d-arg-dmt-lys-phe-nh2 and Endomyocardial-Fibrosis

d-arg-dmt-lys-phe-nh2 has been researched along with Endomyocardial-Fibrosis* in 1 studies

Other Studies

1 other study(ies) available for d-arg-dmt-lys-phe-nh2 and Endomyocardial-Fibrosis

Article	Year
Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway. International journal of molecular medicine, 2021, Volume: 47, Issue:4 Oxidative stress serves a key role in doxorubicin (DOX)‑induced cardiotoxicity. The peptide Szeto‑Schiller (SS)31 is an efficacious antioxidant with the capacity to reduce mitochondrial reactive oxygen species (ROS) levels and scavenge free radicals. Although SS31 is involved in the pathophysiological process of various cardiovascular diseases, the role of SS31 in DOX‑induced cardiotoxicity remains unclear. To explore the effects of SS31 in DOX‑induced cardiotoxicity, the present study first constructed DOX‑induced cardiotoxicity models, in which H9c2 cells were incubated with 1 µM DOX for 24 h and C57BL/6 mice were administered DOX (20 mg/kg cumulative dose). The results of various assays in these models demonstrated that SS31 exhibited a cardioprotective effect Topics: Animals; Antioxidants; Apoptosis; Cardiotonic Agents; Cardiotoxicity; Doxorubicin; Endomyocardial Fibrosis; Male; MAP Kinase Signaling System; Membrane Potential, Mitochondrial; Mice; Mice, Inbred C57BL; Mitochondria; Myocardium; Oligopeptides; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Rats; Reactive Oxygen Species	2021

Article

Year

Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway.

International journal of molecular medicine, 2021, Volume: 47, Issue:4

Oxidative stress serves a key role in doxorubicin (DOX)‑induced cardiotoxicity. The peptide Szeto‑Schiller (SS)31 is an efficacious antioxidant with the capacity to reduce mitochondrial reactive oxygen species (ROS) levels and scavenge free radicals. Although SS31 is involved in the pathophysiological process of various cardiovascular diseases, the role of SS31 in DOX‑induced cardiotoxicity remains unclear. To explore the effects of SS31 in DOX‑induced cardiotoxicity, the present study first constructed DOX‑induced cardiotoxicity models, in which H9c2 cells were incubated with 1 µM DOX for 24 h and C57BL/6 mice were administered DOX (20 mg/kg cumulative dose). The results of various assays in these models demonstrated that SS31 exhibited a cardioprotective effect

Topics: Animals; Antioxidants; Apoptosis; Cardiotonic Agents; Cardiotoxicity; Doxorubicin; Endomyocardial Fibrosis; Male; MAP Kinase Signaling System; Membrane Potential, Mitochondrial; Mice; Mice, Inbred C57BL; Mitochondria; Myocardium; Oligopeptides; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Rats; Reactive Oxygen Species

2021