A calcium channel blocker, manoalide exerts an anti-allergic inflammatory effect through attenuating NF-κB activity

Yeom, Jun-Ho; Kim, Hee-Yun; Lim, Jin‐Ho; Yoon, Kyoung Wan; Kim, Hyung-Min; Jeong, Hyun‐Ja

doi:10.1080/08923973.2021.1988101

Cited by 2 publications

(3 citation statements)

References 33 publications

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“…In the inflammatory state, the infiltration and accumulation of eosinophils, basophils, lymphocytes, and mast cells are increased (Castillo et al, 2018 ; Lyons and Yi, 2021 ). In response to tissue damage, mast cells influence the promotion of the inflammatory response by producing tumor necrosis factor (TNF)-α, interleukin (IL)-1, thymic stromal lymphopoietin (TSLP), IL-6, and IL-8 (Kritas et al, 2020 ; Yeom et al, 2021 ). Recently, mast cell is a key effector cell in SARS-CoV-2-induced inflammation and cytokine storms, according to multiple studies (Kritas et al, 2020 ; Theoharides and Conti, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

“…In the absence of stimulation in cells, NF-κB binds to IκB inhibitor protein (IκBα) and is present in the cytoplasm. When cells are activated by various stimulants, phosphorylation and degradation of IκBα protein occurs, NF-κB is translocated into the nuclear and is activated (Yeom et al, 2021 ). In addition, caspase-1, a member of the cysteine protease family, is involved in the secretion of inflammatory cytokines as an IL-1β converting enzyme (Moon and Kim, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

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Caudatin attenuates inflammatory reaction by suppressing JNK/AP-1/NF-κB/caspase-1 pathways in activated HMC-1 cells

Kim

Kang

Choi

et al. 2023

Food Sci Biotechnol

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One of the interfering factors in Coronavirus disease 2019 (COVID-19) is the cytokine storm, which contributes to hyperinflammation. Mast cells cause COVID-19 hyperinflammation by increasing inflammatory cytokine levels. We investigated whether caudatin, an active compound of Cynanchum auriculatum , could suppress inflammatory response signaling in human mast cell line, HMC-1 cells. Caudatin suppressed activation of c-Jun N-terminal kinase (JNK) and activator protein-1 (AP-1) in HMC-1 cells. Caudatin suppressed nuclear translocation of catalytic subunit (p65) of nuclear factor (NF)-κB by blocking IκBα phosphorylation and degradation. Caudatin also reduced levels of activated-caspase-1 protein and activation of caspase-1. Non-toxic caudatin doses inhibited the mRNA expression and protein synthesis of pro-inflammatory cytokines. A significant finding was that caudatin inhibited JNK/AP-1/NF-κB/caspase-1 signaling molecules, reducing the secretion of inflammatory cytokines. Consequently, we propose that caudatin might be used as a material in health functional foods to alleviate mast cell-mediated inflammatory conditions like COVID-19.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Caudatin attenuates inflammatory reaction by suppressing JNK/AP-1/NF-κB/caspase-1 pathways in activated HMC-1 cells

Kim

Kang

Choi

et al. 2023

Food Sci Biotechnol

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“…Manoalide is a natural sesterterpenoid isolated in 1980 from the marine spongederived West Pacific species Luffariella variabilis [1]. Manoalide has a variety of pharmacological activities, including antibacterial [2], calcium channel blocker [3], analgesic, anti-inflammatory [4], and anticancer properties [5,6]. Manoalide functions by permanently blocking phospholipase A2 (PLA2) with lysine residues [7].…”

Section: Introductionmentioning

confidence: 99%

Manoalide Induces Intrinsic Apoptosis by Oxidative Stress and Mitochondrial Dysfunction in Human Osteosarcoma Cells

et al. 2023

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Osteosarcoma (OS) is the most common primary malignant bone tumor that produces immature osteoid. Metastatic OS has a poor prognosis with a death rate of >70%. Manoalide is a natural sesterterpenoid isolated from marine sponges. It is a phospholipase A2 inhibitor with anti-inflammatory, analgesic, and anti-cancer properties. This study aimed to investigate the mechanism and effect of manoalide on OS cells. Our experiments showed that manoalide induced cytotoxicity in 143B and MG63 cells (human osteosarcoma). Treatment with manoalide at concentrations of 10, 20, and 40 µM for 24 and 48 h reduced MG63 cell viability to 45.13–4.40% (p < 0.01). Meanwhile, manoalide caused reactive oxygen species (ROS) overproduction and disrupted antioxidant proteins, activating the apoptotic proteins caspase-9/-3 and PARP (Poly (ADP-ribose) polymerase). Excessive levels of ROS in the mitochondria affected oxidative phosphorylation, ATP generation, and membrane potential (ΔΨm). Additionally, manoalide down-regulated mitochondrial fusion protein and up-regulated mitochondrial fission protein, resulting in mitochondrial fragmentation and impaired function. On the contrary, a pre-treatment with n-acetyl-l-cysteine ameliorated manoalide-induced apoptosis, ROS, and antioxidant proteins in OS cells. Overall, our findings show that manoalide induces oxidative stress, mitochondrial dysfunction, and apoptosis, causing the cell death of OS cells, showing potential as an innovative alternative treatment in human OS.

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A calcium channel blocker, manoalide exerts an anti-allergic inflammatory effect through attenuating NF-κB activity

Cited by 2 publications

References 33 publications

Caudatin attenuates inflammatory reaction by suppressing JNK/AP-1/NF-κB/caspase-1 pathways in activated HMC-1 cells

Caudatin attenuates inflammatory reaction by suppressing JNK/AP-1/NF-κB/caspase-1 pathways in activated HMC-1 cells

Manoalide Induces Intrinsic Apoptosis by Oxidative Stress and Mitochondrial Dysfunction in Human Osteosarcoma Cells

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