首页|高良姜素调节AMPK/SIRT1/PGC-1α信号通路对高氧致早产大鼠肺损伤的影响

高良姜素调节AMPK/SIRT1/PGC-1α信号通路对高氧致早产大鼠肺损伤的影响

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目的 探讨高良姜素(Ga)对高氧致早产大鼠肺损伤及腺苷酸活化蛋白激酶(AMPK)/沉默信息调节因子1(SIRT1)/过氧化物酶体增殖物激活受体γ辅活化因子1α(PGC-1α)信号通路的影响.方法 建立高氧致早产大鼠肺损伤模型,将大鼠分为对照组(Control组)、模型组(Model组)、Ga低剂量组(Ga-L组)、Ga高剂量组(Ga-H组)、Ga-H+AMPK抑制剂Dorsomorphin组(Ga-H+Dors组);检测大鼠肺湿重/干重比值;H-E染色观察肺组织病理变化;ELISA检测支气管肺泡灌洗液(BALF)肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)水平;试剂盒检测超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)水平;TUNEL染色检测肺组织细胞凋亡情况;Western blot检测Bcl-2相关X蛋白(Bax)、B淋巴细胞瘤-2(Bcl-2)、AMPK、SIRT1、PGC-1α蛋白表达.结果 与Control组相比,Model组早产大鼠肺湿重/干重比值、TNF-α、IL-6、MDA、细胞凋亡率、Bax水平升高,SOD、GSH、Bcl-2、p-AMPK/AMPK、SIRT1、PGC-1α水平降低(P<0.05);与Model组相比,Ga-L、Ga-H组早产大鼠肺湿重/干重比值、TNF-α、IL-6、MDA、细胞凋亡率、Bax 水平降低,SOD、GSH、Bcl-2、p-AMPK/AMPK、SIRT1、PGC-1α 水平升高(P<0.05);Dorsomorphin减弱了 Ga-H对高氧致早产大鼠肺损伤的改善作用.结论 Ga可能通过激活AMPK/SIRT1/PGC-1α通路,抑制炎症、氧化应激和细胞凋亡,减轻高氧致早产大鼠的肺损伤.
Effect of galangin on hyperoxia-induced lung injury in premature rats by regulating the AMPK/SIRT1/PGC-1α signaling pathway
Objective To investigate the effect of galangin(Ga)on hyperoxia-induced lung injury and adenylate ac-tivated protein kinase(AMPK)/silent information regulator factor 1(SIRT1)/peroxisome proliferator-activated receptor γcoactivator 1α(PGC-1α)pathway in premature rats.Methods The hyperoxia induced lung injury model of premature rats was established.The rats were divided into Control group,Model group,low and high dose Ga groups(Ga-L group,Ga-H group),and Ga-H+AMPK inhibitor Dorsomorphin group(Ga-H+Dors group);the wet to dry weight ratio of rat lungs was detected;H-E staining was used to observe pathological changes in lung tissue.ELISA was used to detect tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)levels in bronchoalveolar lavage fluid(BALF).The kits were used to detect levels of super-oxide dismutase(SOD),malondialdehyde(MDA),and glutathione(GSH).TUNEL staining was used to detect apoptosis in lung tissue cells.Western blot was used to detect the expression of BCL2-associated X protein(Bax),B-cell lymphoma-2(Bcl-2),AMPK,SIRT1,and PGC-1α proteins.Results Compared with Control group,the ratio of lung wet weight to dry weight,TNF-α,IL-6,MDA,cell apoptosis rate,and the level of Bax in Model group were increased,the levels of SOD,GSH,Bcl-2,p-AMPK/AMPK,SIRT1,and PGC-1α were reduced(P<0.05);compared with Model group,the ratio of lung wet weight to dry weight,TNF-α,IL-6,MDA,cell apoptosis rate,and the expression level of Bax in Ga-L and Ga-H groups were reduced,the levels of SOD,GSH,Bcl-2,p-AMPK/AMPK,SIRT1,and PGC-1α were increased(P<0.05);Dorsomorphin attenuated the ameliorative effect of Ga-H on lung injury in hyperoxy-induced preterm rats.Conclusion Ga may inhibit inflammation,oxi-dative stress and apoptosis by activating the AMPK/SIRT1/PGC-1α pathway,and alleviate lung injury in premature rats in-duced by hyperoxia.

galanginadenylate activated protein kinase(AMPK)/silent information regulator factor 1(SIRT1)/peroxisome proliferator-activated receptor γ coactivator 1α(PGC-1α)signaling pathwayhyperoxiapremature ratslung in-jury

王雪莲、谭华发

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重庆两江新区人民医院儿科,重庆 401147

高良姜素 腺苷酸活化蛋白激酶/沉默信息调节因子1/过氧化物酶体增殖物激活受体γ辅活化因子1α信号通路 高氧 早产大鼠 肺损伤

2024

中国优生与遗传杂志
中国优生科学协会

中国优生与遗传杂志

CSTPCD
影响因子:0.527
ISSN:1006-9534
年,卷(期):2024.32(3)
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