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Your search keyword '"Senthil Kumar, Kanthasamy Jayabal"' showing total 4 results
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4 results on '"Senthil Kumar, Kanthasamy Jayabal"'

2. Antcin A, a phytosterol regulates SARS‐CoV‐2 spike protein‐mediated metabolic alteration in THP‐1 cells explored by the 1H‐NMR‐based metabolomics approach.

Author

Dakpa, Gyaltsen, Senthil Kumar, Kanthasamy Jayabal, Tsao, Nai‐Wen, and Wang, Sheng‐Yang

Abstract

The mechanism of SARS‐CoV‐2 spike protein‐mediated perturbations of metabolic pathways and modulation of antcin A, a steroid‐like compound isolated from Taiwanofungus camphoratus, are not studied. Here, we investigated the metabolic alteration by SARS‐CoV‐2 spike protein and the regulatory effect of antcin A on SARS‐CoV‐2 spike protein‐induced metabolic changes in the Phorbol 12‐myristate 13‐acetate (PMA)‐induced human monocytes (THP‐1) using proton nuclear magnetic resonance (1H‐NMR) and MetaboAnalyst 5.0 software. The cytotoxic potential of SARS‐CoV‐2 spike protein, antcin A, and dexamethasone was assessed by MTT assay. The metabolomic perturbations and their relation to human coronaviruses' receptors were evaluated by qPCR. This study indicated that the altered metabolites mediated by SARS‐CoV‐2 protein, such as methionine, phosphoenolpyruvic acid, canadine, glutamine, ethanolamine, and phenylalanine, were significantly reversed by antcin A. In addition, antcin A significantly inhibited SARS‐CoV‐2 spike protein‐mediated up‐regulation of TLR‐4 and ACE2 receptors, while GRP78 inhibition was not statistically significant. This is the first study to use 1H‐NMR to investigate SARS‐CoV‐2 spike protein‐induced metabolomic changes in PMA‐induced THP‐1 cells. Antcin A significantly reversed metabolomic alters while dexamethasone failed to fix them. Therefore, we believe that antcin A could be a potential candidate for therapeutic agents for viral infections related to a metabolic abnormality. [ABSTRACT FROM AUTHOR]

Published
2023
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3. Bornyl Cinnamate Inhibits Inflammation-Associated Gene Expression in Macrophage Cells through Suppression of Nuclear Factor-κB Signaling Pathway.

Author

Senthil Kumar, Kanthasamy Jayabal, Justine Li, Gokila Vani, Muthuraj, Yu-Hsin Hsieh, Yueh-Hsiung Kuo, and Sheng-YangWang

Subjects
*ANALYSIS of variance, *CELL culture, *ESSENTIAL oils, *GENE expression, *INFLAMMATION, *MACROPHAGES, *CHINESE medicine, *NITRIC oxide, *RESEARCH funding, *T-test (Statistics), *WESTERN immunoblotting, *DNA-binding proteins, *QUANTITATIVE research, *CARBOCYCLIC acids, *DATA analysis software, *DESCRIPTIVE statistics, *FLUOROIMMUNOASSAY, *CURCUMIN, *IN vitro studies, PREVENTION of disease progression
Abstract

Formosan sweetgum (Liquidamber formosana) is an endemic tree species. Various parts of this tree are used as a traditional Chinese medicine for treating pain, inflammation, and rheumatic disorders. In this study, we investigated the anti-inflammatory potential of bornyl cinnamate, a cinnamic acid derivative from the essential oil of L. formosana. Pretreatment with bornyl cinnamate significantly inhibited lipopolysaccharide-induced proinflammatory molecules, including nitric oxide, prostaglandin-E2, tumor necrosis factor α, and interleukin-1β production, in murine macrophage RAW 264.7 cells. RT-PCR and immunoblotting analysis revealed that the inhibition of the proinflammatory molecules occurred through the downregulation of their corresponding mediator genes. Immunofluorescence and luciferase reporter assays revealed that the inhibition of proinflammatory genes by bornyl cinnamate was caused by the suppression of nuclear translocation and transcriptional activation of the redox-sensitive transcription factor nuclear factor κB. In addition, bornyl cinnamate increased the protein stability of the inhibitor of nuclear factor κB, an endogenous repressor of nuclear factor κB, through inhibition of its phosphorylation and proteasomal degradation. Furthermore, bornyl cinnamate significantly blocked the lipopolysaccharide-induced activation of I-κB kinase α, an upstream kinase of the inhibitor of nuclear factor κB α. Taken together, these results suggest that bornyl cinnamate could inhibit proinflammatory molecules through the suppression of the redox-sensitive nuclear factor κB signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2015
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4. Antcin A, a phytosterol regulates SARS-CoV-2 spike protein-mediated metabolic alteration in THP-1 cells explored by the 1 H-NMR-based metabolomics approach.

Author

Dakpa G, Senthil Kumar KJ, Tsao NW, and Wang SY

Subjects
Humans, SARS-CoV-2 physiology, Spike Glycoprotein, Coronavirus metabolism, THP-1 Cells, Magnetic Resonance Spectroscopy, Dexamethasone, COVID-19 Drug Treatment, COVID-19, Phytosterols
Abstract

The mechanism of SARS-CoV-2 spike protein-mediated perturbations of metabolic pathways and modulation of antcin A, a steroid-like compound isolated from Taiwanofungus camphoratus, are not studied. Here, we investigated the metabolic alteration by SARS-CoV-2 spike protein and the regulatory effect of antcin A on SARS-CoV-2 spike protein-induced metabolic changes in the Phorbol 12-myristate 13-acetate (PMA)-induced human monocytes (THP-1) using proton nuclear magnetic resonance ( 1 H-NMR) and MetaboAnalyst 5.0 software. The cytotoxic potential of SARS-CoV-2 spike protein, antcin A, and dexamethasone was assessed by MTT assay. The metabolomic perturbations and their relation to human coronaviruses' receptors were evaluated by qPCR. This study indicated that the altered metabolites mediated by SARS-CoV-2 protein, such as methionine, phosphoenolpyruvic acid, canadine, glutamine, ethanolamine, and phenylalanine, were significantly reversed by antcin A. In addition, antcin A significantly inhibited SARS-CoV-2 spike protein-mediated up-regulation of TLR-4 and ACE2 receptors, while GRP78 inhibition was not statistically significant. This is the first study to use 1 H-NMR to investigate SARS-CoV-2 spike protein-induced metabolomic changes in PMA-induced THP-1 cells. Antcin A significantly reversed metabolomic alters while dexamethasone failed to fix them. Therefore, we believe that antcin A could be a potential candidate for therapeutic agents for viral infections related to a metabolic abnormality., (© 2022 John Wiley & Sons Ltd.)

Published
2023
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