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目的 :观察永久性大脑中动脉栓塞(permanent middle cerebral artery occlusion,p MCAO)模型大鼠心、肾组织内自噬标志物微管相关蛋白轻链3(LC3)和P62的变化情况,探讨高压氧对心、肾组织自噬的影响及意义。方法:雄性Sprague-Dawley大鼠共75只,随机分为对照组、p MCAO组和高压氧组(p MCAO后给予高压氧处理);每组按造模后6 h和5 d 2个时间点处死大鼠并分成2个亚组。通过改良神经功能缺陷评分(m NSS)评估大鼠神经功能损伤情况,利用2,3,5-氯化三苯基四氮唑(TTC)法测定大鼠脑梗死面积,蛋白质印迹法(Western blotting)检测心、肾组织蛋白表达情况,实时荧光定量(real time)PCR检测组织内基因水平。结果:高压氧干预可有效减少脑缺血损伤后梗死面积,有助于神经功能恢复。除了高压氧6 h亚组的肾组织外,各组心、肾组织LC3和P62的蛋白表达水平变化基本与基因水平相符,且LC3与P62蛋白表达变化趋势基本一致。在大鼠心、肾组织中,脑缺血6 h后LC3-Ⅱ/LC3-Ⅰ和P62表达升高,高压氧处理后下降(P<0.05);缺血后5 d结果基本与6 h相似。结论:脑缺血损伤后心、肾组织内LC3-Ⅱ/LC3-Ⅰ和P62蛋白表达水平上调,高压氧干预后可下调,高压氧可能通过抑制自噬活性减少脑缺血后继发的心、肾损伤。
OBJECTIVE: To observe the changes of LC3 and P62, an autophagy marker, in the heart and kidney tissues of permanent middle cerebral artery occlusion (p MCAO) model rats and to explore whether hyperbaric oxygen Effect on heart and renal autophagy and its significance. Methods: A total of 75 male Sprague-Dawley rats were randomly divided into control group, p MCAO group and hyperbaric oxygen group (hyperbaric oxygen treatment after p MCAO). At 6 h and 5 d after modeling, Rats were sacrificed and divided into 2 subgroups. Neurological impairment was evaluated by improving neurological deficit score (m NSS). Cerebral infarct area was measured by 2,3,5-triphenyltetrazolium chloride (TTC) method. Western blotting ) To detect the expression of heart and kidney tissue protein, real-time PCR to detect the level of gene in the tissue. Results: Hyperbaric oxygen intervention can effectively reduce the area of infarction after cerebral ischemia injury and contribute to nerve function recovery. In addition to hyperbaric oxygen 6 h subgroup of renal tissue, heart and kidney tissue LC3 and P62 protein expression levels in the basic line with the gene level, and LC3 and P62 protein expression trends are basically the same. The expression of LC3-Ⅱ / LC3-Ⅰ and P62 in rat heart and kidney tissue increased 6 h after cerebral ischemia and decreased after hyperbaric oxygen treatment (P <0.05). The results of 5 d after ischemia were similar to those of 6 h . CONCLUSION: The expression of LC3-Ⅱ / LC3-Ⅰ and P62 protein in heart and kidney tissues after focal cerebral ischemia is up-regulated, which may be down-regulated after hyperbaric oxygen intervention. Hyperbaric oxygen may reduce the secondary heart after cerebral ischemia by inhibiting autophagy activity, Kidney injury.