中国医科大学学报2024，Vol.53Issue(6)：501-508,8.DOI:10.12007/j.issn.0258-4646.2024.06.004
自噬抑制急性肾损伤诱导急性肺损伤的分子机制
Molecular mechanism whereby autophagy inhibits acute lung injury induced by acute kidney injury
摘要
Abstract
Objective This study aimed to explore the regulatory role of autophagy in acute kidney injury(AKI)-induced acute liver injury(ALI).Methods Forty-eight male Sprague-Dawley rats were randomly divided into four groups:sham operation group,IRI group,3-MA group and RA group.Except for the sham operation group,a rat model of AKI induced by IRI was established in all groups.The AKI model was established by removing the right kidney,separating the left renal artery,and clamping the left renal artery,followed by reper-fusion for 12,24,48,or 72 h.The 3-MA and RA groups were intraperitoneally injected with 3-MA(15 mg/kg,1 mL)or RA(2 mg/kg,1 mL)12 h before and after IRI treatment.The structure and function of the rat lung and kidney tissues were evaluated,and the expression levels of autophagy-related proteins,oxidative stress,and apoptosis were measured.Results Renal IRI led to ALI after AKI,and the levels of blood urea nitrogen,creatinine,tumor necrosis factor-α,and interleukin-1βwere all significantly increased.In addition,compared to the IRI group,the expression levels of P62 and caspase-3 significantly decreased in the RA group,whereas the expression levels of LC3-Ⅱ/LC3-Ⅰ,Beclin-1,Bcl-2,and ULK1 increased.Autophagy reduced pathological damage to kidney and lung tissues by inhibiting inflammation and oxidative stress and effectively ameliorated AKI-induced ALI.Conclusion Autophagy plays an important role in the regulation of ALI induced by AKI and can be used as a new target for AKI treatment and to reduce complication-related mortality.关键词
自噬/凋亡/急性肾损伤/急性肺损伤/缺血再灌注损伤Key words
autophagy/apoptosis/acute kidney injury/acute lung injury/ischemic reperfusion injury分类
医药卫生引用本文复制引用
袁琦,简禄勇,郭华慧,张星炜,曹海虹,黄仁发..自噬抑制急性肾损伤诱导急性肺损伤的分子机制[J].中国医科大学学报,2024,53(6):501-508,8.基金项目
广东省自然科学基金(2020A1515010566) （2020A1515010566）
深圳市科学技术研究开发基金(JCYJ20190809102413156) （JCYJ20190809102413156）
