發(fā)布時(shí)間：2018-01-26 01:00

  本文關(guān)鍵詞： 高氧肺損傷 長(zhǎng)鏈非編碼RNA NANCI NKX. 小鼠　出處：《中國(guó)當(dāng)代兒科雜志》2017年02期 　論文類(lèi)型：期刊論文

【摘要】：目的探討長(zhǎng)鏈非編碼RNA NANCI在高氧誘導(dǎo)肺損傷新生小鼠肺組織中的表達(dá)變化及對(duì)NKX2.1的調(diào)控作用。方法采用隨機(jī)分組法將48只C57BL/6J新生小鼠隨機(jī)分為空氣組和高氧組,每組24只,各組再隨機(jī)分為生后7 d組、14 d組、21 d組,每組8只�？諝饨M置于室內(nèi)環(huán)境(Fi O2=21%)中飼養(yǎng),高氧組置于高氧箱(保持氧濃度95%)中飼養(yǎng),在各時(shí)間點(diǎn)分別處死兩組動(dòng)物后收集肺組織標(biāo)本。采用蘇木精-伊紅染色法觀察小鼠肺組織病理變化;采用RT-q PCR及Western blot技術(shù)分別檢測(cè)NANCI、NKX2.1的m RNA和蛋白表達(dá)水平。結(jié)果空氣組新生小鼠肺組織NANCI和NKX2.1的m RNA表達(dá)水平7 d最高(P0.05),14 d與21 d呈同水平表達(dá)。與空氣組比較,高氧組肺組織肺泡化程度降低,輻射狀肺泡計(jì)數(shù)(RAC)減少(P0.05),且高氧組RAC值隨高氧處理時(shí)間延長(zhǎng)逐漸降低(P0.05)。各時(shí)間點(diǎn)高氧組NANCI m RNA、NKX2.1 m RNA及其蛋白表達(dá)水平均低于空氣組(P0.05),且隨高氧處理時(shí)間延長(zhǎng)逐漸降低(P0.05)。NKX2.1與NANCI表達(dá)呈正相關(guān)(r=0.585,P=0.003);兩者與高氧組RAC水平均呈正相關(guān)(分別r=0.655、0.541,P0.05)。結(jié)論 NANCI可能主要參與未成熟肺組織發(fā)育;肺組織損傷程度隨高氧暴露時(shí)間的延長(zhǎng)逐漸加重,且NANCI及NKX2.1水平與肺損傷程度相關(guān),提示NANCI/NKX2.1靶基因信號(hào)通路可能參與新生小鼠高氧肺損傷過(guò)程。
[Abstract]:Objective to investigate the long chain noncoding RNA. Changes of NANCI expression in lung tissue of neonatal mice with hyperoxia-induced lung injury and its regulatory effect on NKX2.1. Methods 48 C57BL / 6J newborn mice were randomly divided into empty by random grouping. Gas group and hyperoxia group. 24 rats in each group were randomly divided into two groups: the 7th day postnatal group, 14 d group, 21 d group, 8 rats in each group, and the air group was fed in indoor environment. The rats in the hyperoxia group were fed in the hyperoxia box (keeping oxygen concentration 95). The lung tissue samples were collected after the animals were killed at each time point. The pathological changes of lung tissue were observed by hematoxylin-eosin staining method. NANCI was detected by RT-q PCR and Western blot. Results the expression level of m RNA in lung tissue of newborn mice in air group was highest at 7 days (P 0.05). Compared with the air group, the alveolar degeneration of lung tissue in the hyperoxia group decreased, and the radiative alveolar count decreased (P 0.05). The RAC value of hyperoxia group decreased gradually with the prolongation of hyperoxia treatment time, and NANCI m RNA of hyperoxia group decreased gradually at each time point. The expression level of NKX2.1 m RNA and its protein was lower than that of air group (P 0.05). With the prolongation of hyperoxia treatment time, the expression of P0.05N. NKX2.1 was positively correlated with the expression of NANCI. There was a positive correlation between NANCI and RAC level in hyperoxia group (r = 0.655-0.541P 0.050.Conclusion NANCI may be involved in the development of immature lung tissue. The degree of lung injury increased with the prolongation of hyperoxia exposure time, and the levels of NANCI and NKX2.1 were correlated with the severity of lung injury. These results suggest that NANCI/NKX2.1 target gene signaling pathway may be involved in the process of hyperoxia lung injury in newborn mice.
【作者單位】： 南京醫(yī)科大學(xué)附屬淮安第一醫(yī)院新生兒科;
【基金】：江蘇省臨床醫(yī)學(xué)專(zhuān)項(xiàng)(BL2014063) 淮安市科技攻關(guān)項(xiàng)目(HAS2014010)
【分類(lèi)號(hào)】：R722.1
【正文快照】： 支氣管肺發(fā)育不良(bronchopulmonary dysplasia,BPD)是發(fā)生于早產(chǎn)兒長(zhǎng)期應(yīng)用高濃度氧氣和輔助機(jī)械通氣后的一種慢性肺疾病(chronic lungdisease,CLD),是由生后感染、氣壓傷和容量傷導(dǎo)致的纖維化以及氧毒性等多因素誘發(fā)形成[1],其發(fā)病率隨胎齡和出生體重的減少而增高[2],其發(fā)生

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