本文選題：二十二碳六烯酸　切入點(diǎn)：缺血性腦卒中　出處：《第三軍醫(yī)大學(xué)學(xué)報(bào)》2017年14期

【摘要】：目的探討二十二碳六烯酸(docosahexaenoic acid,DHA)對大鼠缺血性腦卒中神經(jīng)損傷的保護(hù)作用及其機(jī)制。方法利用60只280~330 g成年SD雄性大鼠建立永久性局灶腦梗死模型(permanent middle cerebral artery occlusion,pMCAO),按隨機(jī)數(shù)字表法分為3組(n=20):假手術(shù)組、模型載體空白組(pMCAO+Veh)和模型DHA給藥組(pMCAO+DHA)。建模成功后,按預(yù)設(shè)時(shí)間點(diǎn)對動(dòng)物體質(zhì)量、生存時(shí)間、神經(jīng)功能、腦梗體積等大體指標(biāo)進(jìn)行評測;利用HE、Nissl染色對腦組織形態(tài)學(xué)改變進(jìn)行觀察;Western blot檢測神經(jīng)細(xì)胞自噬相關(guān)蛋白變化規(guī)律。結(jié)果造模后24、72 h,pMCAO+Veh組動(dòng)物體質(zhì)量及生存率較假手術(shù)組出現(xiàn)明顯下降(P0.05),DHA給藥可明顯改善上述指標(biāo),但差異無統(tǒng)計(jì)學(xué)意義(P0.05);pMCAO+Veh組第7天生存率僅為38%,DHA早期干預(yù)可使第7天生存率提高至52%,但2組差異無統(tǒng)計(jì)學(xué)意義(P0.05),DHA可明顯改善由疾病模型造成的神經(jīng)功能,包括認(rèn)知、感覺、運(yùn)動(dòng)功能,從而獲得更高的神經(jīng)功能分?jǐn)?shù)及更少的平衡木錯(cuò)失(P0.05)。建模72 h后TTC染色發(fā)現(xiàn),pMCAO+DHA組較pMCAO+Veh組可減少約17%的梗死體積(P0.05);HE及Nissl染色發(fā)現(xiàn),DHA給藥可顯著減輕皮層梗死區(qū)神經(jīng)細(xì)胞的病理性損傷;Western blot蛋白檢測,DHA可顯著抑制梗死后mTOR表達(dá)(P0.01),同時(shí)增強(qiáng)LC3Ⅰ/Ⅱ表達(dá)(P0.05)。結(jié)論 DHA可顯著減輕由缺血性腦卒中引起的病理性改變,其保護(hù)機(jī)制可能為負(fù)性調(diào)控mTOR通路作用從而激活自噬。
[Abstract]:Objective to investigate the protective effect and mechanism of 22 carbohexaenoic acidoic acid on nerve injury in ischemic stroke rats.Methods A permanent focal cerebral infarction model was established in 60 adult male SD rats (280 ~ 330g). The permanent middle cerebral artery occlusion pMCAOG was divided into three groups according to random digital table: sham-operated group, model vector blank group (pMCAO Veh) and model DHA administration group (pMCAO DHAO).After modeling successfully, the gross indexes such as animal mass, survival time, nerve function and volume of cerebral infarction were evaluated according to preset time points.The changes of neuronal autophagy related proteins were detected by Western blot.Results the mass and survival rate of animals and animals in the pMCAO Veh group were significantly lower than those in the sham operation group.However, there was no significant difference between the two groups. The 7th day survival rate of the P0.05-pMCAO Veh group was only 38%. The early intervention of DHA could increase the survival rate from the 7th day to 52%, but there was no significant difference between the two groups. P0.05 Veh could significantly improve the neurological function caused by the disease model, including cognition and perception.Motor function, resulting in higher neurological function scores and less balance beam missed P0.05.After 72 hours of modeling, TTC staining showed that the infarct volume of pMCAO DHA group was about 17% less than that of pMCAO Veh group, and Nissl staining showed that it could significantly reduce the pathological injury of neurons in cortical infarct area.Postmortem mTOR expressed P0.01a and enhanced LC3 鈪，

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