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Bibliographic Details
Main Authors: Yurchenko, Ekaterina A, Kozhushnaya, Anastasia B, Kolesnikova, Sophia A, Chingizova, Ekaterina A, Menchinskaya, Ekaterina S, Pislyagin, Evgeny A, Kuzmich, Aleksandra S, Aminin, Dmitry L
Format: Artículo científico
Language:en
Published: Journal of natural medicines 2026
Online Access:https://pubmed.ncbi.nlm.nih.gov/41865145/
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Table of Contents:
  • Biological activity of isomalabaricane compounds from the marine sponge Rhabdastrella globostellata. Yurchenko, Ekaterina A Kozhushnaya, Anastasia B Kolesnikova, Sophia A Chingizova, Ekaterina A Menchinskaya, Ekaterina S Pislyagin, Evgeny A Kuzmich, Aleksandra S Aminin, Dmitry L This study aimed to investigate the cytotoxic effects of isomalabaricane stellettins Q-V and globostelletins K-N, recently isolated from the Vietnamese marine sponge Rhabdastrella globostellata, against human cervical cancer HeLa, human melanoma SK-Mel-28, murine neuroblastoma Neuro-2a cells, human normal keratinocytes HaCaT, and rat normal cardiomyocytes H9c2, as well as to study the cardioprotective activity of non-toxic compounds. Stellettins Q and R and globostelletins M and N showed moderate cytotoxic activity against HeLa, SK-Mel-28, Neuro-2a cells as well as normal keratinocytes HaCaT and normal cardiomyocytes H9c2. Stellettin U increased the viability of H9c2 cardiomyocytes treated with nutrient deprivation, high concentration of ATP, TNF-α pro-inflammatory cytokine, and CoCl2-mimicking hypoxia. In an in vitro ischemia model, stellettin U reversed mitochondrial ROS and cardiolipin peroxidation levels. In CoCl2-induced toxicity, intracellular and mitochondrial ROS production, mitochondrial membrane depolarization, and cardiolipin peroxidation levels were normalized following stellettin U treatment. The effect of stellettin U on ATP-induced Ca2+influx led to the assumption that stellettin U protects cardiomyocytes via a P2X7R-dependend pathway. Moreover, the modulation of the NF-κB-dependent anti-inflammatory pathway by stellettin U was confirmed. Thus, it was suggested that stellettin U may protect cardiomyocytes via both canonical NF-κB- and non-canonical P2X7R-dependend pathways.