本文關鍵詞：解偶聯(lián)蛋白2與脂多糖誘導膿毒癥大鼠心肌線粒體損傷的關系　出處：《中國當代兒科雜志》2016年02期 　論文類型：期刊論文

  更多相關文章： 膿毒癥 心肌 線粒體 解偶聯(lián)蛋白 大鼠

【摘要】：目的探討解偶聯(lián)蛋白2(uncoupling protein 2,UCP2)與脂多糖誘導膿毒癥大鼠心肌線粒體損傷的關系。方法通過腹腔注射脂多糖(LPS)建立膿毒癥模型。將40只Sprague-Dawley(SD)雄性大鼠隨機分為5組,每組8只:對照組(腹腔注射生理鹽水)、膿毒癥6 h組(LPS-6 h組)、膿毒癥12 h組(LPS-12 h組)、膿毒癥24 h組(LPS-24 h組)和膿毒癥48 h組(LPS-48 h組)。在相應時間點留取大鼠血清和心臟組織,提取心肌線粒體,通過酶標儀檢測肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)和活性氧(ROS)水平,流式細胞儀檢測線粒體腫脹度和線粒體膜電位(MMP),采用蛋白質免疫印跡試驗(Western blot)測定UCP2蛋白表達水平;電鏡觀察心肌組織線粒體形態(tài)學變化。結果與對照組比較,LPS各組血清CK、CK-MB水平、心肌組織ROS水平和線粒體腫脹度均明顯升高(P0.05),峰值在LPS-24 h組;而LPS各組線粒體膜電位明顯下降(P0.05),LPS-24 h組降至最低。Western blot檢測發(fā)現(xiàn)LPS各組心肌組織UCP2的表達水平較對照組明顯升高(P0.05),峰值在LPS-24 h組。電鏡觀察結果發(fā)現(xiàn)LPS大鼠心肌線粒體腫脹,線粒體膜部分破碎,有空泡形成,LPS-24 h組病變最嚴重。LPS大鼠心肌線粒體ROS水平、線粒體腫脹度與UCP2表達量呈正相關(分別r=0.796、0.893,P0.05);LPS大鼠心肌MMP與UCP2表達量呈負相關(r=-0.903,P0.05)。結論在膿毒癥大鼠模型中,心肌和心肌線粒體都明顯損傷,心肌組織UCP2的表達與線粒體損傷密切相關,推測UCP2可能在膿毒癥心肌線粒體損傷中起重要作用。
[Abstract]:Objective to study uncoupling protein 2 of uncoupling protein 2. The relationship between UCP2) and myocardial mitochondria damage induced by lipopolysaccharide in sepsis rats. Methods the sepsis model was established by intraperitoneal injection of lipopolysaccharide (LPS). Forty Sprague-Dawley rats were selected. SD) male rats were randomly divided into 5 groups. There were 8 rats in each group: control group (intraperitoneal injection of normal saline, sepsis 6 h group, LPS-6 h group, sepsis 12 h group, LPS-12 h group). The rat serum and heart tissue were collected at the corresponding time points to extract myocardial mitochondria from sepsis group (n = 24) and sepsis group (n = 48 h). The levels of creatine kinase (CK), creatine kinase isozyme (CK-MBB) and reactive oxygen species (Ros) were detected by enzyme scale, and mitochondrial swelling degree and mitochondrial membrane potential (MMPs) were measured by flow cytometry (FCM). Western blotting assay was used to detect the expression of UCP2 protein. The changes of myocardial mitochondria morphology were observed by electron microscope. Results compared with the control group, the level of CKK-MB in serum of LPS group was higher than that of LPS group. The level of ROS and the degree of swelling of mitochondria in myocardial tissue were significantly increased (P 0.05), and the peak value was in the LPS-24 h group. However, the mitochondrial membrane potential in LPS group was significantly decreased (P 0.05). The expression of UCP2 in myocardium of LPS group was significantly higher than that of control group (P0.05). The peak value was in LPS-24 h group. The results of electron microscopic observation showed that myocardial mitochondria were swollen, mitochondrial membrane was partially broken and empty vesicles were formed in LPS rats. The level of myocardial mitochondrial ROS, mitochondrial swelling and UCP2 expression were positively correlated in the LPS-24 h group (r 0.796 鹵0.893, respectively). P0.05; There was a negative correlation between the expression of MMP and UCP2 in the myocardium of LPS rats. Conclusion in the sepsis rat model, both myocardial and myocardial mitochondria were significantly damaged. The expression of UCP2 in myocardium is closely related to mitochondrial damage. It is suggested that UCP2 may play an important role in myocardial mitochondrial injury in sepsis.
【作者單位】： 南方醫(yī)科大學珠江醫(yī)院兒科中心;東莞市厚街醫(yī)院兒科;
【基金】：國家自然科學基金(81272070) 廣東省科技計劃項目(2014A020212725)
【分類號】：R459.4
【正文快照】： 膿毒癥是機體對病原的免疫應答反應性疾病,其免疫學特征是宿主自身免疫損傷,進一步可發(fā)展為多器官功能障礙綜合征(MODS)。心臟是膿毒癥的靶器官之一,合并心功能障礙的膿毒癥患者的病死率可高達70%[1-2]。研究發(fā)現(xiàn)活性氧(reactive oxygen species,ROS)生成過多、能量產生和代謝

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