Tai He, Jiang Xiao-Lin, Song Nan, Xiao Hong-He, Li Yue, Cheng Mei-Jia, Yin Xiao-Mei, Chen Yi-Ran, Yang Guan-Lin, Jiang Xiao-Yu, Kuang Jin-Song, Lan Zhi-Ming, Jia Lian-Qun
Key Laboratory of Ministry of Education for Traditional Chinese Medicine Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Department of Nephrology, The Fourth of Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine (Shenzhen Traditional Chinese Medicine Hospital), Guangzhou University of Traditional Chinese Medicine, Shenzhen, China.
Front Med (Lausanne). 2021 May 3;8:617393. doi: 10.3389/fmed.2021.617393. eCollection 2021.
Acute lung injury (ALI), which is induced by renal ischemia-reperfusion (IR), is one of the leading causes of acute renal IR-related death. Obesity raises the frequency and severity of acute kidney injury (AKI) and ALI. Tanshinone IIA (TIIA) combined with cyclosporine A (CsA) was employed to lessen the lung apoptosis led by renal IR and to evaluate whether TIIA combined with CsA could alleviate lung apoptosis by regulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats. Hematoxylin-eosin (HE) staining was used to assess the histology of the lung injury. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was used to assess apoptosis of the lung. Electron microscopy was used to assess mitochondrial morphology in lung cells. Arterial blood gas and pulmonary function were used to assess the external respiratory function. Mitochondrial function was used to assess the internal respiratory function and mitochondrial dynamics and biogenesis. Western blot (WB) was used to examine the PI3K/Akt/Bad pathway-related proteins. TIIA combined with CsA can alleviate lung apoptosis by regulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats.
由肾缺血再灌注（IR）诱导的急性肺损伤（ALI）是急性肾IR相关死亡的主要原因之一。肥胖会增加急性肾损伤（AKI）和ALI的发生频率及严重程度。采用丹参酮IIA（TIIA）联合环孢素A（CsA）来减轻肾IR导致的肺细胞凋亡，并评估TIIA联合CsA是否能通过PI3K/Akt/Bad途径调节线粒体功能来减轻肥胖大鼠的肺细胞凋亡。采用苏木精-伊红（HE）染色评估肺损伤的组织学变化。采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL）评估肺细胞凋亡。采用电子显微镜评估肺细胞中的线粒体形态。采用动脉血气和肺功能评估外呼吸功能。采用线粒体功能评估内呼吸功能以及线粒体动力学和生物发生。采用蛋白质免疫印迹法（WB）检测PI3K/Akt/Bad途径相关蛋白。在肥胖大鼠中，TIIA联合CsA可通过PI3K/Akt/Bad途径调节线粒体功能来减轻肺细胞凋亡。
