scholarly journals Effects of apelin-13 on myocardial ischemia reperfusion injury in streptozotocine induced diabetic rats

2018 ◽  
Vol 119 (06) ◽  
pp. 348-354 ◽  
Author(s):  
I. Gunes ◽  
H. Kartal ◽  
A. D. Dursun ◽  
N. Sungu ◽  
Y. S. Polat ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

scholarly journals N-Acetylcysteine Restores Sevoflurane Postconditioning Cardioprotection against Myocardial Ischemia-Reperfusion Injury in Diabetic Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Jiefu Lin ◽  
Tingting Wang ◽  
Yalan Li ◽  
Mengxia Wang ◽  
Haobo Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Cd36 Expression ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Sevoflurane Postconditioning

The effect of sevoflurane postconditioning (sevo-postC) cardioprotection is compromised in diabetes which is associated with increased oxidative stress. We hypothesized that antioxidant N-Acetylcysteine may enhance or restore sevo-postC cardioprotection in diabetes. Control or streptozotocin-induced Type 1 diabetic rats were either untreated or treated with N-Acetylcysteine for four weeks starting at five weeks after streptozotocin injection and were subjected to myocardial ischemia-reperfusion injury (IRI), in the absence or presence of sevo-postC. Diabetes showed reduction of cardiac STAT3 activation (p-STAT3) and adiponectin with concomitantly increase of FoxO1 and CD36, which associated with reduced sevo-postC cardioprotection. N-Acetylcysteine and sevo-postC synergistically reduced the infarct size in diabetic groups. N-Acetylcysteine remarkably increased cardiac p-STAT3 which was further enhanced by sevo-postC. N-Acetylcysteine but not sevo-postC decreased myocardial FoxO1 while sevo-postC but not N-Acetylcysteine significantly increased myocardiac adiponectin in diabetic rats. It is concluded that late stage diabetic rats displayed reduction of cardiac p-STAT3, adiponectin deficiency, and increase of FoxO1 and CD36 expression, which may be responsible for the loss of myocardial responsiveness to sevo-postC cardioprotection. N-Acetylcysteine restored Sevo-postC cardioprotection in diabetes possibly through enhancing cardiac p-STAT3 and adiponectin and reducing Fox1 and CD36.

scholarly journals Activation of NRF2/FPN1 Pathway Attenuates Myocardial Ischemia-reperfusion Injury in Diabetic Rats by Regulating Iron Homeostasis and Ferroptosis

2021 ◽  
Author(s):  
hao tian ◽  
Yonghong Xiong ◽  
Yi Zhang ◽  
Yan Leng ◽  
Jie Tao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Related Factor ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Purpose Myocardial ischemia-reperfusion injury (IRI) can further worsen cardiac function in ischemic heart disease, and diabetes can increase susceptibility to myocardial IRI. Disorders of iron metabolism are involved in the pathological mechanisms of the most common diseases, such as diabetes, obesity, coronary artery angioplasty, or heart transplantation. Ferroportin1 (FPN1) is the only protein known to be associated with iron release in mammals and is regulated by nuclear factor E2-related factor 2 (NRF2) at the transcriptional level, thus playing an important role in iron homeostasis. Therefore, this study tested whether NRF2/FPN1 pathway plays a beneficial role in the treatment of diabetic myocardial IRI and potential detailed mechanism. Methods In this study, we investigated the effects of ferroptosis in STZ-induced diabetic rats following myocardial IRI in vivo, and its alteration in glucose and hypoxia/reoxygenation-induced cardiomyocytes injury in vitro. Results Cardiac functional and structural damage was detected by Evans blue/TTC double staining, Echocardiography, HE staining and serological indices, CCK-8 assay and ROS production to measure cardiomyocyte viability and oxidative stress level. Additionally, the changes in cell supernatant levels of Fe2+, SOD, MDA, and mRNA and protein expression of ferroptosis marker proteins confirmed the beneficial effects of the NRF2/FPN1 pathway on diabetic myocardial IRI related to iron metabolism and ferroptosis. Conclusions Overall, we find that iron homeostasis-related ferroptosis plays an important role in aggravating myocardial IRI in diabetic rats, and NRF2/FPN1 pathway-mediated iron homeostasis and ferroptosis might be a promising therapeutic target against myocardial IRI in diabetes.

Sign in / Sign up

Export Citation Format

Share Document