本文選題：燈盞花乙素　切入點：缺血再灌注損傷　出處：《醫(yī)學(xué)研究生學(xué)報》2017年09期

【摘要】：目的燈盞花乙素(SCU)可拮抗心肌IR損傷,但SCU是否通過細胞外信號調(diào)節(jié)激酶(ERK1/2)通路拮抗IR所致血管內(nèi)皮細胞損傷尚不清楚。文中探討SCU在缺氧-復(fù)氧(HR)誘導(dǎo)的人心臟微血管內(nèi)皮細胞(HCMEC)損傷中的作用及對ERK1/2信號通路的影響。方法體外培養(yǎng)的HCMEC分別進行正常培養(yǎng)和缺氧12 h-復(fù)氧12 h建立IR模型(HR)處理。正常培養(yǎng)條件下,將HCMEC分為正常對照組、DMSO組、SCU 1μmol/L組和SCU 10μmol/L組。給予HCMEC IR損傷處理后,分為空白對照組、HR模型組、HR+DMSO組、HR+SCU 1μmol/L組和HR+SCU 10μmol/L組。將HCMEC與SCU或DMSO預(yù)孵育2 h后行HR處理。采用MTT法和錐蟲藍染色檢測細胞存活率,并檢測HCMEC的丙二醛(MDA)濃度。Western blot檢測p-ERK1/2、ERK2和GAPDH蛋白表達情況。結(jié)果 MTT檢測結(jié)果顯示,與正常對照組細胞存活率(100%)比較,SCU 1μmol/L組和SCU 10μmol/L組[(110.40±2.34)%和(122±1.25)%]均增加(P0.05);與空白對照組細胞活力(100%)比較,HR模型組[(68.00±4.06)%]下降(P0.05),與HR模型組細胞存活率比較,HR+SCU 1μmol/L組和HR+SCU 10μmol/L組[(90.53±3.67)%、(92.04±2.32)%]增加(P0.05)。錐蟲藍染色顯示,與正常對照組細胞活力[(90.06±1.85)%]比較,SCU 10μmol/L組[(96.78±2.01)%]增加(P0.05);與空白對照組[(91.83±2.34)%]比較,HR模型組細胞存活率[(73.72±4.91)%]下降(P0.01),與HR模型組比較,HR+SCU 10μmol/L組細胞存活率[(87.59±2.64)%]增加(P0.05)。與空白對照組比較,HR模型組、HR+DMSO組MDA明顯增加(P0.01);與HR模型組比較,HR+SCU 1μmol/L組和HR+SCU 10μmol/L組MDA含量減少(P0.05)。與空白對照組比較,HR模型組p-ERK1/2蛋白表達明顯降低(P0.01);與HR模型組比較,HR+SCU 10μmol/L組p-ERK1/2蛋白表達明顯增加(P0.01)。結(jié)論 HR損傷導(dǎo)致HCMEC細胞活力下降、MDA增加和p-ERK1/2蛋白表達降低,SCU通過上調(diào)p-ERK1/2表達而拮抗HCMEC IR損傷。
[Abstract]:Objective to antagonize myocardial IR injury by Erigeron breviscapine (SCU). However, it is not clear whether SCU antagonizes vascular endothelial cell damage induced by IR through the extracellular signal-regulated kinase ERK1 / 2 pathway. In this paper, we investigate the role of SCU in human heart microvascular endothelial cell injury induced by hypoxia and reoxygenation. Methods HCMEC cultured in vitro was treated with normal culture and 12 h hypoxia and 12 h reoxygenation to establish IR model. HCMEC was divided into normal control group (1 渭 mol/L group) and SCU group (10 渭 mol/L group). HR SCU 1 渭 mol/L group and HR SCU 10 渭 mol/L group were divided into two groups. HCMEC was preincubated with SCU or DMSO for 2 hours. Cell survival rate was detected by MTT method and trypanosome blue staining. The malondialdehyde (MDA) concentration of HCMEC. Western blot was used to detect the expression of p-ERK1 / 2 ERK2 and GAPDH protein. Compared with the normal control group, the cell survival rate of SCU 1 渭 mol/L group and SCU 10 渭 mol/L group [110.40 鹵2.34% and 122 鹵1.25%] increased P0.05%, compared with the blank control group, the cell viability of HR model group [68.00 鹵4.06%] decreased P0.05%, and the cell survival rate of HR SCU 1 渭 mol/L group and HR SCU 10 渭 mol/L group was higher than that of HR model group. [90.53 鹵3.67] increased by 92.04 鹵2.32%. Trypanosoma blue staining showed, Compared with the normal control group [90.06 鹵1.85%], the cell viability of the SCU 10 渭 mol/L group [96.78 鹵2.01U%] increased P0.05%, compared with the blank control group [91.83 鹵2.34%], the cell viability of the HR model group [73.72 鹵4.91%] decreased P0.01U, and the cell survival rate of the HR SCU 10 渭 mol/L group [87.59 鹵2.641g] increased than that of the blank control group [87.59 鹵2.641U], and increased the cell viability of the HR SCU 10 渭 mol/L group (87.59 鹵2.641g%), compared with the control group (91.83 鹵2.34g%) and the HR model group (93.72 鹵4.91g%). Compared with HR model group, HR SCU 1 渭 mol/L group and HR SCU 10 渭 mol/L group decreased MDA content in HR SCU 1 渭 mol/L group and HR SCU 10 渭 mol/L group. Compared with blank control group, p-ERK1/2 protein expression in HR model group decreased significantly (P 0.01), and that in HR SCU 10 渭 mol/L group was significantly lower than that in HR model group, and that in HR SCU 10 渭 mol/L group was significantly lower than that in HR model group. Conclusion the activity of HCMEC cells decreased after HR injury and the expression of p-ERK1/2 protein decreased. Sch U antagonized HCMEC IR damage by upregulating the expression of p-ERK1/2.
【作者單位】： 昆明醫(yī)科大學(xué)第一附屬醫(yī)院心內(nèi)科;昆明醫(yī)科大學(xué)病理教研室;昆明醫(yī)科大學(xué)云南省天然藥物藥理重點實驗室;
【基金】：國家自然科學(xué)基金(81560072) 云南省科學(xué)技術(shù)廳-昆明醫(yī)科大學(xué)應(yīng)用基礎(chǔ)研究聯(lián)合專項資金(2014FB037)
【分類號】：R54
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本文編號：1689078