FNF-12, a novel benzylidene-chromanone derivative, attenuates inflammatory response in in vitro and in vivo asthma models mediated by M2-related Th2 cytokines via MAPK and NF-kB signaling

Abohassan, Mohammad; Shahrani, Mesfer Al; Alshahrani, Mohammad Y.; Begum, Naseem; Radhakrishnan, S.; Rajagopalan, Prasanna

doi:10.1007/s43440-021-00325-0

Cited by 7 publications

(8 citation statements)

References 52 publications

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“…Moreover, phosphorylation of MAPKs (p38 MAPK, Erk, and JNK) can regulate a variety of cellular activities, including gene expression, differentiation, and differentiation in response to external stimuli. 49 Anti-MAPK inhibitors have been manufactured with the intention of managing a wide range of inflammatory disorders. 50 In this study, UPE promotes the stability of eosinophils and mast cells.…”

Section: Discussionmentioning

confidence: 99%

“…The nuclear translocation of AP‐1, which transcribes and generates cytokines, is facilitated by these MAPKs. Moreover, phosphorylation of MAPKs (p38 MAPK, Erk, and JNK) can regulate a variety of cellular activities, including gene expression, differentiation, and differentiation in response to external stimuli 49 . Anti‐MAPK inhibitors have been manufactured with the intention of managing a wide range of inflammatory disorders 50 .…”

Section: Discussionmentioning

confidence: 99%

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Undaria pinnatifida ameliorates nasal inflammation by inhibiting eosinophil and mast cell activation and modulating the NF‐κB/MAPKs signaling pathway

Yu,

Fan,

Nguyen

et al. 2024

Immunity Inflam & Disease

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BackgroundAllergic rhinitis (AR) is the most prevalent form of atopic disease. Undaria pinnatifida has potent antioxidative, antidiabetic, and anti‐inflammatory properties.AimsWe investigated the immunomodulatory effect of Undaria pinnatifida extract (UPE) on allergic inflammation in an AR mouse model.Materials & MethodsMice were sensitized and intranasally challenged with ovalbumin (OVA), and the Th1/Th2 and Th17/Treg‐related cytokines and histopathology were exanimated after UPE treatments. Enzyme‐linked immunosorbent assay was performed using serum samples and NALF to detect OVA‐specific immunoglobulins and inflammatory cytokines. Mitogen‐activated protein kinases (MAPKs) were measured by western blotting analysis, and an in vitro study measured mast cell activation induced by compound 48/80.ResultsAfter UPE treatment, nasal and lung allergy symptoms, nasal mucosal swelling, and goblet cell hyperplasia were ameliorated. Oral UPE regulated the balance of Th1/Th2 and Th17/Treg cell differentiation in AR mice in a dose‐dependent manner. In addition, UPE attenuated the migration of eosinophils and mast cells to the nasal mucosa by suppressing nuclear factor kappa B (NF‐κB)/MAPKs. The levels of anti‐OVA IgE and IgG1 were also decreased.DiscussionUPE inhibited inflammation by regulating the NF‐κB/MAPKs signaling pathway and supressing the activation of critical immune cells such as eosinophils and mast cells.ConclusionUPE may have therapeutic potential for AR.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Undaria pinnatifida ameliorates nasal inflammation by inhibiting eosinophil and mast cell activation and modulating the NF‐κB/MAPKs signaling pathway

Yu,

Fan,

Nguyen

et al. 2024

Immunity Inflam & Disease

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“…The canonical pathway of NF‐κB signaling has been shown to respond to hypoxia 46 . Studies have indicated a link between NF‐κB activation and asthma, 47 and the NF‐κB pathway can regulate the inflammatory immune response in asthma through Th2 reactions 48 . The NF‐κB pathway is considered a key regulatory pathway for modulating Th2 inflammation in allergic diseases such as asthma, involved in the activation of various inflammatory cells and the production of inflammatory mediators, such as IL‐4, IL‐5, and IL‐13 49 .…”

Section: Discussionmentioning

confidence: 99%

“… 46 Studies have indicated a link between NF‐κB activation and asthma, 47 and the NF‐κB pathway can regulate the inflammatory immune response in asthma through Th2 reactions. 48 The NF‐κB pathway is considered a key regulatory pathway for modulating Th2 inflammation in allergic diseases such as asthma, involved in the activation of various inflammatory cells and the production of inflammatory mediators, such as IL‐4, IL‐5, and IL‐13. 49 The immunohistochemical results of NF‐κB in this study suggest that preconditioning with low oxygen levels induces more severe Th2‐related inflammatory responses in asthma, and NF‐κB maybe involved in this process.…”

Section: Discussionmentioning

confidence: 99%

Intermittent hypoxic pretreatment exacerbates house dust mite‐induced asthma airway inflammation

Meng,

Zhang,

Que

et al. 2024

Immunity Inflam & Disease

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BackgroundAsthma is widely recognized as an inflammatory disorder. In the context of this inflammatory microenvironment, the involvement of hypoxia and its impact on related pathways have drawn considerable attention. However, the exact role of hypoxia, a prevalent environmental factor, in the development and progression of asthma remains poorly understood.MethodsMice were treated with house dust mite (HDM) extracts for 23 days to induce asthma. Mice were divided into room air (RA) group and intermittent hypoxic (IH) group by exposing to different conditions and IH preconditioning (IHP) were underwent to the above groups before the hypoxic regimen. Airway inflammation in mice was evaluated by airway hyperresponsiveness, excessive mucus secretion, and recruitment of inflammatory cells. Immunohistochemistry was employed to quantify the expression levels of NF‐κB. Subsequently, the dose of allergen was modified to investigate whether the impact of hypoxia on asthma is affected by different doses of allergens.ResultCompared to the RA and IH groups, HDM‐treated mice in the IHP group exhibited aggravated inflammatory cell infiltration and airway hyperresponsiveness (p＜.05). Moreover, there was an increased release of inflammatory mediators and higher expression levels of NF‐κB (p＜.05). Importantly, the impact ia on asthma was found to be influenced by high dose of allergen (p＜.05).ConclusionIHP treatment potentially exacerbates HDM‐induced airway inflammation in asthma, with the involvement of NF‐κB, particularly under high‐dose allergen stimulation.

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“…On the other hand, previous studies also suggested the other signaling which were associated with the polarization of M2 macrophages. For example, MAPK and NF‐κB activation could lead to the M2 polarization of macrophages (Abohassan et al, 2021); Akt signaling was confirmed to be positively correlated with macrophage M2 polarization (K. Zhang, Chen, et al, 2021). Thus, more pathways involved in IGF2BP3‐mediated macrophage M2 polarization need to be further explored.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of IGF2BP3 inhibits the tumorigenesis of gallbladder cancer and modifies tumor microenvironment

Qin

Zhang

Lei

et al. 2022

Drug Development Research

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Gallbladder cancer (GBC) ranks seventh among the gastrointestinal cancers. Messenger RNAs (mRNAs) could regulate the progression of GBC. For the purpose of exploring the targets for GBC treatment, RNA sequencing was used to identify the differential expressed mRNAs between GBC and adjacent tissues. Next, CCK8 assay was used to assess the cell viability, and cell proliferation was investigated by colony formation assay. Flow cytometry was performed to evaluate the cell apoptosis. Protein and mRNA expression were analyzed by western blot and RT‐qPCR, respectively. Transwell was performed to evaluate the cell metastasis. GBC‐derived exosomes were isolated with ultracentrifugation. To evaluate the function of exosomes in GBC, in vivo model of GBC was constructed. The data revealed IGF2BP3 was identified to be upregulated in GBC, and IGF2BP3 silencing was able to decrease GBC cell proliferation by promoting the apoptosis. The migration and invasion of GBC cells were reduced by IGF2BP3 knockdown. Silencing of IGF2BP3 obviously suppressed the level of p‐STAT3 in GBC cells. Meanwhile, GBC cell‐derived exosomes notably promoted macrophage M2 polarization via carrying IGF2BP3, and then the polarized macrophages promoted the malignant behavior of GBC cells. Furthermore, exosomes markedly promoted the tumor growth of GBC via promoting macrophage M2 polarization. In summary, knockdown of IGF2BP3 suppressed the malignant behavior of GBC cells. Additionally, knockdown of IGF2BP3 modified tumor microenvironment during the progression of GBC. Thus, these findings might provide a new theoretical basis for exploring a strategies against GBC.

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FNF-12, a novel benzylidene-chromanone derivative, attenuates inflammatory response in in vitro and in vivo asthma models mediated by M2-related Th2 cytokines via MAPK and NF-kB signaling

Cited by 7 publications

References 52 publications

Undaria pinnatifida ameliorates nasal inflammation by inhibiting eosinophil and mast cell activation and modulating the NF‐κB/MAPKs signaling pathway

Undaria pinnatifida ameliorates nasal inflammation by inhibiting eosinophil and mast cell activation and modulating the NF‐κB/MAPKs signaling pathway

Intermittent hypoxic pretreatment exacerbates house dust mite‐induced asthma airway inflammation

Knockdown of IGF2BP3 inhibits the tumorigenesis of gallbladder cancer and modifies tumor microenvironment

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