JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2021
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IF 5.279
Yaozhong Hu,Jiaxin Gu,Yi Wang,Jing Lin,Huaning Yu,Feier Yang,Sihao Wu,Jia Yin,Huan Lv,Xuemeng Ji,Shuo Wang
Tea polyphenol of epigallocatechin-3-gallate (EGCG) has been verified to possess multiple biological activities. Interleukin-23 (IL-23) is a heterodimeric cytokine consisting of two subunits of IL-23p19 and IL-12p40, with the functionality in regulating the production of cytokines under physiological or pathological conditions. By serendipity, the raised expression of IL-23 was observed after treating cells with EGCG, whereas the detailed mechanism remains poorly understood. This study was proposed to investigate the signaling related to EGCG-induced IL-23. The raised expression of IL-23 was confirmed primarily by intraperitoneally injecting with different concentrations of EGCG (0, 20, 50, 80 mg/kg) into BALB/c mice, and the raised expression was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Results from enzyme-linked immunosorbent assay (ELISA) revealed the increase of IL-23 in serum from 116.09 to 153.90 pg/mL after treating with EGCG. The same results were also observed in RAW264.7 and peritoneal macrophages after treating with EGCG (0, 1, 5, 10, 25 μM) with the increased tendency of IL-23 in cultural medium (7.98 to 25.38 pg/mL for RAW264.7; 3.64 to 260.93 pg/mL for peritoneal macrophages). After preliminary exploration of the signaling related to the increased IL-23, the classical signaling pathways and key transcription factors, such as nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK) signaling pathways, and interferon regulatory factor 5 (IRF5), were demonstrated with no relevant contribution. A further study revealed the involvement of the key transcription factor of BATF2, which could antagonistically modulate the transcription and translation of IL-23. The signaling of STAT3-BATF2-c-JUN/ATF2-IL-23 has been further verified in RAW264.7 macrophages using the STAT3 inhibitor of AG490 and the activator of Colivelin TFA. The results indicated that EGCG inhibits the phosphorylation of STAT3 to facilitate the decreased level of BATF2, which contributed to the increased level of IL-23 by the enhancing heterodimerization of c-JUN and ATF2.
研究领域:
免疫学
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药理学
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
American Journal of Translational Research
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2018
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IF 3.061
Qin Zhu,Peifen Zheng,Xinyu Chen,Feng Zhou,Qiaona He,Yuefeng Yang
Ulcerative colitis (UC) is a chronic and nonspecific intestinal inflammatory disease, which may increase the risk of colon cancer. Andrographolide is a main active component of Andrographis paniculata . The anti-inflammatory ability of andrographolide suggested its potential therapeutic effect against UC. In the present study, elevated serum concentrations of proinflammatory factors, including (TNF)-α, interleukin (IL)-1β, IL-6 and IL-23, as well as increased percentages of Th17 cells (IL-17+CD4+ cells) in CD4+ cells were detected in UC patients compared to that in healthy donors. These data suggested that Th17 immune responses may involve in the pathogenesis of UC. Experimental colitis mouse model was then established. The results of hematoxylin and eosin staining demonstrated the therapeutic effect of andrographolide on colitis. Enzyme-linked immunosorbent assay (ELISA), flow cytometry and western blotting analyses showed that andrographolide could decreased the levels of proinflammatory factors TNF-α, IL-1β, IL-6 and IL-17A in the serum and in the colon tissues, reduced the percentages of Th17 cells in CD4+ cells, and suppressed the levels of IL-23, IL-17A, ROR-γt (key transcription factor of Th17 cells) and p-STAT3 in the colon tissues. Further, peripheral blood mononuclear cells (PBMCs) were isolated from UC patients and treated with various concentrations of andrographolide (0, 10, 20 and 30 μg/ml). Andrographolide also showed inhibitory effects on the levels of proinflammatory factors, the percentages of Th17 cells and the expression of relative proteins. Similar results were obtained in lipopolysaccharide-treated normal PBMCs. These data suggested that andrographolide may inhibit Th17 immune response via STAT3 signaling. In conclusion, we demonstrated that andrographolide inhibited the activity of IL-23/IL-17 axis and down-stream pro-inflammatory factors so as to suppress inflammation response, resulting in the relieving of UC.
研究领域:
免疫学
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药理学
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炎症性肠病
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DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2024
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IF 4.4
Chen Xinlu,Gong Luyao,Wang Yuanyuan,Ye Chen,Guo Huanhuan,Gao Shen,Chen Jiyuan,Wang Zhuo,Gao Yuan
Introduction: Metastatic castration-resistant prostate cancer (mCRPC) patients face challenges due to limited treatment options. About 50% of patients with mCRPC have a functional loss of phosphatase and tensin homology deleted on chromosome 10 (PTEN), leading to tumor progression, metastasis, and immune suppression. Moreover, elevated IL-23 produced by myeloid-derived suppressor cells (MDSCs) is found in CRPC patients, driving tumor progression. Therefore, a combination strategy based on PTEN restoration and IL-23 inhibition may block CRPC progression and metastasis.Methods: The antitumor effect of restoring PTEN expression combined with the IL-23 inhibitor Apilimod was studied in a mouse model of bone metastasis CRPC and mouse prostate cancer RM-1 cells. To verify the targeting ability of PTEN DNA coated with lipid nanoparticles (LNP@PTEN) in vitro and in vivo. In addition, RT-qPCR and flow cytometry were used to investigate the related mechanisms of the antitumor effect of LNP@PTEN combined with Apilimod.Results: LNPs exhibited significant tumor-targeting and tumor accumulation capabilities both in vitro and in vivo, enhancing PTEN expression and therapeutic efficacy. Additionally, the combination of LNP@PTEN with the IL-23 inhibitor Apilimod demonstrated enhanced inhibition of tumor growth, invasion, and metastasis (particularly secondary organ metastasis) compared to other groups, and extended the survival of mice to 41 days, providing a degree of bone protection. These effects may be attributed to the PTEN function restoration combined with IL-23 inhibition, which help reverse immune suppression in the tumor microenvironment by reducing MDSCs recruitment and increasing the CD8+/CD4+ T cell ratio.Discussion: In summary, these findings highlight the potential of LNPs for delivering gene therapeutic agents. And the combination of LNP@PTEN with Apilimod could achieve anti-tumor effects and improve tumor microenvironment. This combinational strategy opens new avenues for the treatment of mCRPC.
研究领域:
肿瘤学
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分子生物学
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纳米技术
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免疫治疗
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2026
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IF 5.6
Qing Liu,Jing Liu,Ziren Wang,Yihang Zheng,Yujuan Li,Jianhua Huang,Yachao Jiang,Xiaoyong Lei,Junjie Wang
Tangeretin (Tan) is an anti-psoriatic bioactive ingredient derived from Citri Reticulatae Pericarpium . • Validated Tan's anti-psoriatic efficacy via imiquimod-induced mouse model and LPS-stimulated RAW264.7 macrophage model. • Molecular docking predicted the specific amino acid residue sites involved in Tan's competitive inhibition of IL-23/IL-23R binding. • Tan alleviates psoriasis by inhibiting the IL-23/IL-23R signaling pathway. • Tan can be developed as a novel, potent, and targeted agent for psoriasis treatment. Psoriasis is a chronic immune-mediated skin disease characterized by strong genetic susceptibility and autoimmune components. Identifying lead compounds from natural products for psoriasis has been proposed as a promising therapeutic strategy. Citri Reticulatae Pericarpium (CRP) is a traditional Chinese medicine material rich in polymethoxy flavonoids with anti-inflammatory, antioxidant, and immunomodulatory activities. Whereas, the bioactive constituents of CRP responsible for anti-psoriatic effects and its underlying mechanism have yet to be elucidated. In this study, we employed network pharmacology analysis to pinpoint tangeretin (Tan) as the major anti-psoriatic component of CRP, and further systematically evaluated its anti-psoriatic effects and investigated its underlying mechanisms . Tan significantly attenuated IMQ-induced psoriasiform skin lesions in mice, as evidenced by the remarkably decrease in erythema, scaling, skin thickness, inflammatory cell infiltration, and several inflammatory factors. Further mechanism revealed that Tan inhibited the binding of IL-23 to the IL-23 receptor, and suppressed downstream JAK2/STAT3 and MAPK activation, thereby reducing inflammation and attenuating psoriasis progression. Overall, these findings provide strong evidence for Tan represents to be developed into a therapeutic candidate for psoriasis management. Our study also provides a scientific rationale for the therapeutic application of CRP against psoriasis.
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DOI
高影响因子
IMMUNOLOGY AND CELL BIOLOGY
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2026
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IF 3.3
Yadi Li,Xiaoqian Zhou,Zhusheng Yang,Xiumin Yang,Aihua Wei
Psoriasis, a chronic inflammatory skin disease, involves dysregulated immune responses and keratinocyte hyperproliferation. The role of salt-inducible kinase 2 (SIK2) in modulating interleukin-23 (IL-23) secretion via C–X–C motif chemokine ligand 5 (CXCL5) in neutrophils has not been fully explored. We combined in vivo and in vitro approaches to examine SIK2's role in an imiquimod (IMQ)-induced psoriasis model and activated neutrophils. Mice underwent intradermal injections of lentiviruses overexpressing SIK2, CXCL5, or both, while in vitro experiments involved transfecting activated neutrophils with these constructs. Assessments included ear thickness, cellular and neutrophil infiltration through histological and immunofluorescence techniques, and analysis of gene and protein expressions via quantitative real-time PCR (qRT-PCR), immunohistochemistry (IHC), and Western blot. Additionally, cell viability, proliferation, and cytokine levels in N -formylmethionyl-leucyl-phenylalanine (fMLF) treated neutrophils were evaluated using cell-counting kit-8 (CCK8), 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and Enzyme-Linked Immunosorbent Assay (ELISA). Overexpression of SIK2 significantly reduced ear thickness, cellular and neutrophil infiltration, IL-1β, tumor necrosis factor-alpha (TNF-α), CXCL5, IL-23 and phosphorylated Yes-associated protein (p-YAP) levels, and increased SIK2 levels in IMQ mice model, but overexpression of CXCL5 reversed these effects. In vitro , SIK2 overexpression resulted in reduced cell viability and proliferation, with corresponding reductions in IL-1β, IL-17, IL-23, and Matrix Metallopeptidase 9 levels, whereas overexpression of CXCL5 reversed these effects. Our findings suggest that SIK2 acts as a critical modulator in psoriasis by influencing CXCL5-mediated IL-23 secretion in neutrophils, underscoring the potential of SIK2 as a therapeutic target to alleviate the inflammatory responses in psoriasis.
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DOI
高影响因子
Frontiers in Cellular and Infection Microbiology
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2022
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IF 6.073
Zhang Haiting,Wei Yu,Jia Huanhuan,Chen Diling,Tang Xiaocui,Wang Jian,Chen Meili,Guo Yinrui
It is very important to understand the communication and interaction mechanisms between the host and its resident microorganisms on host physiology and for precise diagnosis and treatment. Although intestinal fungi and bacteria dysbiosis is increasingly linked to ankylosing spondylitis (AS), their mechanisms of action have been rarely illustrated. In this paper, fecal samples from 10 AS monkeys and 10 healthy controls were collected to systematically characterize the gut mycobiota and microbiota in AS monkeys by 16S rRNA and ITS2 DNA sequencing. Our results showed the gut fungi of Kazachstania pintolopesii, Saccharomycetaceae, Kazachstania, and Saccharomyceteles. Saccharomycetes were specially enriched in AS, and the microbiota of AS monkeys was characterized by an increased abundance of Clostridia, Clostridiales, Ruminococcaceae, and Prevotella 2, using Line Discriminant Analysis Effect Size. Compared to healthy controls, decreased ITS2/16S biodiversity ratios and altered bacterial–fungal interkingdom networks were observed in AS monkeys. Oral administration of K. pintolopesii activates IL-17RA pathway and induce inflammatory reaction in the colonic tissue of C57BL/6 mice, as well as multiple AS phenotypes, including fungal and bacterial dysbiosis, immune responses of NK cells, platelets, T cells, leukocytes, B-cell activation, rheumatoid arthritis, and inflammatory bowel disease. We also found the secreted products of K. pintolopesii could activate the IL-17RA pathway, which induces PANoptosis in macrophage RAW264.7 cells. Much worse, the PANoptosis products could promote the proliferation and morphological changes of K. pintolopesii, which resulted in much more K. pintolopesii and a severe inflammatory reaction. Interestingly, the inflammatory factor TNF-α can promote the morphological transformation of Candida albicans and K. pintolopesii, which is worthy of further study. The characteristic fungi in all these findings implied that fungal and bacterial dysbiosis have a close link to AS and that their communication and interaction indeed play an important role in autoimmune responses, and K. pintolopesii could be a potential marker microorganism in AS, although its specific mechanism is not fully elucidated.
研究领域:
免疫学
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微生物学
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风湿病学
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分子生物学
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2026
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IF 4.7
Jia-Yi Dou,Chen-Yu Wang,Sai-Hu Liu,Chong Gao,Shuang Zheng,Li-Hua Lian,Zhen-Yu Cui,Ji-Xing Nan,Yan-Ling Wu
Pterostilbene (PTE) is a natural stilbene compound abundantly found in various small berries such as blueberry and grape, and exhibits multiple health promoting potentials and excellent pharmacological activities, especially antioxidant and anti-inflammatory activities. This study explored the protective effects of PTE on pulmonary fibrogenesis and inflammation and its underlying mechanisms. TGF-β-stimulated BEAS-2B or primary lung fibroblasts (LFs) were cultured with PTE or pirfenidone (PFD). Mice were received intratracheal instillation of bleomycin (BLM) and administered PTE or PFD. IL-23/ATP6V 0 D 2 -deficient BEAS-2B were treated with TGF-β or PTE. Primary LFs were stimulated with conditioned medium from TGF-β-primed RLE-6TN (CM) and treated with PTE. In vitro , PTE inhibited TGF-β-induced BEAS-2B cell migration, extracellular matrix (ECM) deposition, epithelial-mesenchymal transition (EMT) and inflammation. In BLM-induced mice, PTE reduced lung index and IL-1β levels in BALF, and improved histopathological changes. PTE inhibited BLM-induced fibrogenesis, EMT, inflammation and immune cell infiltration through blocking IL-23 and activating ATP6V 0 D 2 . In TGF-β-induced BEAS-2B, PTE decreased IL-23, increased ATP6V 0 D 2 and ATP levels, and disrupted the interaction between IL-23 and ATP6V 0 D 2 . In IL-23-deficient BEAS-2B, PTE further elevated ATP6V 0 D 2 and decreased α-SMA, Vimentin and IL-1β expressions. ATP6V 0 D 2 deficiency attenuated the anti-fibrotic and anti-inflammatory effects of PTE in TGF-β-induced BEAS-2B. PTE also inhibited fibrogenesis, EMT, and inflammation in activated-primary LFs and blocked CM-triggered primary LFs activation by regulating IL-23-ATP6V 0 D 2 axis. In conclusion, PTE ameliorated pulmonary fibrosis targeting IL-23/ATP6V 0 D 2 pathway, especially remodeling the local microenvironment of alveolar epithelial cells and fibroblasts, which might be a novel therapeutic strategy against pulmonary fibrosis.
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产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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2018
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IF 2.559
Chuiming Jia,Dejuan Kong,Yiwei Guo,Lianqiao Li,Lina Quan
Bortezomib (BTZ) is one of the most frequently used drugs in treatment of multiple myeloma (MM), but drug-resistance often occurs and limits its clinical efficacy. Annexin A1 (ANXA1) is upregulated in MM, and its knockdown enhances chemosensitivity in MM. However, whether ANXA1 inhibition can increase antitumor activity of BTZ in MM cells remains unknown. In the present study, Cell Counting Kit-8 (CCK-8) and colony formation assays showed that ANXA1 silencing combined with BTZ treatment led to a more significant inhibition of MM cell proliferation than each treatment alone. Cell apoptosis was dramatically promoted in MM cells following silencing of ANXA1 and BTZ administration versus that in ANXA1-silenced alone or BTZ-treated alone cells, as evidenced by decreased expression of phosphorylated signal transducers and activators of transcription 3 and BCL2, and increased expression of BAX. Moreover, we demonstrated that the levels of IL-6 and IL-23 were markedly downregulated in ANXA1-silenced and BTZ-treated MM cells. Furthermore, the combination of ANXA1 knockdown and BTZ treatment distinctly suppressed tumor growth in vivo compared with BTZ treatment alone. Taken together, our results show that downregulation of ANXA1 enhances antitumor activity of BTZ in MM in vitro and in vivo , indicating that ANXA1 may be a promising target for enhancing the chemosensitivity of MM to BTZ.
研究领域:
肿瘤学
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血液学
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分子生物学
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药理学
✓ 已验证
DOI
PubMed
高影响因子
ANNALS OF MEDICINE
·
2025
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IF 4.3
Yun Yang,Lengqiu Guo,Jinghua Yu,Wei Peng,Qi Wang,Lan Wei,Xihua Chen,Chunyan Min,Xiaogang Jiang,Song Zhu,Haixin Zhao,Zhenyu Xuan,Jianzhong Yu,Jian Zhang
Background Da-Yuan-Yin Decoction (DYY), used since the early Qing Dynasty in China for damp-heat syndrome, was evaluated for its comprehensive protective effects.Materials and methods Rats received a high-fat/high-sugar diet for 14 days, then daily exposure to high temperature/humidity (31.0 ± 0.5°C, 85%-95%) for 10 hours over 14 days. Damp-heat syndrome was induced on day 29 via intraperitoneal lipopolysaccharide (LPS) injections (1 mg/kg and 0.5 mg/kg after 4 hours). Two hours post-modeling, rats received DYY (400 or 800 mg/kg/day) orally for 5 days. Symptoms were scored. On day 33, kidney, spleen, tongue, lung, liver, stomach, and colon tissues underwent histopathological and immunochemical/immunofluorescence analysis. Serum levels of inflammation factors, C-reactive protein (CRP), cell-free DNA (cfDNA), myeloperoxidase (MPO), and superoxide dismutase (SOD) were quantified. Complete blood count (CBC), blood biochemistry, short-chain fatty acids (SCFAs), gut microbiota composition in the colon, and metabolites in the cecum were analyzed.Results DYY significantly reduced symptom scores and decreased CRP level, while also regulating parameters in CBC and biochemical profiles. The treatment ameliorated tissue damage in the kidney, spleen, tongue, lung, liver, stomach, and colon. DYY downregulated citrullinated histone H3 (Cit H3), polyclonal peptidylarginine deiminase 4 (PADI4), and MPO expressions in the lung, stomach, and colon. Furthermore, it modulated inflammatory responses, suppressed the interleukin-23 (IL-23)/janus kinase-2 (JAK2)/signal transduction and transcription activator-3 (STAT3) signaling pathway and enhanced antioxidant activity. DYY administration significantly increased total SCFA content. The intervention restored gut microbiota diversity and abundance, while ameliorating metabolic dysregulation.Conclusion Systemic pathophysiological alterations were observed in rats with damp-heat syndrome. The comprehensive protective effects of DYY involved suppression of neutrophil extracellular traps (NETs) formation through downregulation of PADI4 expression, modulation of inflammatory responses, inhibition of the IL-23/JAK2/STAT3 signaling pathway, restoration of intestinal microecological balance and metabolic homeostasis, and enhancement of antioxidant.
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产品关联
DOI
PubMed
高影响因子
Advanced Science
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2024
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IF 14.3
Zi Yi Wang,Ze Qiang Zhao,Yu Jun Sheng,Ke Jun Chen,Bo Zhi Chen,Xin Dong Guo,Yong Cui
Psoriasis is a chronic, immune-mediated disorder characterized by immune regulation disorders and abnormal keratinocyte proliferation. Deucravacitinib (Deu), a selective oral Tyrosine Kinase 2 (TYK2) inhibitor, shows promise in treating psoriasis but may cause systemic side effects and fail to address persistent localized thickened lesions. Herein, a self-locking microneedle (MN) patch with a polyvinyl alcohol (PVA) inner ring loaded with Deu is developed, designed to penetrate the transdermal barriers and dissolve rapidly, downregulating the IL-23/IL-17 pathway and serve as the first line of defense against the spread of skin-originated inflammation. Additionally, Calcipotriol (Cal), a vitamin D derivative, is incorporated into a methacrylated hyaluronic acid (HAMA) backing layer and outer ring that mimics occlusive administration, maintaining localized skin surface retention for prolonged anti-proliferative therapy. The Deu@Cal MN demonstrates satisfactory adhesiveness due to swelling-mediated mechanical interlocking via the outer ring, ensuring targeted drug release at lesion site. Besides its effectiveness in alleviating both skin inflammation and proliferation, it inhibits the differentiation of Th17 cells in the spleen, suggesting potential to reduce systemic inflammation. These findings offer a new therapeutic approach for treating psoriasis and other autoimmune and inflammatory conditions.
研究领域:
药学
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皮肤科
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免疫学
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材料科学
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产品关联
DOI
PubMed
高影响因子
Theranostics
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2021
·
IF 11.556
Yuce Li,Yuchen Lou,Yu Chen,Jing Yang,Danqi Li,Biling Jiang,Jiajia Lan,Jingjing Wen,Yangxue Fu,Yamin Zhang,Juan Tao,Jintao Zhu
Immune-mediated inflammatory diseases (IMIDs) are characterized by immune dysregulation and severe inflammation caused by the aberrant and overactive host immunological response. Mycophenolic acid (MPA)-based immunosuppressive drugs are potential treatments for IMIDs because of their mild side-effect profile; however, their therapeutic effects are limited by the high albumin binding rate, unsatisfactory pharmacokinetics, and undefined cellular uptake selectivity. Methods: Polysaccharide mycophenolate was synthesized by conjugating MPA molecules to dextran (a typical polysaccharide widely used in drug delivery) and encapsulated extra free MPA molecules to fabricate MPA@Dex-MPA nanoparticles (NPs). The efficacy of these NPs for mediating immunosuppression and treatment of IMIDs was evaluated in imiquimod-induced psoriasis-like skin inflammation in Balb/c mice, a representative IMID model. Results: The MPA@Dex-MPA NPs exhibited high MPA loading efficiency, low albumin binding rates, and sustained MPA release, resulting in improved pharmacokinetics in vivo . Compared to free MPA, MPA@Dex-MPA NPs induced more robust therapeutic effects on IMIDs. Mechanistic studies indicated that MPA@Dex-MPA NPs were primarily distributed in dendritic cells (DCs) and significantly suppressed the overactivated DCs in vivo and in vitro . Furthermore, the recovered DCs rehabilitated the IL-23/Th17 axis function and significantly ameliorated imiquimod-induced psoriasis-like skin inflammation. Importantly, MPA@Dex-MPA NPs showed favorable safety and biocompatibility in vivo . Conclusion: Our results indicated the polysaccharide mycophenolate-based NPs to be highly promising for IMID treatment.
研究领域:
药学
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免疫学
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纳米技术
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炎症研究
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产品关联
DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
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2020
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IF 4.831
Zili Lei,Yanhong Yang,Shaomin Liu,Yuting Lei,Lanxiang Yang,Xueying Zhang,Wanwan Liu,Huijuan Wu,Changyuan Yang,Jiao Guo
In the present study, the effects of dihydroartemisinin (DHA) on inflammatory bowel diseases (IBD) mice model induced by dextran sulfate sodium (DSS) were determined. Hematoxylin and eosin staining was used to assess the intestines of mice treated with DSS and DHA. The expression of inflammatory factors and cell junction-associated genes was measured using reverse transcription-quantitative PCR (RT-qPCR) and Western blot. The effects of DSS and DHA on the gut microbiome were measured using 16S recombinant (r) DNA gene analysis. DHA could improve the diarrhea and bloody stool induced by DSS, and decrease the serum levels of TNF-α, IL-1β and IL-23 of the DSS group. DHA could notably reduce the infiltration of the inflammatory cells and significantly decrease the expression of TNF-α and IL-1β in the intestines of the DSS treated mice. The expression of cell junction-associated genes such as EpCAM and Claudins, were down-regulated in the DSS group, and DHA could recover the expression of these cell junction-associated genes. The 16S rDNA gene analysis demonstrated that Bacteroidetes and Verrucomicrobia decreased, while Firmicutes and Proteobacteria increased in the DSS group, and DHA could recover the abundance of these gut bacteria altered by DSS. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that DHA could partly recover the pathways altered by DSS. DHA could obviously ameliorate the symptoms of IBD induced by DSS by regulation of the expression of inflammation and cell junction-associated genes and gut microbiota, suggesting its potential for the treatment of IBD.
研究领域:
药理学
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免疫学
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胃肠病学
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微生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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