角質(zhì)細(xì)胞生長(zhǎng)因子-2對(duì)煙霧吸入所致肺損傷修復(fù)作用的實(shí)驗(yàn)研究
發(fā)布時(shí)間：2019-01-26 10:47
【摘要】：目的觀察角質(zhì)細(xì)胞生長(zhǎng)因子-2對(duì)煙霧吸入所致肺損傷的修復(fù)作用,并研究其相關(guān)機(jī)制。方法新西蘭大白兔120只制成煙霧吸入性損傷模型,隨機(jī)平均分為五組:0mg/kg組:致傷兔不作處理;PBS組:致傷后4小時(shí),霧化吸入磷酸緩沖鹽溶液(PBS)5ml,每日1次,連續(xù)7日;1mg/kg組:致傷后4小時(shí),霧化吸入KGF-2(1mg/Kg,溶于5ml PBS),每日1次,連續(xù)7日;2mg/kg組:致傷后4小時(shí),霧化吸入KGF-2(2mg/K g,溶于5ml PBS),每日1次,連續(xù)7日;5mg/kg組:致傷后4小時(shí),霧化吸入KGF-2(5mg/K g,溶于5ml PBS),每日1次,連續(xù)7日;每組動(dòng)物分別于治療1d、3d、5d、7d后,在各時(shí)相點(diǎn)行動(dòng)脈血?dú)夥治?放血處死,收集標(biāo)本,Western blot法測(cè)定肺組織中肺表面活性蛋白A(SP-A)、血管內(nèi)皮生長(zhǎng)因子(VEGF)及Bcl-2蛋白水平,Real time PCR檢測(cè)肺組織中肺表面活性蛋白A、血管內(nèi)皮生長(zhǎng)因子及Bcl-2蛋白mRNA水平,TUNEL檢測(cè)細(xì)胞凋亡情況,并觀察肺組織病理改變。結(jié)果(1)與0mg/kg組比較,PBS組煙霧吸入性損傷兔的PaO2、PaCO2均無顯著差異(P0.05);致傷后,生存時(shí)間對(duì)PaO2、PaCO2均有影響(P0.01),隨著生存時(shí)間延長(zhǎng),PaO2、PaCO2總體變化具有上升趨勢(shì);霧化吸入KGF-2對(duì)煙霧吸入性損傷兔PaCO2無明顯影響(P0.05),對(duì)PaO2有影響(P0.01),能夠提高PaO2,以5mg/kg組與各組比較差異均顯著(P0.05),且KGF-2與時(shí)間有交互作用(P0.05),5mg/kg組,在第7d提高氧分壓最明顯。(2)與0mg/kg組比較,PBS組動(dòng)物肺組織中SP-A、VEGF、Bcl-2含量及相關(guān)mRNA表達(dá)均無顯著差異(P0.05);致傷后,生存時(shí)間對(duì)SP-A、VEGF、Bcl-2含量及相關(guān)mRNA表達(dá)均有影響(P0.01),隨著生存時(shí)間延長(zhǎng),SP-A、VEGF、Bcl-2含量及相關(guān)mRNA表達(dá)總體變化均具有增加趨勢(shì);霧化吸入KGF-2對(duì)致傷動(dòng)物肺組織中SP-A、VEGF、Bcl-2含量及相關(guān)mRNA表達(dá)均有影響(P0.01),能夠提高肺組織中SP-A、VEGF、Bcl-2含量及相關(guān)mRNA表達(dá),以5mg/kg組與各組比較差異均顯著(P0.05),且KGF-2與時(shí)間有交互作用(P0.01),5mg/kg組,在第7d提高肺組織中SP-A、VEGF、Bcl-2含量及相關(guān)mRNA表達(dá)最明顯。(3)與0mg/kg組比較,PBS組動(dòng)物肺組織細(xì)胞凋亡指數(shù)無顯著差異(P0.05);致傷后,生存時(shí)間對(duì)肺組織細(xì)胞凋亡指數(shù)有影響(P0.01),隨著生存時(shí)間延長(zhǎng),肺組織細(xì)胞凋亡指數(shù)總體變化具有降低趨勢(shì);霧化吸入KGF-2對(duì)動(dòng)物肺組織細(xì)胞凋亡指數(shù)有影響(P0.01),能夠降低肺組織細(xì)胞凋亡指數(shù),以5mg/kg組與各組比較差異均顯著(P0.05),且KGF-2與時(shí)間有交互作用(P0.01),5mg/kg組,在第7d降低肺組織細(xì)胞凋亡指數(shù)最明顯。(4)肺組織病理檢查顯示,與傷后第1天相比,各組動(dòng)物第7天肺部損傷表現(xiàn)均較前減輕,各組相比,以5mg/Kg組動(dòng)物損傷減輕最為明顯。結(jié)論KGF-2對(duì)煙霧吸入所致肺損傷具有修復(fù)作用。其修復(fù)作用可能與KGF-2增加煙霧吸入性損傷的肺表面活性蛋白A合成,促進(jìn)肺新生血管形成,以及抑制肺損傷細(xì)胞凋亡這三方面機(jī)制有關(guān)。
[Abstract]:Objective to investigate the repair effect of keratinocyte growth factor 2 (KGF 2) on lung injury induced by smoke inhalation and its related mechanism. Methods 120 New Zealand white rabbits were randomly divided into five groups: 0mg/kg group: the injured rabbits were not treated; In PBS group, 4 hours after injury, (PBS) 5 ml of phosphate buffer solution was inhaled once a day for 7 days, while in 1mg/kg group, KGF-2 (1 mg / kg) dissolved in 5ml PBS), once daily for 7 days, 4 hours after injury. In 2mg/kg group, KGF-2 (2mg/K g, dissolved in 5ml PBS), once a day for 7 days) was inhaled 4 hours after injury. In 5mg/kg group, KGF-2 (5mg/K g, dissolved in 5ml PBS), once a day for 7 days) was inhaled 4 hours after injury. The animals in each group were treated for 1 day, 3 days, 5 days and 7 days later. Arterial blood gas analysis was performed at each time point, and blood was put to death. The lung surfactant protein A (SP-A) in lung tissue was determined by, Western blot method. The levels of vascular endothelial growth factor (VEGF) and Bcl-2 protein were detected by, Real time PCR, and the levels of pulmonary surfactant protein A, vascular endothelial growth factor (VEGF) and Bcl-2 protein mRNA in lung tissue were detected by, Real time PCR. Apoptosis was detected by TUNEL, and the pathological changes of lung tissue were observed. Results (1) there was no significant difference in PaO2,PaCO2 between PBS group and 0mg/kg group (P0.05). After injury, the survival time had an effect on PaO2,PaCO2 (P0.01). With the prolongation of survival time, the overall change of PaO2,PaCO2 showed an upward trend. Aerosol inhalation of KGF-2 had no significant effect on PaCO2 in rabbits with smoke inhalation injury (P0.05), but had an effect on PaO2 (P0.01), and could improve PaO2, significantly in 5mg/kg group compared with each group (P0.05). There was interaction between KGF-2 and time (P0.05). In 5mg/kg group, the increase of oxygen partial pressure was the most obvious on the 7th day. (2) compared with 0mg/kg group, SP-A,VEGF, in lung tissue of PBS group was more obvious than that of PBS group. There was no significant difference in Bcl-2 content and related mRNA expression (P0.05). After injury, survival time had an effect on SP-A,VEGF,Bcl-2 content and related mRNA expression (P0.01). With the prolongation of survival time, the content of SP-A,VEGF,Bcl-2 and the expression of related mRNA increased. Aerosol inhalation of KGF-2 had an effect on the expression of SP-A,VEGF,Bcl-2 and related mRNA in lung tissue of injured animals (P0.01), and could increase the content of SP-A,VEGF,Bcl-2 and the expression of related mRNA in lung tissue. The difference between 5mg/kg group and each group was significant (P0.05), and there was interaction between KGF-2 and time (P0.01). In 5mg/kg group, the SP-A,VEGF, in lung tissue was increased on the 7th day. Bcl-2 content and related mRNA expression was the most obvious. (3) compared with 0mg/kg group, the apoptosis index of lung tissue in PBS group had no significant difference (P0.05). After injury, survival time had an effect on the apoptosis index of lung tissue (P0.01), and with the prolongation of survival time, the overall change of apoptosis index of lung tissue showed a decreasing trend. Aerosol inhalation of KGF-2 had an effect on the apoptosis index of lung tissue (P0.01), and could decrease the apoptosis index of lung tissue. The difference between 5mg/kg group and each group was significant (P0.05). KGF-2 had interaction with time (P0.01). In 5mg/kg group, the apoptosis index of lung tissue was significantly decreased on the 7th day. (4) the pathological examination of lung tissue showed that compared with the first day after injury, the apoptosis index of lung tissue was significantly decreased in 5mg/kg group. On the 7th day, lung injury was alleviated in all groups, especially in 5mg/Kg group. Conclusion KGF-2 can repair lung injury induced by smoke inhalation. The repair effect of KGF-2 may be related to the increase of pulmonary surfactant A synthesis in smoke inhalation injury, the promotion of pulmonary angiogenesis, and the inhibition of apoptosis of lung injury cells.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R563
[Abstract]:Objective to investigate the repair effect of keratinocyte growth factor 2 (KGF 2) on lung injury induced by smoke inhalation and its related mechanism. Methods 120 New Zealand white rabbits were randomly divided into five groups: 0mg/kg group: the injured rabbits were not treated; In PBS group, 4 hours after injury, (PBS) 5 ml of phosphate buffer solution was inhaled once a day for 7 days, while in 1mg/kg group, KGF-2 (1 mg / kg) dissolved in 5ml PBS), once daily for 7 days, 4 hours after injury. In 2mg/kg group, KGF-2 (2mg/K g, dissolved in 5ml PBS), once a day for 7 days) was inhaled 4 hours after injury. In 5mg/kg group, KGF-2 (5mg/K g, dissolved in 5ml PBS), once a day for 7 days) was inhaled 4 hours after injury. The animals in each group were treated for 1 day, 3 days, 5 days and 7 days later. Arterial blood gas analysis was performed at each time point, and blood was put to death. The lung surfactant protein A (SP-A) in lung tissue was determined by, Western blot method. The levels of vascular endothelial growth factor (VEGF) and Bcl-2 protein were detected by, Real time PCR, and the levels of pulmonary surfactant protein A, vascular endothelial growth factor (VEGF) and Bcl-2 protein mRNA in lung tissue were detected by, Real time PCR. Apoptosis was detected by TUNEL, and the pathological changes of lung tissue were observed. Results (1) there was no significant difference in PaO2,PaCO2 between PBS group and 0mg/kg group (P0.05). After injury, the survival time had an effect on PaO2,PaCO2 (P0.01). With the prolongation of survival time, the overall change of PaO2,PaCO2 showed an upward trend. Aerosol inhalation of KGF-2 had no significant effect on PaCO2 in rabbits with smoke inhalation injury (P0.05), but had an effect on PaO2 (P0.01), and could improve PaO2, significantly in 5mg/kg group compared with each group (P0.05). There was interaction between KGF-2 and time (P0.05). In 5mg/kg group, the increase of oxygen partial pressure was the most obvious on the 7th day. (2) compared with 0mg/kg group, SP-A,VEGF, in lung tissue of PBS group was more obvious than that of PBS group. There was no significant difference in Bcl-2 content and related mRNA expression (P0.05). After injury, survival time had an effect on SP-A,VEGF,Bcl-2 content and related mRNA expression (P0.01). With the prolongation of survival time, the content of SP-A,VEGF,Bcl-2 and the expression of related mRNA increased. Aerosol inhalation of KGF-2 had an effect on the expression of SP-A,VEGF,Bcl-2 and related mRNA in lung tissue of injured animals (P0.01), and could increase the content of SP-A,VEGF,Bcl-2 and the expression of related mRNA in lung tissue. The difference between 5mg/kg group and each group was significant (P0.05), and there was interaction between KGF-2 and time (P0.01). In 5mg/kg group, the SP-A,VEGF, in lung tissue was increased on the 7th day. Bcl-2 content and related mRNA expression was the most obvious. (3) compared with 0mg/kg group, the apoptosis index of lung tissue in PBS group had no significant difference (P0.05). After injury, survival time had an effect on the apoptosis index of lung tissue (P0.01), and with the prolongation of survival time, the overall change of apoptosis index of lung tissue showed a decreasing trend. Aerosol inhalation of KGF-2 had an effect on the apoptosis index of lung tissue (P0.01), and could decrease the apoptosis index of lung tissue. The difference between 5mg/kg group and each group was significant (P0.05). KGF-2 had interaction with time (P0.01). In 5mg/kg group, the apoptosis index of lung tissue was significantly decreased on the 7th day. (4) the pathological examination of lung tissue showed that compared with the first day after injury, the apoptosis index of lung tissue was significantly decreased in 5mg/kg group. On the 7th day, lung injury was alleviated in all groups, especially in 5mg/Kg group. Conclusion KGF-2 can repair lung injury induced by smoke inhalation. The repair effect of KGF-2 may be related to the increase of pulmonary surfactant A synthesis in smoke inhalation injury, the promotion of pulmonary angiogenesis, and the inhibition of apoptosis of lung injury cells.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R563
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