Sevo IR). The patients in the control group only underwent thoracotomy without ligation of the coronary artery and the ischemia / reperfusion group loosened the ligation line 30 minutes after the successful ligation of the coronary artery and reperfused the coronary artery for 180 minutes. In the sevoflurane post-treatment group, the coronary artery was successfully ligated, the thoracic ligation was closed for 30 minutes, the ligation line was released, and 2.4% sevoflurane was inhaled continuously for 5 min, then reperfused for 180 min. The degree of myocardial infarction was determined by the levels of lactate dehydrogenase (LDH) and creatine kinase (CK) (CK) and the area of myocardial infarction (AMI). The expression of Caspase-9 was detected by Western blot. The expression of Caspase-9 was detected by RT-PCR. Results: after sevoflurane treatment, the area of left ventricular myocardial infarction and the levels of LDH and CK were reduced after ischemia / reperfusion injury. Compared with ischemia / reperfusion group, cardiac myocyte apoptosis was significantly decreased in sevoflurane post treatment group (P0.05). Myocardial specific Mi RNA-133a decreased significantly during ischemia / reperfusion and increased after sevoflurane treatment (P0.05), and the m RNA expression of apoptosis-related protein Bax and Caspase-9 was down-regulated by sevoflurane post-treatment. Upregulation of m RNA expression of Bcl-2 (P0.05). Western blot also confirmed that sevoflurane post-treated group significantly decreased the expression of Caspase-9 protein compared with ischemia / reperfusion group (P0.05). Conclusion: sevoflurane post treatment can up-regulate the expression of Micro RNA-133a and reduce the anti-apoptosis target of apoptosis. Micro RNA-133a may play an important role in the myocardial protection of sevoflurane.
【學位授予單位】：新疆醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2016
【分類號】：R614

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