本文選題：缺血再灌注損傷 + 老年大鼠��； 參考：《中南大學(xué)》2012年碩士論文

【摘要】：目的： 探討血紅素氧合酶-1(Heme oxygenase-1)對(duì)老年大鼠缺血再灌注損傷(ischemia/reperfusion injury, IRI)'腎臟的抗凋亡作用及其機(jī)制。 方法： 25月齡健康雄性Wistar大鼠隨機(jī)分為正常對(duì)照組、I/R組、CoPP組、ZnPP組和CoPP+SB203580組。成功建模后24h,取腎臟組織,分別用RT-PCR和Western blot檢測(cè)HO-1蛋白的表達(dá)；免疫組化檢測(cè)Caspase-3的表達(dá)；流式細(xì)胞術(shù)檢測(cè)腎組織細(xì)胞凋亡情況；Western blot檢測(cè)P38MAPK的磷酸化的情況。 結(jié)果： RT-PCR和Western blot結(jié)果顯示：對(duì)照組腎組織中存在HO-1分子的mRNA和蛋白的表達(dá)；與對(duì)照組相比,I/R組HO-1的表達(dá)明顯增加,HO-1誘導(dǎo)劑CoPP增加了HO-1的表達(dá),HO-1抑制制劑ZnPP抑制了HO-1的表達(dá)。免疫組化結(jié)果顯示I/R組Caspase-3表達(dá)水平明顯升高,與I/R組比較,CoPP組腎組織Caspase-3表達(dá)水平顯著降低,而ZnPP組和CoPP+SB203580組Caspase-3表達(dá)水平￡顯著升高。流式細(xì)胞術(shù)結(jié)果顯示,I/R組細(xì)胞凋亡率明顯升高,與I/R組比較,CoPP組細(xì)胞凋亡率顯著降低,而ZnPP組和CoPP+SB203580組細(xì)胞凋亡率明顯升高；Western blot結(jié)果顯示I/R組p38MAPK的磷酸化水平明顯升高,HO-1誘導(dǎo)劑CoPP促進(jìn)了p38MAPK的磷酸化,HO-1抑制劑ZnPP抑制了p38MAPK的磷酸化,SB203580同樣抑制了p38MAPK的磷酸化。 結(jié)論： HO-1對(duì)老年大鼠缺血再灌注損傷的保護(hù)作用可能是通過(guò)激活P38MAPK的磷酸化,抑制凋亡因子的表達(dá),減少細(xì)胞凋亡,從而減輕腎臟損傷及功能障礙來(lái)實(shí)現(xiàn)。
[Abstract]:Aim: to investigate the antiapoptotic effect of heme oxygenase-1 on ischemia/reperfusion injury-reperfusion injury (IRI) 'kidney in aged rats and its mechanism. Methods: healthy male Wistar rats aged 25 months were randomly divided into two groups: normal control group (I / R group) and Copp group (ZnPP group) and CoPP SB203580 group. The expression of HO-1 protein was detected by RT-PCR and Western blot, the expression of Caspase-3 was detected by immunohistochemistry, the apoptosis of renal tissue was detected by flow cytometry and the phosphorylation of P38 MAPK was detected by Western blot. Results: the results of RT-PCR and Western blot showed that the expression of HO-1 mRNA and protein existed in the control group. Compared with the control group, the expression of HO-1 in IPA / R group was significantly increased, and the expression of HO-1 was increased by CoPP, the inducer of HO-1, and the expression of HO-1 was inhibited by ZnPP, an inhibitor of HO-1. The results of immunohistochemistry showed that the expression of Caspase-3 was significantly increased in I / R group. Compared with I / R group, the expression level of Caspase-3 in renal tissue of Caspase-3 was significantly decreased, while that of Caspase-3 in ZnPP group and Copp SB203580 group was significantly higher than that in I / R group. The results of flow cytometry showed that the apoptosis rate of I- / R group was significantly higher than that of I- / R group, but the apoptosis rate of ZnPP group and Copp SB203580 group was significantly higher than that of I / R group. Western blot showed that the phosphorylation level of p38 MAPK was significantly increased in I / R group. Copp promoted the phosphorylation of p38 MAPK and inhibited the phosphorylation of p38 MAPK, SB203580 and p38 MAPK, as well as the phosphorylation of p38 MAPK. Conclusion: the protective effect of HO-1 on ischemia-reperfusion injury in aged rats may be achieved by activating phosphorylation of p38 MAPK, inhibiting the expression of apoptotic factor and reducing apoptosis, thereby reducing renal injury and dysfunction.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類(lèi)號(hào)】：R-332;R692

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