Caffeic acid methyl ester inhibits mast cell activation through the suppresion of MAPKs and NF-κB signaling in RBL-2H3 cells

Park, Jin‐Young; Lee, Hee Jae; Han, Eun‐Taek; Han, Jin‐Hee; Park, Won Sun; Kwon, Yong Soo; Wang, Chun

doi:10.1016/j.heliyon.2023.e16529

Cited by 4 publications

(4 citation statements)

References 51 publications

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“…RBL-2H3 cells, a rat basophilic leukemia cell line, are commonly used in immunological research because the cells release histamine and other inflammatory mediators in response to various allergic stimuli. 34 We previously confirmed that COX-2 expression was significantly increased with the treatment of PMA and A23187 in RBL-2H3 cells. 35 To validate the results from the computational study, the inhibitory activity of the drugs (celecoxib, ibuprofen, and vismodegib) was examined by measuring the PGE 2 levels in PMA/A23187-challenged RBL-2H3 cells.…”

Section: ■ Results and Discussionsupporting

confidence: 56%

“…Prostaglandin E2 (PGE 2 ) is a major prostaglandin produced by COX-2 in response to inflammatory stimuli. RBL-2H3 cells, a rat basophilic leukemia cell line, are commonly used in immunological research because the cells release histamine and other inflammatory mediators in response to various allergic stimuli . We previously confirmed that COX-2 expression was significantly increased with the treatment of PMA and A23187 in RBL-2H3 cells .…”

Section: Results and Discussionmentioning

confidence: 85%

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Vismodegib Identified as a Novel COX-2 Inhibitor via Deep-Learning-Based Drug Repositioning and Molecular Docking Analysis

Yasir,

Park,

Han

et al. 2023

ACS Omega

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Artificial intelligence algorithms have been increasingly applied in drug development due to their efficiency and effectiveness. Deep-learning-based drug repurposing can contribute to the identification of novel therapeutic applications for drugs with other indications. The current study used a trained deep-learning model to screen an FDA-approved drug library for novel COX-2 inhibitors. Reference COX-2 data sets, composed of active and decoy compounds, were obtained from the DUD-E database. To extract molecular features, compounds were subjected to RDKit, a cheminformatic toolkit. GraphConvMol, a graph convolutional network model from DeepChem, was applied to obtain a predictive model from the DUD-E data sets. Then, the COX-2 inhibitory potential of the FDA-approved drugs was predicted using the trained deep-learning model. Vismodegib, an anticancer agent that inhibits the hedgehog signaling pathway by binding to smoothened, was predicted to inhibit COX-2. Noticeably, some compounds that exhibit high potential from the prediction were known to be COX-2 inhibitors, indicating the prediction model’s liability. To confirm the COX-2 inhibition activity of vismodegib, molecular docking was carried out with the reference compounds of the COX-2 inhibitor, celecoxib, and ibuprofen. Furthermore, the experimental examination of COX-2 inhibition was also carried out using a cell culture study. Results showed that vismodegib exhibited a highly comparable COX-2 inhibitory activity compared to celecoxib and ibuprofen. In conclusion, the deep-learning model can efficiently improve the virtual screening of drugs, and vismodegib can be used as a novel COX-2 inhibitor.

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Section: ■ Results and Discussionsupporting

confidence: 56%

Section: Results and Discussionmentioning

confidence: 85%

Vismodegib Identified as a Novel COX-2 Inhibitor via Deep-Learning-Based Drug Repositioning and Molecular Docking Analysis

Yasir,

Park,

Han

et al. 2023

ACS Omega

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“…25 They are activated by phosphorylation and cause the transcription of several cytokines to produce inflammatory mediators such as tumor necrosis fctor-α (TNF-α) and interleukins (ILs). [26][27][28] Previous studies have shown that cerebral ischemia is closely related to p38MAPK and JNKs. 8,29 As p38MAPK activation is involved in ischemia-induced neurological injury, blocking it may protect brain tissue from ischemia damage by decreasing the production of inflammatory mediators and blocking the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

“… 25 They are activated by phosphorylation and cause the transcription of several cytokines to produce inflammatory mediators such as tumor necrosis fctor‐α (TNF‐α) and interleukins (ILs). 26 , 27 , 28 …”

Section: Discussionmentioning

confidence: 99%

Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β

Zheng,

Zhang,

Dong

et al. 2023

Immunity Inflam & Disease

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ObjectiveTissue injury and inflammation are two potential outcomes of cerebral ischemia–reperfusion (I/R) injury. Salvianolic acid B (Sal B), isolated from the roots of Salvia miltiorrhiza, is one of the major water‐soluble compounds with a wide range of pharmacological effects including antioxidant, anti‐inflammatory, antiproliferative, and neuroprotective effects. In the present study, we explored the neuroprotective effects and potential mechanisms of Sal B after I/R injury.MethodsWe induced cerebral ischemia in male CD‐1 mice through transient (60 min) middle cerebral artery occlusion (tMCAO), and then injected Sal B (30 mg/kg) intraperitoneally. Neurological deficits, infarct volumes, and brain edema were assessed at 24 and 72 h after tMCAO. We detected the expression of Toll‐like receptor 4 (TLR4), phosphorylated‐p38 mitogen‐activated protein kinase (P‐p38 MAPK), phosphorylated c‐Jun amino (N)‐terminal kinases (p‐JNK), nuclear factor‐κB (NF‐κB), and interleukin‐1β (IL‐1β) in the brain tissue.ResultsCompared with the tMCAO group, Sal B significantly improved neurological deficits, reduced infarct size, attenuated cerebral edema, and downregulated the expression of pro‐inflammatory mediators TLR4, p‐p38MAPK, p‐JNK, nuclear NF‐κB, and IL‐1β in brain tissue after I/R injury.ConclusionWe found that Sal B protects brain tissues from I/R injury by activating its anti‐inflammatory properties.

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Urolithin B inhibits LPS-induced macrophage M1 polarization via miR155-5p mediated MAPK/NF-кB pathway

Tuohudaali,

Ji,

Ding

et al. 2024

Journal of Asian Natural Products Research

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Caffeic acid methyl ester inhibits mast cell activation through the suppresion of MAPKs and NF-κB signaling in RBL-2H3 cells

Cited by 4 publications

References 51 publications

Vismodegib Identified as a Novel COX-2 Inhibitor via Deep-Learning-Based Drug Repositioning and Molecular Docking Analysis

Vismodegib Identified as a Novel COX-2 Inhibitor via Deep-Learning-Based Drug Repositioning and Molecular Docking Analysis

Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β

Urolithin B inhibits LPS-induced macrophage M1 polarization via miR155-5p mediated MAPK/NF-кB pathway

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