目的 通過(guò)觀察ip丙泊酚對(duì)腦缺血再灌注大鼠海馬區(qū)神經(jīng)細(xì)胞的影響, 探討丙泊酚對(duì)臨床圍手術(shù)期預(yù)防腦缺血再灌注損傷的作用。方法 SD大鼠60只隨機(jī)分為丙泊酚組、假手術(shù)組和模型組。采用大腦中動(dòng)脈線栓法制作左側(cè)大腦動(dòng)脈栓塞模型。在缺血再灌注前10 min時(shí), 丙泊酚組ip丙泊酚50 mg/kg, 模型組ip給予等量生理鹽水。假手術(shù)組只進(jìn)行頸部切開、縫合操作而不進(jìn)行缺血再灌注實(shí)驗(yàn)。缺血再灌注24 h采集腦組織。TTC染色法測(cè)定大鼠左側(cè)腦組織梗死面積, 免疫組化檢測(cè)大鼠腦組織海馬區(qū)Caspase-3的表達(dá), 原位雜交檢測(cè)大鼠海馬組織Caspase-3 mRNA的轉(zhuǎn)錄水平。結(jié)果 與模型組比較, 丙泊酚組腦組織灰白色區(qū)域明顯縮小, 改善了腦組織梗死面積, 海馬區(qū)Caspase-3的陽(yáng)性表達(dá)和Caspase-3 mRNA的轉(zhuǎn)錄水平明顯降低(P<0.01)。結(jié)論 丙泊酚干預(yù)對(duì)大鼠腦缺血再灌注損傷有保護(hù)作用, 其機(jī)制可能通過(guò)干預(yù)Caspase-3相關(guān)的細(xì)胞凋亡信號(hào)傳導(dǎo)途徑來(lái)完成。

Objective To observe the effects of propofol ip injection on hippocampus nervous after cerebral ischemia-reperfusion injury, to study the prevention of propofol to cerebral ischemia-reperfusion injury during clinical peroperative period. Methods Sixty SD rats were randomly divided into propofol group, Sham group, and model group. Left cerebral arterial embolism models were made. At 10 min before cerebral ischemia-reperfusion, rats in propofol group were ip administered propofol (50 mg/kg), and physiological saline was given to Sham group. Rats in model group were done the same operation except cerebral ischemia-reperfusion and propofol. At 24 h after ischemia reperfusion, the tissues were collected. The areas of left cerebral infarct of rats were measured by TTC staining method, Caspase-3 express in hippocampus was measured by immunohistochemical methods, and transcriptional levels of Caspase-3 mRNA were detected by in situ hybridization test. Results Compared with model group, gray area obviously shrank and incanus areas were improved in propofol group. The expression of Caspase-3 and transcriptional levels of Caspase-3 mRNA in hippocampus of rats in propofol group were lower than those in model group, with significant differences between two groups (P < 0.01). Conclusion Propofol intervention before ischemia-reperfusion maybe prevent ischemia reperfusion injury, and the mechanism is related to the apoptosis signal transduction pathway through Caspase-3 mediation.

河北省自然科學(xué)基金資助項(xiàng)目(H2012405016);河北北方學(xué)院自然科學(xué)研究計(jì)劃項(xiàng)目(120176)