scholarly journals Protective effect of distillated Nerium oleander on heart of type 2 diabetic rats

2015 ◽  
Vol 116 (07) ◽  
pp. 451-456
Author(s):  
M. Ayaz ◽  
F. Baba ◽  
N. Akgun ◽  
A. L. Bas ◽  
K. Uney ◽  
...  
Keyword(s):  
Protective Effect ◽  
Diabetic Rats ◽  
Nerium Oleander ◽  
Type 2 Diabetic

scholarly journals Adiponectin Ameliorates Lung Ischemia-Reperfusion Injury Through SIRT1-Pink1 Signaling-Mediated Mitophagy in Type 2 Diabetic Rats

2021 ◽  
Author(s):  
Tao Jiang ◽  
Tianhua Liu ◽  
Xijin Deng ◽  
Wengang Ding ◽  
Ziyong Yue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Transplantation ◽  
Protective Effect ◽  
Mitochondrial Dysfunction ◽  
Small Interfering Rna ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Interfering Rna ◽  
Type 2 Diabetic

Abstract BackgroundDiabetes mellitus (DM) is a key contributing factor to the poor survival in lung transplantation recipients. Mitochondrial dysfunction is recognized as a critical mediator in the pathogenesis of diabetic lung ischemia-reperfusion (IR) injury. The protective effects of adiponectin have been demonstrated in our previously study, but the underlying mechanism remained unclear. Here we demonstrated an important role of mitophagy in the protective effect of adiponectin during diabetic lung IR injury.Methods High-fat diet-fed streptozotocin-induced type 2 diabetic rats as recipients were exposed to adiponectin with or without administration of the SIRT1 inhibitor EX527 following lung transplantation. To unravel the mechanisms underlying the action of adiponectin, rat pulmonary microvascular endothelial cells were transfected with SIRT1 small-interfering RNA or Pink1 small-interfering RNA and then subjected to in vitro diabetic lung IR injury.ResultsMitophagy was impaired in the diabetic lung subjected to IR injury, accompanied by increased oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction. Adiponectin induced mitophagy and attenuated subsequent diabetic lung IR injury by improving lung functional recovery, suppressing oxidative damage, diminishing inflammation, decreasing cell apoptosis, and preserving mitochondrial function. However, both inhibitors of mitophagy and knockdown of Pink1 suppressed mitophagy, and reduced the protective action of adiponectin. Furthermore, we demonstrated that APN affected Pink1 stabilization via the SIRT1 signaling pathway, and knockdown of SIRT1 suppressed Pink1 expression and compromised the protective effect of adiponectin.ConclusionThese data demonstrated that adiponectin attenuated reperfusion-induced oxidative stress, inflammation, apoptosis and mitochondrial dysfunction via activation of SIRT1-Pink1 signaling-mediated mitophagy in diabetic lung IR injury.

scholarly journals Adiponectin ameliorates lung ischemia–reperfusion injury through SIRT1-PINK1 signaling-mediated mitophagy in type 2 diabetic rats

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Tao Jiang ◽  
Tianhua Liu ◽  
Xijin Deng ◽  
Wengang Ding ◽  
Ziyong Yue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Transplantation ◽  
Protective Effect ◽  
Mitochondrial Dysfunction ◽  
Small Interfering Rna ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Interfering Rna ◽  
Type 2 Diabetic

Abstract Background Diabetes mellitus (DM) is a key contributing factor to poor survival in lung transplantation recipients. Mitochondrial dysfunction is recognized as a critical mediator in the pathogenesis of diabetic lung ischemia–reperfusion (IR) injury. The protective effects of adiponectin have been demonstrated in our previous study, but the underlying mechanism remains unclear. Here we demonstrated an important role of mitophagy in the protective effect of adiponectin during diabetic lung IR injury. Methods High-fat diet-fed streptozotocin-induced type 2 diabetic rats were exposed to adiponectin with or without administration of the SIRT1 inhibitor EX527 following lung transplantation. To determine the mechanisms underlying the action of adiponectin, rat pulmonary microvascular endothelial cells were transfected with SIRT1 small-interfering RNA or PINK1 small-interfering RNA and then subjected to in vitro diabetic lung IR injury. Results Mitophagy was impaired in diabetic lungs subjected to IR injury, which was accompanied by increased oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction. Adiponectin induced mitophagy and attenuated subsequent diabetic lung IR injury by improving lung functional recovery, suppressing oxidative damage, diminishing inflammation, decreasing cell apoptosis, and preserving mitochondrial function. However, either administration of 3-methyladenine (3-MA), an autophagy antagonist or knockdown of PINK1 reduced the protective action of adiponectin. Furthermore, we demonstrated that APN affected PINK1 stabilization via the SIRT1 signaling pathway, and knockdown of SIRT1 suppressed PINK1 expression and compromised the protective effect of adiponectin. Conclusion These data demonstrated that adiponectin attenuated reperfusion-induced oxidative stress, inflammation, apoptosis and mitochondrial dysfunction via activation of SIRT1- PINK1 signaling-mediated mitophagy in diabetic lung IR injury.

Protective effect of telmisartan on pancreatic β cells of type 2 diabetic rats

2008 ◽  
Vol 32 (3) ◽  
pp. S56-S56
Author(s):  
Ya Qi Chen ◽  
Wan Qin Xiao ◽  
Shao Wen Tian ◽  
Jing Zhang ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Diabetic Rats ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Type 2 Diabetic

The protective effect of 1alpha, 25-dihydroxyvitamin d3 and metformin on liver in type 2 diabetic rats

2017 ◽  
Vol 173 ◽  
pp. 235-244 ◽  
Author(s):  
Samah Elattar ◽  
Suzanne Estaphan ◽  
Enas A Mohamed ◽  
Ahmed Elzainy ◽  
Mary Naguib
Keyword(s):  
Protective Effect ◽  
Diabetic Rats ◽  
Dihydroxyvitamin D3 ◽  
Type 2 Diabetic
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