Baicalin ameliorates experimental inflammatory bowel disease through polarization of macrophages to an M2 phenotype

Zhu, Wei; Jin, Zaishun; Yu, Jianbo; Liang, Jun; Qing-dong, Yang; Li, Fujuan; Shi, Xuekui; Zhu, Xiaodong; Zhang, Xiaoli

doi:10.1016/j.intimp.2016.03.030

Cited by 105 publications

(54 citation statements)

References 23 publications

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“…The IRF signaling pathway, along with several transcription factor, such as STAT3, STAT6, PPARγ, and KLF-4, were reported to promote the M2 macrophage phenotype. Up-regulation of IRF4 and down-regulation of IRF5 after the addition of baicalin consolidated the result of M2 polarization [42]. A similar finding was obtained by Zhu et al (2016), who reported alleviated inflammatory bowel disease by switching macrophages (CD14 + monocytes isolated peripheral blood mononuclear cells) from M1 state to M2 by intervention of the pentacyclic triterpene Lupeol.…”

Section: Role Of Macrophages In Intestinal and Colorectal Diseasesupporting

confidence: 66%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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Macrophages can polarize into two different states (M1 and M2), which play contrasting roles during pathogenesis or tissue damage. M1 polarized macrophages produce pro-inflammatory cytokines and mediators resulting in inflammation, while M2 macrophages have an anti-inflammatory effect. Secretion of appropriate cytokines and chemokines from macrophages can lead to the modification of the microenvironment for bridging innate and adaptive immune responses. Increasing evidence suggests that polarized macrophages are pivotal for disease progression, and the regulation of macrophage polarization may provide a new approach in therapeutic treatment of inflammation-related diseases, including cancer, obesity and metabolic diseases, fibrosis in organs, brain damage and neuron injuries, and colorectal disease. Polarized macrophages affect the microenvironment by secreting cytokines and chemokines while cytokines or mediators that are produced by resident cells or tissues may also influence macrophages behavior. The interplay of macrophages and other cells can affect disease progression, and therefore, understanding the activation of macrophages and the interaction between polarized macrophages and disease progression is imperative prior to taking therapeutic or preventive actions. Manipulation of macrophages can be an entry point for disease improvement, but the mechanism and potential must be understood. In this review, some advanced studies regarding the role of macrophages in different diseases, potential mechanisms involved, and intervention of drugs or phytochemicals, which are effective on macrophage polarization, will be discussed.

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Section: Role Of Macrophages In Intestinal and Colorectal Diseasesupporting

confidence: 66%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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“…Moreover, as the major bioactive constituents in S. baicalensis , baicalin and its aglycones baicalein can protect injured intestinal epithelial cells (Yao et al, 2016) and active autophagy in cancer cells (Li-Weber, 2009). The mechanism research further demonstrated that baicalin might be able to promote the polarization of macrophages to an M2 phenotype to relieve ulcerative colonic inflammation (Zhu et al, 2016). Afterward, other studies also shown that BB could protect intestinal epithelial cells and inhibit mTORC1 in human cancer cells (Aryal et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Quantitative Evaluation of the Compatibility Effects of Huangqin Decoction on the Treatment of Irinotecan-Induced Gastrointestinal Toxicity Using Untargeted Metabolomics

et al. 2017

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Huangqin decoction (HQD), a traditional Chinese medicine (TCM), has been widely used to treat gastrointestinal syndrome in China for thousands of years. Chemotherapy drug irinotecan (CPT-11) is used clinically to treat various kinds of cancers but limited by its side effects, especially delayed diarrhea. Nowadays, HQD has been proved to be effective in attenuating the intestinal toxicity induced by CPT-11. HQD consists of four medicinal herbs including Scutellaria baicalensis Georgi, Glycyrrhiza uralensis Fisch, Paeonia lactiflora Pall, and Ziziphus jujuba Mill. Due to its complexity, the role of each herb and the multi-herb synergistic effects of the formula are poorly understood. In order to quantitatively assess the compatibility effects of HQD, mass spectrometry-based untargeted metabolomics studies were performed. The serum metabolic profiles of rats administered with HQD, single S. baicalensis decoction, S. baicalensis-free decoction and baicalin/baicalein combination were compared. A time-dependent trajectory upon principal component analysis was firstly used to visualize the overall differences. Then metabolites deregulation score and relative area under the curve were calculated and used as parameters to quantitatively evaluate the compatibility effects of HQD from the aspect of global metabolic profile and the specifically altered metabolites, respectively. The collective results indicated that S. baicalensis played a crucial role in the therapeutic effect of HQD on irinotecan-induced diarrhea. Both HQD and SS decoction regulated glycine, serine and threonine pathway. This study demonstrated that metabolomics was a promising tool to elucidate the compatibility effects of TCM or combinatorial drugs.

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“…Mangiferin downregulates IRF5 expression, and therefore inhibits the activation of macrophages and the release of proinflammatory cytokines (13). Baicalin alleviates dextran sodium sulfate-induced colitis by decreasing LPS-induced IRF5 expression (14). Nanoparticle-delivered IRF5 siRNA promotes efficient transition of macrophages from M1 to M2 and functional recovery after spinal cord injury in mice (15).…”

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confidence: 99%

An Oligodeoxynucleotide with AAAG Repeats Significantly Attenuates Burn-induced Systemic inflammatory Responses by inhibiting interferon Regulatory Factor 5 Pathway

Xiao

et al. 2017

Mol Med

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Previously, we showed that an oligodeoxynucleotide (ODN) with AAAG repeats (AAAG ODN) rescued mice from fatal acute lung injury (ALI) induced by influenza virus and inhibited production of tumor necrosis factor-α (TNF-α) in the injured lungs. However, its underlying mechanisms remain to be elucidated. Upon the bioinformatic analysis revealing that the sequence of AAAG ODN is in consensus with the interferon regulatory factor 5 (IRF5) binding site in the cis-regulatory elements of proinflammatory cytokines, we tried to explore whether AAAG ODN could attenuate burn injury-induced systemic inflammatory responses by inhibiting the IRF5 pathway. Using a mouse model with sterile systemic inflammation induced by burn injury, we found that AAAG ODN prolonged the lifespan of the mice, decreased the expression of IRF5 in the injured skin, reduced the production of TNF-α and IL-6 in the blood and injured skin, and attenuated the ALI. These effects were correlated with AAAG ODN-mediated inhibition of nuclear translocation of IRF5. The data suggest that AAAG ODN could act as a cytoplasmic decoy capable of interfering the function of IRF5 and be developed as a drug candidate for the treatment of inflammatory diseases. online address: http://www.molmed.org

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Baicalin ameliorates experimental inflammatory bowel disease through polarization of macrophages to an M2 phenotype

Cited by 105 publications

References 23 publications

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Quantitative Evaluation of the Compatibility Effects of Huangqin Decoction on the Treatment of Irinotecan-Induced Gastrointestinal Toxicity Using Untargeted Metabolomics

An Oligodeoxynucleotide with AAAG Repeats Significantly Attenuates Burn-induced Systemic inflammatory Responses by inhibiting interferon Regulatory Factor 5 Pathway

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