The effect of levosimendan on lung damage after myocardial ischemia reperfusion in rats in which experimental diabetes was induced

Alkan, Metin; Çelik, Ali; Bilge, Mustafa; Kiraz, Hasan Ali; Kip, Gülay; Özer, Abdullah; Şıvgın, Volkan; Erdem, Özlem; Arslan, M; Kavutçu, Mustafa

doi:10.1016/j.jss.2014.08.038

Cited by 20 publications

(10 citation statements)

References 29 publications

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“…The consequence of these pulmonary involvements confers fragility to diabetic lungs, when they underwent an acute or chronic pulmonary and/or cardiac disease (e.g., myocardial IR). Consistent with the previous studies [ 7 ], our present study have demonstrated that diabetic lungs are more vulnerable to myocardial IR, indicated by our results that diabetic rats subjected to myocardial IR showed serious ALI with higher lung injury score and WET/DRY ratio, and lower PaO 2 as compared with that in control rats.…”

Section: Discussionsupporting

confidence: 93%

“…Previous studies indicated that myocardial IR could also cause injury in distant organs, and the lung can be one of the most affected organs [ 5 , 6 ]. Further studies suggested that acute lung injury (ALI) induced by myocardial IR in diabetes was more serious than that in nondiabetics [ 7 ]. However, there are little relevant reports concerning the potential mechanism of ALI induced by myocardial IR under diabetic condition.…”

Section: Introductionmentioning

confidence: 99%

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The Roles of Autophagy in Acute Lung Injury Induced by Myocardial Ischemia Reperfusion in Diabetic Rats

Zhang

et al. 2018

Journal of Diabetes Research

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Patients with diabetes are vulnerable to myocardial ischemia reperfusion (IR) injury, which may also induce acute lung injury (ALI) due to overaccumulation of reactive oxygen species (ROS) and inflammation cytokine in circulation. Despite autophagy plays a significant role in diabetes and pulmonary IR injury, the role of autophagy in ALI secondary to myocardial IR in diabetes remains largely elusive. We aimed to investigate pulmonary autophagy status and its roles in oxidative stress and inflammation reaction in lung tissues from diabetic rats subjected to myocardial IR. Control or diabetic rats were either treated with or without autophagy inducer rapamycin (Rap) or autophagy inhibitor 3-methyladenine (3-MA) before myocardial IR, which was achieved by occluding the left anterior descending coronary artery for 30 min and followed by reperfusion for 120 min. Diabetic rats subjected to myocardial IR showed more serious ALI with higher lung injury score and WET/DRY ratio and lower PaO2 as compared with control rats, accompanied with impaired autophagy indicated by reduced LC-3II/LC-3I ratio and Beclin-1 expression, decreased superoxide dismutase (SOD) activity, and increased 15-F2t-Isoprostane formation in lung tissues, as well as increased levels of leukocyte count and proinflammatory cytokines in BAL fluid. Improving autophagy with Rap significantly attenuated all these changes, but the autophagy inhibitor 3-MA exhibited adverse or opposite effects as Rap. In conclusion, diabetic lungs are more vulnerable to myocardial IR, which are involved in impaired autophagy. Improving autophagy could attenuate ALI induced by myocardial IR in diabetic rats, possibly through inhibiting inflammatory reaction and oxidative stress.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

The Roles of Autophagy in Acute Lung Injury Induced by Myocardial Ischemia Reperfusion in Diabetic Rats

Zhang

et al. 2018

Journal of Diabetes Research

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“…The neutrophil infiltration/aggregation, alveolar wall thickening, and excessive production of alveolar interstitial collagen were manifested in diabetic mice, which is consistent with previous reports on diabetic lung injury. 72,73 Likewise, a similar phenotype was observed in the mice with antibiotic-induced gut dysbiosis. It is worthwhile to note that the heat maps between STZ-induced diabetic mice and antibiotic-induced gut dysbiosis are similar.…”

Section: Discussionsupporting

confidence: 57%

Gut-Lung Dysbiosis Accompanied by Diabetes Mellitus Leads to Pulmonary Fibrotic Change through the NF-κB Signaling Pathway

Wang

et al. 2021

The American Journal of Pathology

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“…The basal membranes were thickened, along with an intense inflammatory reaction in diabetic lungs [ 22 ]. The structures of lung tissue and lamellar bodies showed collapse in DM group [ 23 ], neutrophil infiltration or aggregation and alveolar wall thickening in lung tissue were significantly higher in the DM group than in the control group [ 24 ]. In diabetic lung models, histological examination with Sirius red and eosin and hemotoxylin staining showed fibrosis along with massive inflammatory cell infiltration [ 25 ].…”

Section: Morphological Changes In Diabetic Lung Injurymentioning

confidence: 99%

Potential Biochemical Mechanisms of Lung Injury in Diabetes

Zheng¹,

Wu²,

Jin³

et al. 2017

Aging and disease

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Accumulating evidence has shown that the lung is one of the target organs for microangiopathy in patients with either type 1 or type 2 diabetes mellitus (DM). Diabetes is associated with physiological and structural abnormalities in the diabetic lung concurrent with attenuated lung function. Despite intensive investigations in recent years, the pathogenic mechanisms of diabetic lung injury remain largely elusive. In this review, we summarize currently postulated mechanisms of diabetic lung injury. We mainly focus on the pathogenesis of diabetic lung injury that implicates key pathways, including oxidative stress, non-enzymatic protein glycosylation, polyol pathway, NF-κB pathway, and protein kinase c pathway. We also highlight that while numerous studies have mainly focused on tissue or cell damage in the lung, studies focusing on mitochondrial dysfunction in the diabetic lung have remained sketchy. Hence, further understanding of mitochondrial mechanisms of diabetic lung injury should provide invaluable insights into future therapeutic approaches for diabetic lung injury.

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The effect of levosimendan on lung damage after myocardial ischemia reperfusion in rats in which experimental diabetes was induced

Cited by 20 publications

References 29 publications

The Roles of Autophagy in Acute Lung Injury Induced by Myocardial Ischemia Reperfusion in Diabetic Rats

The Roles of Autophagy in Acute Lung Injury Induced by Myocardial Ischemia Reperfusion in Diabetic Rats

Gut-Lung Dysbiosis Accompanied by Diabetes Mellitus Leads to Pulmonary Fibrotic Change through the NF-κB Signaling Pathway

Potential Biochemical Mechanisms of Lung Injury in Diabetes

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