本文選題：β腎上腺素能受體 + 心肌細胞　； 參考：《臨床心血管病雜志》2017年01期

【摘要】：目的:探討β3腎上腺素能受體(β3-AR)對SD大鼠乳鼠心肌肥大的影響及其機制。方法:體外培養(yǎng)SD大鼠乳鼠心肌細胞,用攜帶β3-AR基因的慢病毒轉染細胞后,用去甲腎上腺素(NE)誘導細胞48h,建立心肌細胞肥大模型。實驗分4組:空白對照組(Control組)、心肌肥厚組(NE組)、β3-AR基因轉染+NE組(β3-AR組)、空病毒轉染+NE組(空病毒組)。用免疫熒光法鑒定心肌細胞,倒置熒光顯微鏡觀察病毒轉染組綠色熒光蛋白(GFP)表達,免疫印跡法(Western Blot)檢測β3-AR、絲裂原活化蛋白激酶p38(p38MAPK)、細胞外信號調控激酶(ERK1/2)、磷酸化p38MAPK(p-p38MAPK)和ERK(p-ERK1/2)及原癌基因c-myc、c-fos蛋白水平的表達。結果:(1)慢病毒介導β3-AR基因轉染心肌細胞,β3-AR表達較空白對照組明顯升高。(2)用Western Blot檢測各實驗組細胞原癌基因c-myc、c-fos表達,其中NE組、β3-AR組、空病毒組表達均高于空白對照組,其中β3-AR組cmyc、c-fos表達明顯高于NE組。(3)NE組、β3-AR組、空病毒組p38MAPK及ERK1/2的磷酸化水平較空白對照組明顯上調,其中β3-AR組表達最高。結論:慢病毒介導的β3-AR基因轉染使心肌細胞有效高表達β3-AR,β3-AR可能通過MAPK通路促進心肌肥厚。
[Abstract]:Aim: to investigate the effect of 尾 3 adrenoceptor (尾 3 AR) on myocardial hypertrophy in neonatal SD rats and its mechanism. Methods: neonatal SD rat cardiomyocytes were cultured in vitro. The cells were transfected with lentivirus carrying 尾 3-AR gene and induced by norepinephrine (NE) for 48h to establish cardiomyocyte hypertrophy model. The experiment was divided into four groups: control group (blank control group), NE group (myocardial hypertrophy group), NE group (尾 3-AR group) transfected with 尾 3-AR gene, and NE group (empty virus group) transfected with empty virus. The expression of green fluorescent protein (GFP) in viral transfection group was observed by reverse fluorescence microscope. Western blot was used to detect the expression of 尾 3-AR, p38 MAPK, ERK1 / 2, phosphorylated p38 MAPK and ERK (p-ERK1 / 2) and proto-oncogene c-mycc-fos. Results: (1) the expression of 尾 _ 3-AR gene was significantly higher than that of the blank control group. (2) the expression of proto-oncogene c-mycnc-fos was detected by Western blot, and the expression of c-mycfs in NE group, 尾 _ 3-AR group and empty virus group was higher than that in blank control group. The expression of c-fos in 尾 3-AR group was significantly higher than that in NE group. (3) the phosphorylation levels of p38 MAPK and ERK1 / 2 in NE group, 尾 3-AR group and empty virus group were significantly higher than those in control group, and the highest expression was found in 尾 3-AR group. Conclusion: lentivirus-mediated 尾 _ 3-AR gene transfection can effectively overexpression 尾 _ 3-AR. 尾 _ 3-AR may promote myocardial hypertrophy through MAPK pathway.
【作者單位】： 新疆石河子大學醫(yī)學院第一附屬醫(yī)院心內二科;新疆醫(yī)科大學第一附屬醫(yī)院心臟中心;
【基金】：國家自然科學基金-地區(qū)科學基金項目(No:81260028) 石河子大學科學技術研究發(fā)展計劃“自然科學與技術創(chuàng)新”團隊創(chuàng)新項目(No:2011ZRKXTD-07)
【分類號】：R541.6

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