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Malabaricone C, a constituent of spice Myristica malabarica, exhibits anti-inflammatory effects via modulation of cellular redox

The present study primarily focuses on the efficacy of Malabaricone C (Mal C) as an anti-inflammatory agent. Mal C inhibited mitogen-induced T-cell proliferation and cytokine secretion. Mal C significantly reduced cellular thiols in lymphocytes. N-acetyl cysteine (NAC) restored cellular thiol levels...

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Detalles Bibliográficos
Autores principales: Patwardhan, Raghavendra S, Kundu, Kshama, Purohit, Vaitashi, Kumar, Binita Kislay, Singh, Beena, Thoh, Maikho, Undavia, Khushboo, Bhilwade, Hari N, Nayak, Sandip K, Sharma, Deepak, Sandur, Santosh K
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer India 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10040911/
https://www.ncbi.nlm.nih.gov/pubmed/36971326
http://dx.doi.org/10.1007/s12038-023-00329-3
Descripción
Sumario:The present study primarily focuses on the efficacy of Malabaricone C (Mal C) as an anti-inflammatory agent. Mal C inhibited mitogen-induced T-cell proliferation and cytokine secretion. Mal C significantly reduced cellular thiols in lymphocytes. N-acetyl cysteine (NAC) restored cellular thiol levels and abrogated Mal C-mediated inhibition of T-cell proliferation and cytokine secretion. Physical interaction between Mal C and NAC was evinced from HPLC and spectral analysis. Mal C treatment significantly inhibited concanavalin A-induced phosphorylation of ERK/JNK and DNA binding of NF-κB. Administration of Mal C to mice suppressed T-cell proliferation and effector functions ex vivo. Mal C treatment did not alter the homeostatic proliferation of T-cells in vivo but completely abrogated acute graft-versus-host disease (GvHD)-associated morbidity and mortality. Our studies indicate probable use of Mal C for prophylaxis and treatment of immunological disorders caused due to hyper-activation of T-cells. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12038-023-00329-3.