Berberine suppresses IL-33-induced inflammatory responses in mast cells by inactivating NF-κB and p38 signaling

Li, Weihua; Yin, Ning; Tao, Wenting; Wang, Qian; Fan, Hong; Wang, Zhigang

doi:10.1016/j.intimp.2018.11.009

Cited by 26 publications

(16 citation statements)

References 42 publications

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“…The occurrence and development of sepsis have close correlations with inflammatory responses mediated by the TLR signaling pathway. Activated TLR can activate the downstream kinases p38 MAPK and IκB and the transcription factor NF-κB 18 . P38 MAPK is a member of the MAPK family.…”

Section: Discussionmentioning

confidence: 99%

Effect of IL-33 on pyroptosis of macrophages in mice with sepsis via NF-κB/p38 MAPK signaling pathway

Cai

2021

Acta Cir. Bras.

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Purpose: To demonstrate the effect of IL-33 on the macrophage pyroptosis in mice with sepsis through the NF-kB/p38 MAPK signal pathway. Methods: In total, 24 C57BL/6 mice were divided into the sham operation group (sham) and the cecal ligation and puncture group (CLP). After CLP, 24 IL-33-/-mice were divided into the IL-33-/-group and the IL-33-/-intervention group. The latter group was intraperitoneally injected with IL-33. Mouse mortality was observed after CLP. Macrophage apoptosis in peritoneal lavage fluid was detected by flow cytometry. Serum inflammatory factor level was detected by ELISA. Apoptotic protein expression and NF-κB/p38 MAKP signaling pathway protein expression were detected by qRT-PCR and Western blot. Results: Knocking out IL-33 significantly reduced the mortality of CLP mice, as well as the mRNA expression of IL-33 and the levels of serum inflammatory factors, including IL-33, IL-1β, and IL-18. It also reduced the rate of macrophage apoptosis and the expression of the apoptotic protein caspase-1 p10; increased the expression of IκBα; and reduced the protein expression of NF-κB and p38 MAPK. These effects were reversed after exogenous injection of IL-33. Conclusion: IL-33 can increase the level of macrophage pyroptosis in mice with sepsis (by activating the NF-kB/ p38MAPK signal pathway) and the mortality of these mice.

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Section: Discussionmentioning

confidence: 99%

Effect of IL-33 on pyroptosis of macrophages in mice with sepsis via NF-κB/p38 MAPK signaling pathway

Cai

2021

Acta Cir. Bras.

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“…Berberine is one kind of alkaloid component, and it has been demonstrated to possess various bioactivities such as anti-inflammatory, antitumor, and antioxidant properties (Dkhil et al, 2017; Almeer et al, 2018; Kim et al, 2018; Xu et al, 2018; Li et al, 2019). It has been reported that berberine could exert its protective effects against DSS colitis by improving intestinal barrier function and reducing inflammation and oxidative stress; and berberrubine, which has been reported to possess an anti-colitis effect similar to that of berberine with a much smaller dosage, is one of the metabolites of berberine (Yu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Berberine Protects Mice Against Dextran Sulfate Sodium-Induced Colitis by Activating mTORC1 Pathway

Liu

Pang

et al. 2019

Front. Pharmacol.

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Berberine is a plant alkaloid that can be extracted from many Chinese herbs. It has been reported that berberine could protect mice from ulcerative colitis, but the mechanism remains unclear. The current study’s aim was to determine the potential mechanism by which berberine exhibits its anti-inflammatory function. Mice with colitis induced by dextran sulfate sodium (DSS) were administered with berberine at 50 mg/kg by gavage. Berberine significantly increased the proportion of regulatory T cells (Treg cells). The targeted metabolomics analysis was then performed to find that glutamine and glutamate metabolism played an important role in the process of regulating immune response. mTORC1 pathway was reported to closely relate with glutamine metabolism. As a result, the relative expression levels of downstream effector genes of mTORC were further determined, and data obtained showed that berberine could significantly increase the relative expression levels of S6K1 and 4EBP1. In addition, rapamycin was used to inhibit mTORC1 signaling, and it was found that colon length, disease associated index (DAI), and proportion of Treg cells of mice in the rapamycin-DSS group were not different from those of mice in the rapamycin/berberine-DSS group. Together, these results suggest that berberine exhibits significant protective effects against DSS colitis by activating the mTORC1 pathway to increase the proportion of Treg cells.

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“…The natural molecule berberine may be particularly useful in cases of PANS/PANDAS because of its antibacterial properties, but also because it can inhibit mast cells [ 370 , 371 ] and improve brain circulation [ 372 ]. In addition, high doses of Vitamin D3 are recommended, because this vitamin has been found to be present at low levels in mothers and/or children with ASD [ 371 , 373 , 374 , 375 ] and also decreases atopic responses [ 376 ].…”

Section: Treatment Approachesmentioning

confidence: 99%

Ways to Address Perinatal Mast Cell Activation and Focal Brain Inflammation, including Response to SARS-CoV-2, in Autism Spectrum Disorder

2021

JPM

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The prevalence of autism spectrum disorder (ASD) continues to increase, but no distinct pathogenesis or effective treatment are known yet. The presence of many comorbidities further complicates matters, making a personalized approach necessary. An increasing number of reports indicate that inflammation of the brain leads to neurodegenerative changes, especially during perinatal life, “short-circuiting the electrical system” in the amygdala that is essential for our ability to feel emotions, but also regulates fear. Inflammation of the brain can result from the stimulation of mast cells—found in all tissues including the brain—by neuropeptides, stress, toxins, and viruses such as SARS-CoV-2, leading to the activation of microglia. These resident brain defenders then release even more inflammatory molecules and stop “pruning” nerve connections, disrupting neuronal connectivity, lowering the fear threshold, and derailing the expression of emotions, as seen in ASD. Many epidemiological studies have reported a strong association between ASD and atopic dermatitis (eczema), asthma, and food allergies/intolerance, all of which involve activated mast cells. Mast cells can be triggered by allergens, neuropeptides, stress, and toxins, leading to disruption of the blood–brain barrier (BBB) and activation of microglia. Moreover, many epidemiological studies have reported a strong association between stress and atopic dermatitis (eczema) during gestation, which involves activated mast cells. Both mast cells and microglia can also be activated by SARS-CoV-2 in affected mothers during pregnancy. We showed increased expression of the proinflammatory cytokine IL-18 and its receptor, but decreased expression of the anti-inflammatory cytokine IL-38 and its receptor IL-36R, only in the amygdala of deceased children with ASD. We further showed that the natural flavonoid luteolin is a potent inhibitor of the activation of both mast cells and microglia, but also blocks SARS-CoV-2 binding to its receptor angiotensin-converting enzyme 2 (ACE2). A treatment approach should be tailored to each individual patient and should address hyperactivity/stress, allergies, or food intolerance, with the introduction of natural molecules or drugs to inhibit mast cells and microglia, such as liposomal luteolin.

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Berberine suppresses IL-33-induced inflammatory responses in mast cells by inactivating NF-κB and p38 signaling

Cited by 26 publications

References 42 publications

Effect of IL-33 on pyroptosis of macrophages in mice with sepsis via NF-κB/p38 MAPK signaling pathway

Effect of IL-33 on pyroptosis of macrophages in mice with sepsis via NF-κB/p38 MAPK signaling pathway

Berberine Protects Mice Against Dextran Sulfate Sodium-Induced Colitis by Activating mTORC1 Pathway

Ways to Address Perinatal Mast Cell Activation and Focal Brain Inflammation, including Response to SARS-CoV-2, in Autism Spectrum Disorder

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