本文選題：高壓氧　切入點(diǎn)：創(chuàng)傷性腦損傷　出處：《中國(guó)康復(fù)醫(yī)學(xué)雜志》2017年11期 　論文類型：期刊論文

【摘要】：目的:觀察高壓氧治療對(duì)腦損傷大鼠認(rèn)知功能的影響及海馬區(qū)CCL2及其受體CCR2的表達(dá)變化。方法:75只成年雄性SD大鼠按數(shù)字表法隨機(jī)分為假手術(shù)組(Sham組)、腦外傷組(TBI組)和高壓氧治療組(HBOT組),每組各25只。HBOT組和TBI組均采用Feeney自由落體法制作腦外傷模型,HBOT組每天進(jìn)行HBO治療;Sham組暴露硬腦膜不予打擊。運(yùn)用Morris水迷宮測(cè)試認(rèn)知功能;熒光免疫雙標(biāo)檢測(cè)海馬CA1區(qū)CCL2和CCR2的表達(dá)。實(shí)時(shí)定量PCR測(cè)定損傷側(cè)海馬CCL2和CCR2mRNA的表達(dá)情況。結(jié)果:Morris水迷宮測(cè)試結(jié)果顯示,HBOT組高壓氧治療后7d、14d和21d平均潛伏期下降,同時(shí)穿越平臺(tái)次數(shù)增多,與TBI組相比,差異均有顯著性意義(P0.05);免疫熒光雙染法檢測(cè)顯示,大鼠TBI后海馬CA1區(qū)CCL2主要表達(dá)在星形膠質(zhì)細(xì)胞,CCR2主要表達(dá)在神經(jīng)元;實(shí)時(shí)定量PCR顯示,腦損傷后3—21d損傷側(cè)海馬CCL2 mRNA、CCR2 mRNA水平明顯上升,差異有顯著性意義;高壓氧治療后海馬CCL2 mRNA明顯下降,與TBI組相比,7d組、14d組及21d組差異有顯著性意義(P0.05)。高壓氧治療7d、14d后海馬CCR2 mRNA明顯下降,與TBI組相比,7d組及14d組差異有顯著性意義(P0.05)。結(jié)論:HBO治療可以改善創(chuàng)傷性腦損傷大鼠認(rèn)知功能,其機(jī)制可能與海馬CCL2/CCR2表達(dá)下調(diào)有關(guān)。
[Abstract]:Objective: to observe the effect of hyperbaric oxygen therapy on cognitive function and the expression of CCL2 and its receptor CCR2 in hippocampus of rats with brain injury. Methods: 75 adult male SD rats were randomly divided into sham group and brain injury group according to digital table. HBOT group (25 rats in each group) and hyperbaric oxygen treatment group (HBOT group) and TBI group were treated with HBO every day to treat the dura mater exposed to the dura mater. The cognitive function was tested by Morris water maze. The expression of CCL2 and CCR2 in hippocampal CA1 was detected by fluorescence immunoassay, and the expression of CCL2 and CCR2mRNA in injured hippocampus was measured by real-time quantitative PCR. Results the results of water maze test showed that the mean latency of HBOT group was decreased on day 14 and day 21 after hyperbaric oxygen therapy. At the same time, the frequency of crossing the platform increased, compared with the TBI group, the difference was significant (P 0.05). The results of immunofluorescence double staining showed that the expression of CCL2 in the CA1 area of hippocampus was mainly in astrocytes and neurons after TBI, and the real-time quantitative PCR showed that the CCL2 was mainly expressed in the neurons. The level of CCL2 mRNA-CCR2 mRNA in the hippocampus of the injured side increased significantly after 3 to 21 days of brain injury, and the CCL2 mRNA in the hippocampus decreased significantly after hyperbaric oxygen treatment. Compared with TBI group, there was a significant difference between 14 d group and 21 d group in TBI group. CCR2 mRNA in hippocampus decreased significantly after hyperbaric oxygen treatment for 7 d and 14 d after hyperbaric oxygen therapy. Compared with TBI group, there was a significant difference between 7 d group and 14 day group (P 0.05). Conclusion the treatment of TBI can improve the cognitive function of traumatic brain injury rats, and its mechanism may be related to the down-regulation of CCL2/CCR2 expression in hippocampus.
【作者單位】： 南通大學(xué)附屬醫(yī)院;
【分類號(hào)】：R651.15
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本文編號(hào)：1625507