Role of mesenchymal stem cells‐derived exosomes on inflammation, apoptosis, fibrosis and telocyte modulation in doxorubicin‐induced cardiotoxicity: A closer look at the structural level DOI

Reda Abdelnasser Imam,

Basma Emad Aboulhoda,

Maha M. Amer

et al.

Microscopy Research and Technique, Journal Year: 2024, Volume and Issue: 87(7), P. 1598 - 1614

Published: March 5, 2024

Abstract Cardiotoxicity induced by doxorubicin (Dox) is a major complication in cancer patients. Exosomes (Ex) derived from mesenchymal cells could be promising therapeutic for various heart diseases. This study investigated the role of Ex Dox‐induced cardiotoxicity and its mechanistic insights, using Sacubitril/valsartan (S/V) as reference drug widely recommended failure management. The involved 24 Wistar rats, divided into control, Dox, Dox + S/V, groups. rats were assessed cardiac enzymes, inflammatory oxidative stress markers. Immunohistochemical expression caspase‐1, nuclear factor erythroid 2‐related 2 (NrF2), E‐Cadherin, CD117/c‐kit, Platelet‐derived growth factor‐α (PDGFα) was evaluated. P53 Annexin V PCR. Histological examination performed hematoxylin eosin Sirius red stains. ameliorated adverse pathological changes significantly decreased enzymes also exerted antifibrotic antiapoptotic effect tissue. treatment improved NrF2 immunohistochemistry, up‐regulated E‐Cadherin immune expression, restored telocyte markers CD117/c‐kit PDGFα. can mitigate acting an anti‐inflammatory, antioxidant, antiapoptotic, agents, restoring telocytes modulating epithelial transition. Research Highlights exhibit positive CD90 CD105 whereas showing −ve CD 34 flow cytometry. restore immunohistochemical alleviate myocardial apoptosis, fibrosis.

Language: Английский

Role of Trimetazidine in Ameliorating Endothelial Dysfunction: A Review DOI Creative Commons
Yusof Kamisah, Hamat Hamdi Che Hassan

Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(4), P. 464 - 464

Published: April 5, 2024

Endothelial dysfunction is a hallmark of cardiovascular diseases, contributing to impaired vasodilation, altered hemodynamics, and atherosclerosis progression. Trimetazidine, traditionally used for angina pectoris, exhibits diverse therapeutic effects on endothelial dysfunction. This review aims elucidate the mechanisms underlying trimetazidine's actions its potential as agent associated disorders. Trimetazidine enhances vasodilation hemodynamic function by modulating nitric oxide synthase activity, production, endothelin-1. It also ameliorates metabolic parameters, including reducing blood glucose, mitigating oxidative stress, dampening inflammation. Additionally, trimetazidine exerts antiatherosclerotic inhibiting plaque formation promoting stability. Moreover, it regulates apoptosis angiogenesis, fostering cell survival neovascularization. Understanding multifaceted underscores disorders, warranting further investigation clinical translation.

Language: Английский

Citations

5
Knockdown of Galectin-3 confers myocardial protection against ischemia-reperfusion injury, modulating oxidative stress, inflammatory response, and the peroxisome proliferator-activated receptor g signaling pathway DOI Open Access
Duo Chen, Jingyu Wen, Wei Zang

et al.

CytoJournal, Journal Year: 2025, Volume and Issue: 22, P. 49 - 49

Published: May 6, 2025

Objective Ischemia-reperfusion (I-R) injury in the myocardium is a considerable challenge cardiovascular medicine, posing severe threat to life. Given that galectin-3 possibly regulates myocardial I-R damage, this study aims investigate detailed mechanisms underlying galectin-3’s effects on injury. Material and Methods The expression levels of vivo vitro models were determined by Western blot quantitative real-time polymerase chain reaction. inflammatory factors oxidative stress measured with an enzyme-linked immunosorbent assay, extent tissue damage was assessed using hematoxylin-eosin staining. influence peroxisome proliferator-activated receptor g (PPARg) signaling pathway-related proteins blot. Results Myocardial associated increased expression, blood creatine kinase-myocardial band kinase favorably correlated messenger RNA mice cardiac damage. inhibition alleviated response, promoted reactive oxygen species production cells. Furthermore, mouse model exhibited decreased linked PPARg pathway, but enhanced these proteins. Conclusion Galectin-3 plays crucial role exacerbating injury, its up-regulation stress, responses, protective pathway. alleviation harmful suggests targeting potential therapeutic method for reducing

Language: Английский

Citations

0
Effect of Selenium nanoparticles on Paraquat-induced-neuroinflammation and oligodendocyte modulation: Implication of the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway DOI

Reda Abdelnasser Imam,

Fatma E. Hassan, Isra H. Ali

et al.

Tissue and Cell, Journal Year: 2024, Volume and Issue: 89, P. 102454 - 102454

Published: June 19, 2024

Language: Английский

Citations

2
Role of mesenchymal stem cells‐derived exosomes on inflammation, apoptosis, fibrosis and telocyte modulation in doxorubicin‐induced cardiotoxicity: A closer look at the structural level DOI

Reda Abdelnasser Imam,

Basma Emad Aboulhoda,

Maha M. Amer

et al.

Microscopy Research and Technique, Journal Year: 2024, Volume and Issue: 87(7), P. 1598 - 1614

Published: March 5, 2024

Abstract Cardiotoxicity induced by doxorubicin (Dox) is a major complication in cancer patients. Exosomes (Ex) derived from mesenchymal cells could be promising therapeutic for various heart diseases. This study investigated the role of Ex Dox‐induced cardiotoxicity and its mechanistic insights, using Sacubitril/valsartan (S/V) as reference drug widely recommended failure management. The involved 24 Wistar rats, divided into control, Dox, Dox + S/V, groups. rats were assessed cardiac enzymes, inflammatory oxidative stress markers. Immunohistochemical expression caspase‐1, nuclear factor erythroid 2‐related 2 (NrF2), E‐Cadherin, CD117/c‐kit, Platelet‐derived growth factor‐α (PDGFα) was evaluated. P53 Annexin V PCR. Histological examination performed hematoxylin eosin Sirius red stains. ameliorated adverse pathological changes significantly decreased enzymes also exerted antifibrotic antiapoptotic effect tissue. treatment improved NrF2 immunohistochemistry, up‐regulated E‐Cadherin immune expression, restored telocyte markers CD117/c‐kit PDGFα. can mitigate acting an anti‐inflammatory, antioxidant, antiapoptotic, agents, restoring telocytes modulating epithelial transition. Research Highlights exhibit positive CD90 CD105 whereas showing −ve CD 34 flow cytometry. restore immunohistochemical alleviate myocardial apoptosis, fibrosis.

Language: Английский

Citations

1