Abstract
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.
Highlights
Acute kidney injury (AKI), as a common complication, is very serious, and even life-threatening in critically patients [1]
IR and IR can both decrease the blood pH, arterial partial pressure of carbon dioxide (PaCO2), and arterial partial pressure of oxygen (PaO2) especially IR (p < 0.05), and they can be increased by Tanshinone IIA (TIIA), cyclosporine A (CsA), and TIIA+CsA (p < 0.05), while pretreatment with TIIA+CsA was higher than TIIA and CsA (p < 0.05; Figure 1A)
The tidal volume (TV), minute ventilation (MV), peak inspiratory force (PIF), peak expiratory force (PEF), and exhale force metaphase (EF50) were decreased by IR and IR, especially the IR (p < 0.05), which were decreased by TIIA, CsA, and TIIA+CsA (p < 0.05), and pretreatment with TIIA+CsA was higher than TIIA and CsA (p < 0.05)
Summary
Acute kidney injury (AKI), as a common complication, is very serious, and even life-threatening (high mortality) in critically patients [1]. The major cause of AKI is renal ischemia-reperfusion (IR) [2]. It. Lung Apoptosis Induced by Renal Ischemia-Reperfusion is worth noting that respiratory failure rather than kidney failure is the main cause of death induced by AKI [5]. Lung endothelial cell inflammation and apoptosis induce ALI following AKI induced by renal IR [7, 8]. As a potential mediator between lung and kidney injury, pulmonary microvascular endothelial cells (PMVECs) express proapoptosis and proinflammation genes, which can change after AKI is induced by renal IR [7, 8]. To our knowledge, no study has explored the change of mitochondrial function in the lung following renal IR in obese rats
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