本文選題：β-石竹烯　切入點(diǎn)：腦缺血再灌注　出處：《重慶醫(yī)科大學(xué)》2016年碩士論文

【摘要】：目的:探討β-石竹烯(β-Caryophyllene,BCP)對(duì)腦缺血再灌注(ischemiareperfusion,I-R)損傷大鼠的保護(hù)作用及其機(jī)制。觀察其對(duì)核因子相關(guān)因子2(2NF-E2-related factor,Nrf2)/血紅素氧合酶1(Heme oxygenase-1,HO-1)通路的作用。方法:1.將78只SD大鼠隨機(jī)分為六組:假手術(shù)(Sham)組;模型(I-R)組;β-石竹烯34mg·kg-11組;β-石竹烯102 mg·kg-1組;β-石竹烯306mg·kg-1組;尼莫地平組6mg·kg-1。采用線栓法建立大鼠大腦中動(dòng)脈栓塞(Middle Cerebral Artery Occlusion,MCAO)模型,缺血1.5h,再灌注24h后,采用雙盲法進(jìn)行神經(jīng)行為學(xué)評(píng)分;TTC染色法測(cè)定腦梗死體積;透射電鏡(Transmission electron microscopy,TEM)和尼氏染色法(Nissl)觀察海馬神經(jīng)元病理變化;原位末端凋亡法(TUNEL)檢測(cè)海馬神經(jīng)元凋亡情況;2.將60只SD大鼠隨機(jī)分為五組:假手術(shù)(Sham)組;模型組(I-R);β-石竹烯34 mg·kg-1組;β-石竹烯102 mg·kg-1組;β-石竹烯306 mg·kg-1組。測(cè)定MCAO大鼠海馬中超氧化物歧化酶(superoxide dismutase,SOD)、過(guò)氧化氫酶(Catalase,CAT)、丙二醛(Malondialdehyde,MDA)、一氧化氮(Nitric oxide,NO)、脂質(zhì)過(guò)氧化物(Lipid peroxidation,LPO)含量;Western法和定量PCR法檢測(cè)假手術(shù)(Sham)組;模型組(I-R);β-石竹烯306 mg·kg-1組Nrf2及HO-1蛋白及基因的表達(dá)。結(jié)果:1.與Sham組相比,I-R組神經(jīng)行為學(xué)評(píng)分升高,腦梗死面積明顯增加。β-石竹烯(102mg·kg-1、306 mg·kg-1)與尼莫地平組可不同程度改善MCAO大鼠神經(jīng)行為學(xué)障礙,減少腦梗死面積;同時(shí),β-石竹烯(102mg·kg-1、306 mg·kg-1)與尼莫地平組可減輕海馬神經(jīng)元病理缺損及細(xì)胞凋亡情況;2.與Sham組相比,I-R組SOD、CAT活性明顯降低,MDA、LPO、NO含量明顯增多。與I-R組相比,β-石竹烯(102mg·kg-1、306 mg·kg-1)中,SOD、CAT活性明顯增高,MDA、LPO、NO含量明顯降低;β-石竹烯(306mg·kg-1)Nrf2、HO-1蛋白及基因的表達(dá)明顯增多。結(jié)論:β-石竹烯對(duì)腦缺血再灌注大鼠具有神經(jīng)保護(hù)作用,此作用可能與調(diào)控Nrf2/HO-1通路有關(guān)。
[Abstract]:Aim: to investigate the protective effect of 尾 -Caryophyllene (尾 -Caryophyllene BCP) on cerebral ischemia-reperfusion injury in rats and its mechanism.To investigate the effect of NRF _ 2 / 1(Heme oxygenase 1(Heme oxygenase-1 (HO-1) pathway on the nuclear factor-related factor 2(2NF-E2-related factor-nrf2 / heme oxygenase 1 (1(Heme oxygenase-1) pathway.Method 1: 1.Seventy-eight SD rats were randomly divided into six groups: sham-operated group; model I-Rgroup; 尾 -caryophylene 34mg kg-11 group; 尾 -caryophyllene 102mg kg-1 group; 尾 -caryophylene 306mg kg-1 group; Nimodipine group 6mg kg-1.The middle Cerebral Artery occlusion model of middle cerebral artery (MCAO) was established by thread occlusion. After 1.5 hours of ischemia and 24 hours of reperfusion, the volume of cerebral infarction was measured by the method of neurobehavioral score and TTC staining.The pathological changes of hippocampal neurons were observed by transmission electron microscopy (TEM) and transmission electron microscopy (TEM) and Nissl staining (Nissll), and the apoptosis of hippocampal neurons was detected by in situ terminal terminal apoptosis (Tunel).Sixty SD rats were randomly divided into five groups: sham group, model group, 尾 -caryophyllene 34 mg kg-1 group, 尾 -caryophyllene 102mg kg-1 group, 尾 -caryophyllene 306 mg kg-1 group.嫻嬪畾MCAO澶ч紶嫻烽┈涓秴姘у寲鐗╂鍖栭叾(superoxide dismutase,SOD),榪囨哀鍖栨阿閰，

本文編號(hào)：1704773