Preconditioning and anti-apoptotic effects of Metformin and Cyclosporine-A in an isolated bile duct-ligated rat heart

Moheimani, Hamid Reza; Amiriani, Taghi; Alizadeh, Ali Mohammad; Jand, Yahya; Shakiba, Delaram; Ensan, Parham Sayyah; Jafarzadeh, Fatemeh; Rajaei, Maryam; Enayati, Ahmad Ali; Pourabouk, Mona; Aliazadeh, Shahriar; Pourkhani, Amir Hoshang; Mazaheri, Zohreh; Zeyghami, Mohammad Ali; Dehpour, Ahmad Reza; Khori, Vahid

doi:10.1016/j.ejphar.2020.173807

Cited by 5 publications

(5 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cyclosporine is a calcineurin inhibitor known for its immunomodulatory properties that prevent organ transplant rejection and treat several inflamma-tory and autoimmune circumstances by targeting the ca/calmodulin-calcineurin pathway. In addition to its primary feature, cyclosporine showed beneficial roles in different experimental models e.g., anti-oxidant and anti-apoptotic properties against testicular torsion/detorsion while administered alone or combined to nortriptyline in rats [26], cardioprotective effects in cirrhotic cardiomyopathy by regulating apoptosis and phosphorylated AMP-activated protein kinase (pAMPK) in mitochondria [27], and attenuation of morphine tolerance in human glioblastoma cell line [28].…”

Section: Discussionmentioning

confidence: 99%

The Possible Protective Effects of Ondansetron and Tropisetron on Optic Nerve Crush Injury in Rats

et al. 2022

View full text Add to dashboard Cite

Background This study aimed to evaluate the potential neuroprotective effect of cyclosporine – a calcineurin inhibitor–, ondansetron, and tropisetron-5-hydroxytryptamine (serotonin) 3 receptor (5-HT3R) antagonists–, on optic nerve crush (ONC) injury in rats. Moreover, underlying signaling activities of their beneficial neuroprotective effects were studied. Methods Adult male rats were treated with the intravitreal administration of cyclosporine (1.6 mM), ondansetron (100 nM), and tropisetron (100 nM) immediately after the induction of ONC. Subsequently, on 7th day after surgery, the rats’ retinas were extracted, and the expression of apoptotic regulators (Bax and Bcl-2) and calcineurin were studied by western blot analysis. Results The induction of ONC injury was associated to higher expression of Bax and calcineurin, while Bcl-2 expression was considerably decreased in these animals. Intravitreal treatment with cyclosporine (1.6 mM), ondansetron (100 nM), and tropisetron (100 nM) significantly attenuated the increased expression of Bax and calcineurin. Moreover, the treatment with these agents resulted in an elevated expression of Bcl-2 in the retina. Conclusion Our findings indicate that cyclosporine, ondansetron, and tropisetron protect against ONC injury in rats, possibly via the suppression of apoptosis and modulation of calcineurin activity directly and via 5-HT3 receptors. Moreover, immunoblotting showed that tropisetron was more effective as opposed to ondansetron. Further studies are needed to evaluate the precise mechanism behind cyclosporine, ondansetron, and tropisetron activities.

show abstract

Section: Discussionmentioning

confidence: 99%

The Possible Protective Effects of Ondansetron and Tropisetron on Optic Nerve Crush Injury in Rats

et al. 2022

View full text Add to dashboard Cite

show abstract

“…For example, metformin reduces collagen IIIA1, α-SMA, and CD68 levels after 2 weeks of reperfusion and improves fibrotic remodeling ( Loi et al, 2021 ). Furthermore, metformin and cyclosporin A exert cardiac protection by regulating the balance between AMPK and apoptosis in the mitochondria of bile duct-ligated rats ( Moheimani et al, 2021 ).…”

Section: Interventions For Cardiac Fibrosismentioning

confidence: 99%

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Yin

Pan

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Cardiac fibrosis plays an indispensable role in cardiac tissue homeostasis and repair after myocardial infarction (MI). The cardiac fibroblast-to-myofibroblast differentiation and extracellular matrix collagen deposition are the hallmarks of cardiac fibrosis, which are modulated by multiple signaling pathways and various types of cells in time-dependent manners. Our understanding of the development of cardiac fibrosis after MI has evolved in basic and clinical researches, and the regulation of fibrotic remodeling may facilitate novel diagnostic and therapeutic strategies, and finally improve outcomes. Here, we aim to elaborate pathophysiology, examination and intervention of cardiac fibrosis after MI.

show abstract

“…According to Messaoudi et al, metformin can improve cardiac function in diabetic CVDs, which can be attributed not only to the antidiabetic treatment but also to the promotion of cardiac mitochondrial functions via AMPK-targeted mitochondrial protection (Whittington et al, 2013). Moheimani et al showed the protective effects of metformin in I/R rat hearts ex vivo, with a significant decrease in the infarct area by modulating phosphorylation of AMPK (Moheimani et al, 2021). According to the review by Varjabedian et al, metformin is a safe clinical drug, with the most serious side effect being acidosis.…”

Section: Targeting the Ampk Pathwaymentioning

confidence: 99%

Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment

Yang

Guo

Feng

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Cardiovascular diseases (CVDs) are serious public health issues and are responsible for nearly one-third of global deaths. Mitochondrial dysfunction is accountable for the development of most CVDs. Mitochondria produce adenosine triphosphate through oxidative phosphorylation and inevitably generate reactive oxygen species (ROS). Excessive ROS causes mitochondrial dysfunction and cell death. Mitochondria can protect against these damages via the regulation of mitochondrial homeostasis. In recent years, mitochondria-targeted therapy for CVDs has attracted increasing attention. Various studies have confirmed that clinical drugs (β-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor-II blockers) against CVDs have mitochondrial protective functions. An increasing number of cardiac mitochondrial targets have shown their cardioprotective effects in experimental and clinical studies. Here, we briefly introduce the mechanisms of mitochondrial dysfunction and summarize the progression of mitochondrial targets against CVDs, which may provide ideas for experimental studies and clinical trials.

show abstract

Preconditioning and anti-apoptotic effects of Metformin and Cyclosporine-A in an isolated bile duct-ligated rat heart

Cited by 5 publications

References 53 publications

The Possible Protective Effects of Ondansetron and Tropisetron on Optic Nerve Crush Injury in Rats

The Possible Protective Effects of Ondansetron and Tropisetron on Optic Nerve Crush Injury in Rats

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment

Contact Info

Product

Resources

About