Berberine Differentially Modulates the Activities of ERK, p38 MAPK, and JNK to Suppress Th17 and Th1 T Cell Differentiation in Type 1 Diabetic Mice

Cui, Guoliang; Qin, Xia; Zhang, Yuebo; Gong, Zhaohui; Ge, Baoxue; Zang, Ying

doi:10.1074/jbc.m109.012674

Cited by 178 publications

(137 citation statements)

References 46 publications

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“…It also exhibits antitumor, antimicrobial, and even antidiabetic effects (31)(32)(33)(34)(35)(36). Moreover, a recent report suggested that BBR may be efficacious in experimental type I diabetes (37), raising the possibility of its use as a treatment for autoimmune diseases. This study was undertaken to investigate the novel regulatory properties and underlying mechanism of BBR in an autoimmune disease model.…”

mentioning

confidence: 99%

Regulation of Th1 and Th17 Cell Differentiation and Amelioration of Experimental Autoimmune Encephalomyelitis by Natural Product Compound Berberine

Qin

Guo

Wan

et al. 2010

The Journal of Immunology

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104

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Berberine (BBR), an isoquinoline alkaloid derived from plants, is widely used as an anti-inflammatory remedy in traditional Chinese medicine. In this study, we showed that BBR was efficacious in the amelioration of experimental autoimmune encephalomyelitis (EAE) through novel regulatory mechanisms involving pathogenic Th1 and Th17 cells. BBR inhibited differentiation of Th17 cells and, to a lesser degree, Th1 cells through direct actions on the JAK/STAT pathway, whereas it had no effect on the relative number of CD4+Foxp3+ regulatory T cells. In addition, BBR indirectly influenced Th17 and Th1 cell functions through its effect on the expression and function of costimulatory molecules and the production of IL-6, which was attributable to the inhibition of NF-κB activity in CD11b+ APCs. BBR treatment completely abolished the encephalitogenicity of MOG35–55-reactive Th17 cells in an adoptive transfer EAE model, and the same treatment significantly inhibited the ability of MOG35–55-reactive Th1 cells to induce EAE. This study provides new evidence that natural compounds, such as BBR, are of great value in the search for novel anti-inflammatory agents and therapeutic targets for autoimmune diseases.

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confidence: 99%

Regulation of Th1 and Th17 Cell Differentiation and Amelioration of Experimental Autoimmune Encephalomyelitis by Natural Product Compound Berberine

Qin

Guo

Wan

et al. 2010

The Journal of Immunology

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104

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“…Although mice lacking T cells, B cells, and NK cells can still develop colitis in response to DSS (4,10), Th1/Th2 responses have been reported to modulate macrophage-induced inflammation in DSS-induced colitis model (9). Berberine has been reported to decrease Th17 and Th1 cytokine production and Th1 and Th17 cell differentiation in a Type 1 diabetic mouse model (8). Fig.…”

mentioning

confidence: 99%

“…Furthermore, berberine's immunoregulatory potentials have been demonstrated. Berberine has been shown to inhibit human immunodeficiency virus (HIV) protease inhibitor-induced TNF and IL-6 production in macrophages (45) and enhance progression of Type 1 diabetes in mice and decrease Th17 and Th1 cytokine production, and Th17 and Th1 cell differentiation by regulation of mitogen-activated protein kinase (MAPK) pathways in this mouse model (8).…”

mentioning

confidence: 99%

Berberine promotes recovery of colitis and inhibits inflammatory responses in colonic macrophages and epithelial cells in DSS-treated mice

Yan

Wang

Shi

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

162

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Inflammatory bowel disease (IBD) results from dysregulation of intestinal mucosal immune responses to microflora in genetically susceptible hosts. A major challenge for IBD research is to develop new strategies for treating this disease. Berberine, an alkaloid derived from plants, is an alternative medicine for treating bacterial diarrhea and intestinal parasite infections. Recent studies suggest that berberine exerts several other beneficial effects, including inducing anti-inflammatory responses. This study determined the effect of berberine on treating dextran sulfate sodium (DSS)-induced intestinal injury and colitis in mice. Berberine was administered through gavage to mice with established DSS-induced intestinal injury and colitis. Clinical parameters, intestinal integrity, proinflammatory cytokine production, and signaling pathways in colonic macrophages and epithelial cells were determined. Berberine ameliorated DSS-induced body weight loss, myeloperoxidase activity, shortening of the colon, injury, and inflammation scores. DSS-upregulated proinflammatory cytokine levels in the colon, including TNF, IFN-γ, KC, and IL-17 were reduced by berberine. Berberine decreased DSS-induced disruption of barrier function and apoptosis in the colon epithelium. Furthermore, berberine inhibited proinflammatory cytokine production in colonic macrophages and epithelial cells in DSS-treated mice and promoted apoptosis of colonic macrophages. Activation of signaling pathways involved in stimulation of proinflammatory cytokine production, including MAPK and NF-κB, in colonic macrophages and epithelial cells from DSS-treated mice was decreased by berberine. In summary, berberine promotes recovery of DSS-induced colitis and exerts inhibitory effects on proinflammatory responses in colonic macrophages and epithelial cells. Thus berberine may represent a new therapeutic approach for treating gastrointestinal inflammatory disorders.

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“…BBR was able to activate ERK1/2 signaling in mice as reported earlier [28]. We tested whether ERK1/2 pathway is involved in BBR-induced neuroprotective effects in PC12 cells.…”

Section: Bbr Stimulated the Erk1/2 Signaling Pathway In Pc12 Cellsmentioning

confidence: 94%

Berberine Protects against Hydrogen Peroxide-Induced Oxidative Damage in PC12 Cells through Activation of ERK1/2 Pathway

Liu¹,

Zeng²,

Gaur³

et al. 2017

Clin Exp Pharmacol

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Oxidative stress is a much-recognized phenomenon linked with the progression of Neurodegenerative Diseases (NDs) due to imbalances in redox homeostasis. Increasing evidence indicates that excessive Reactive Oxygen Species (ROS), impairing the physiological functions of neurons via inducing cell apoptosis, is the main cause of NDs. The drug candidates are required that can effectively protect neurons from oxidative stress insult to slow down the process of neurodegenerative diseases. In present study, we investigated the protective effect and the underlying mechanisms of berberine (BBR, an isoquinoline alkaloid isolated from the herb Rhizoma coptidis, against oxidative damage in PC12 cells. It was found that BBR was able to suppress hydrogen peroxide (H 2 O 2 )-induced cell death in PC12 cells. Flow cytometry revealed that BBR significantly reduced the apoptosis of PC12 cells exposed to H 2 O 2 . Western blot analysis displayed that BBR stimulated the extracellular regulated ERK1/2 survival signaling, while application of PC12 cells with ERK1/2 pathway inhibitor PD98059 blocked the neuroprotective effect of BBR. These results together indicated that BBR is a potential protectant, and it protects PC12 cells against H 2 O 2 toxicity through activated the ERK1/2 pathway.

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Berberine Differentially Modulates the Activities of ERK, p38 MAPK, and JNK to Suppress Th17 and Th1 T Cell Differentiation in Type 1 Diabetic Mice

Cited by 178 publications

References 46 publications

Regulation of Th1 and Th17 Cell Differentiation and Amelioration of Experimental Autoimmune Encephalomyelitis by Natural Product Compound Berberine

Regulation of Th1 and Th17 Cell Differentiation and Amelioration of Experimental Autoimmune Encephalomyelitis by Natural Product Compound Berberine

Berberine promotes recovery of colitis and inhibits inflammatory responses in colonic macrophages and epithelial cells in DSS-treated mice

Berberine Protects against Hydrogen Peroxide-Induced Oxidative Damage in PC12 Cells through Activation of ERK1/2 Pathway

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