BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
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2021
·Vol. 85
·期 8
·1809-1817
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IF 2.043
Li Qiang,Zhai Chunmiao,Wang Guodong,Zhou Jia,Li Weiguang,Xie Liquan,Shi Zhanli
Ginsenoside Rh1 (Rh1) has anti-inflammatory effects in asthma mice, but the underlying mechanism remains unclear. BALB/c mice were sensitized and challenged with ovalbumin (OVA) to construct asthma model. Mice received Rh1 or tiotropium bromide 0.5 h before OVA challenge. Airway morphology and airway remodeling were assessed by HE staining and Masson's trichrome staining, respectively. Th1/Th2 cytokines in serum or broncho alveolar lavage fluid (BALF) were measured by ELISA kits. Rh1 significantly alleviated the lung resistance and airway resistance, and reduced the number of total inflammation cells, eosinophils, neutrophils, and lymphocytes in BALF of the asthmatic mice. The morphological changes and collagen deposition of airway were also reduced by Rh1 in asthmatic mice. The increase of Eotaxin, IL-4, IL-5, IL-13, and IL-33 and the decrease of IL-12 and IFN-γ in both BALF and serum of OVA exposed mice were reversed by Rh1. Rh1 attenuates OVA-induced asthma in the mice model by regulating Th1/Th2 cytokines balance.
研究领域:
免疫学
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药理学
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呼吸病学
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DOI
PubMed
高影响因子
CELL BIOLOGY INTERNATIONAL
·
2017
·Vol. 41
·期 6
·611-621
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IF 1.831
Yaojie Niu,Qiumei Dong,Rongheng Li
To investigate the efficacy and mechanisms of matrine, a component derived from Sophora flavescens in treatment of rheumatoid arthritis (RA), a rat model of RA was established. Compared to control rats, matrine significantly mitigated inflammation and severity of RA (paw volume and articular index (AI) score). Using either mice splenic T cells stimulated with PMA/ionomycin or rat splenic T cells, the levels of Th1 and Th2 responses were determined by flow cytometry, quantitative RT-PCR, and ELISA. Furthermore, the levels of NF-κBp65 (RelA), IκBα, and phosphor-IκBα in T cells were determined by Western blot. Our study found that matrine modulated the imbalance of Th1 and Th2 cytokine responses in rats with RA by reducing the levels of Th1 cytokines (IFN-γ, TNF-α, IL-1β), but increasing Th2 cytokine (IL-4 and IL-10) through attenuating the NF-κB signaling in T cells, suggesting matrine as a promising drug for intervention of RA.
研究领域:
免疫学
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药理学
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风湿病学
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DOI
PubMed
高影响因子
MEDICAL SCIENCE MONITOR
·
2020
·
IF 1.918
Wenlan Wang,Xiaoming Luo,Qin Zhang,Xujun He,Zhifang Zhang,Xinxin Wang
Background Bifidobacteria are among the probiotics used in treating intestinal diseases and are rarely used for allergic asthma treatment. The present study investigated the mechanism of B. infantis in treating allergic asthma in mice. Material/Methods A total of 40 male Balb/c mice were randomized into control, ovalbumin (OVA), montelukast (Mon), and B. infantis (B10) groups, and allergic asthma was induced in the OVA, Mon, and B10 groups. Airway reactivity was measured on day 29 by methacholine at various doses. The numbers of total cells and inflammatory cells in bronchoalveolar lavage fluid (BALF) were counted by blood cell counter and Diff-Quik staining. Hematoxylin-eosin (HE) staining was performed to observe inflammatory cell infiltration in lung tissues. Total IgE and OVA-specific IgE in serum were measured by ELISA. Mucin 5AC expression was detected by Western blot to evaluate airway obstruction. The levels of Th1 (IFN-γ, IL-2) and Th2 (IL-4, IL-5, IL-13) cytokines in BALF and tissues were detected by ELISA and qRT-PCR, respectively. Results The mice in the OVA group had airway hyperreactivity, while the symptoms in the B10 group and Mon group were effectively relieved. B10 reduced the number of inflammatory cells in BALF as well as inflammatory cell infiltration in tissues. Moreover, the levels of total serum IgE, OVA-specific IgE, and Mucin 5AC were increased in the OVA group, but were reduced in the Mon group and B10 group. B. infantis increased the levels of Th1 cytokines and decreased those of Th2 cytokines. Conclusions B. infantis can reduce the infiltration of inflammatory cells induced by OVA-specific antibodies in mice. B. infantis has therapeutic effects on allergic asthma by promoting Th1 and inhibiting Th2 immune responses.
研究领域:
免疫学
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微生物学
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肺科学
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过敏
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL TOXICOLOGY
·
2020
·Vol. 35
·期 9
·982-990
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IF 3.118
Liyang Yao,Yizhou Tang,Bolu Chen,Wuding Hong,Xinyue Xu,Yang Liu,Zoraida P. Aguilar,Hengyi Xu
In this work, we aimed to evaluate the adverse effects and the mechanism of intestinal barrier caused by titanium dioxide nanoparticles (TiO 2 NPs). Here, the effects of two different dosages (300 and 1200 mg/kg) of TiO 2 NPs on female mice (n = 5) were investigated. After 28-day oral exposure, the results of Ti content were significantly increased in the ileum in comparison with the control. The histopathological structure index of the ileum was significantly changed after TiO 2 NPs exposure; villi height and crypt depth were decreased and increased, respectively. Meanwhile, TiO 2 NPs treatment also significantly altered the transcription levels of genes. First, the GATA-3 and STAT-4 were upregulation and downregulation, respectively. Second, gene expressions of the Zonula Occludens-1, claudin ( CLDN ) -12 , occludin, and myosin light chain kinase were significantly upregulated, while the CLDN-3 was decreased. Finally, the caspase-3 , caspase-9 , and caspase-12 were upregulated. The results of TUNEL staining indicated apoptosis in the ileum. In general, TiO 2 NPs treatment significantly changed the intestine physical barrier in a dose-dependent manner. The toxicity of TiO 2 NPs could be through the imbalance in the Th1/Th2.
研究领域:
毒理学
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免疫学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Journal of Thoracic Disease
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2018
·
IF 1.804
Xiaoxia Lu,Huicong Fu,Feng Han,Yurong Fang,Jiali Xu,Liqiong Zhang,Qing Du
Background Urban particulate matter (PM) contributes to the increasing number of people with asthma, which is closely related to the development of industrialization. Especially, PM with an aerodynamic diameter of <2.5 µm (PM2.5) enhances the risk of damaging respiratory organs. It has reported that PM2.5-induced pathological changes could be considered as a remarkable molecular mechanism of PM2.5-mediated cytotoxicity in respiratory disease and even lung cancer. Methods In this study, we have investigated the effects of PM2.5 on ovalbumin (OVA)-induced asthma mice and the therapeutic effect of Lipoxin A4 (LXA 4 ) on improving the poor pathology. Results The exposure of PM2.5 showed that both cytokines of T helper-2 (Th2) cells and transcription factors of group 2 innate lymphoid cells (ILC2s) were significantly increased, and inflammatory cell infiltration occurred in lung tissue. The LXA 4 was used to treat asthma, which was an effective option in reducing inflammatory cytokines and relieving pathological symptoms, probably by regulating the Th1/Th2 balance. Conclusions These results suggest that PM2.5-induced inflammation plays a key role in the progression of asthma mice. In addition, LXA 4 has a significant therapeutic effect on asthma, which indicates the direction for the treatment of asthma related inflammatory diseases.
研究领域:
免疫学
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呼吸病学
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环境健康
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DOI
PubMed
高影响因子
INFLAMMATION
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2019
·Vol. 42
·期 4
·1179-1189
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IF 2.939
Xue Yu-Long,Zhang Sheng-Xiao,Zheng Chao-Feng,Li Yu-Feng,Zhang Li-Hui,Hao Yu-Fei,Wang Shu,Li Xue-Wen
Signal transducer and activator of transcription 4 (STAT4) has been implicated in the progression of myocarditis. The aim of the current study was to investigate the role by which STAT4 influences autoimmune myocarditis in an attempt to identify a theoretical therapeutic perspective for the condition. After successful establishment of an autoimmune myocarditis rat model, the expression patterns of STAT4, NF-κB pathway–related genes, Th1 inflammatory cytokines (IFN-γ and IL-2), and Th2 inflammatory cytokines (IL-6 and IL-10) were subsequently determined. The rats with autoimmune myocarditis were treated with oe-STAT4 or sh-STAT4 lentiviral vectors to evaluate the role of STAT4 in autoimmune myocarditis, or administrated with 1 mL 10 μmol/L of BAY11-7082 (the NF-κB pathway inhibitor) via tail vein to investigate the effect of the NF-κB pathway on autoimmune myocarditis. Finally, cell apoptosis was evaluated. The serum levels of IFN-γ and IL-2, extent of IκBα and P65 phosphorylation, and the expression of STAT4 were elevated, while the serum levels of IL-6 and IL-10 as well as the expression of IκBα were reduced among the rats with autoimmune myocarditis, which was accompanied by an increase in the apoptotic cells. More importantly, the silencing of STAT4 or the inhibition of the NF-κB pathway was detected to result in a decrease in the serum levels of IFN-γ and IL-2 and an elevation of the serum levels of IL-6 and IL-10, and inhibited myocardial cell apoptosis in rats with autoimmune myocarditis. Moreover, STAT4 silencing was also observed to decrease the extent of IκBα and P65 phosphorylation while acting to elevate the expression of IκBα. Taken together, silencing of STAT4 could hinder the progression of autoimmune myocarditis by balancing the expression of Th1/Th2 inflammatory cytokines via the NF-κB pathway, which may provide a novel target for experimental autoimmune myocarditis (EAM) treatment.
研究领域:
免疫学
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心脏病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
·
2021
·
IF 2.73
Jinhui Dong,Ou Xu,Jianxing Wang,Chunguang Shan,Xiumin Ren
Objective Luteolin has an anti-allergic effect but its mechanism is not clear. This study attempted to determine the mechanisms of luteolin in rhinitis.Methods Allergic rhinitis rat model was established by ovalbumin (OVA) stimulation. Then, the rats were treated with normal saline, luteolin, or lipopolysaccharide (LPS) for 14 days. Nasal symptoms were scored; the histopathological changes of nasal mucosa were detected by hematoxylin–eosin staining. Serum levels of Th1 type cytokines (IFN-γ, IL-2), Th2 type cytokines (IL-4, IL-5, IL-13), and OVA-specific IgE (sIgE) were determined by ELISA. The expressions of Toll-like receptor 4 (TLR4) and p65 in nasal mucosa were detected by Western blot or immunohistochemistry.Results Luteolin decreased symptom scores, specifically, the scores in control group, model group, model + 0.1 mg/kg luteolin, model + 1 mg/kg luteolin, and model + 10 mg/kg luteolin groups were 0.63 ± 0.52, 7.88 ± 0.83, 1.38 ± 0.52, 2.75 ± 0.46, and 5.00 ± 0.53, respectively. Luteolin ameliorated nasal mucosa inflammation by promoting the down-regulated levels of Th1 type cytokines, and suppressing the up-regulated levels of Th2 type cytokines, OVE-sIgE, TLR4, and p65. LPS further increased symptom scores, aggravated nasal mucosa inflammation, improved the unbalance of Th1/Th2 type cytokines, and lowered the expressions of OVE-sIgE, TLR4, and p65. Moreover, LPS reversed the effect of luteolin on allergic rhinitis rats.Conclusion Luteolin ameliorated inflammation and Th1/Th2 imbalance via regulating the TLR4/NF-κB pathway in allergic rhinitis rats. This study provided novel evidence that luteolin could be used as a candidate drug in allergic rhinitis treatment.
研究领域:
免疫学
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药理学
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过敏
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Xueru Wang,Waseem Ali,Kanglei Zhang,Yonggang Ma,Hui Zou,Xishuai Tong,Jiaqiao Zhu,Ruilong Song,Hongyan Zhao,Zongping Liu,Wenxuan Dong
Cadmium (Cd) has adverse effects on organisms. Serine is an essential nutritional factor and its nutritional value is extremely high for body. To explore the effects of serine on spleen toxicity induced by Cd in mice, cadmium chloride (CdCl 2 , 50 mg/L) and serine (50 g/L) were individually administered or co-administrated in drinking water of mice for 18 weeks. Results demonstrated that Cd exposure induced splenic toxicity and serine against the toxicity damage caused by Cd in mice. Under Cd stress, trace element homeostasis was disturbed, the mice's body weight and spleen index were increased, and splenic morphology and ultrastructure were altered. Furthermore, Cd exposure led to the cell populations disorder, which in turn triggers cell death. Notably, Cd treatment induced oxidative stress and inflammation, increased M1/M2 (iNOS, CD68) and Th1/Th2 (T-bet, CD4) levels, decreased M1/M2 (Arg1) and Th1/Th2 (GATA3) levels, while disrupted the macrophages and lymphocytes homeostasis, which trigged apoptosis and pyroptosis in spleen. In contrast, serine supplementation changed the levels of Cd and other elements, weakened Cd-induced tissue damage and inflammation, enhanced antioxidant capacity, significantly restored cell homeostasis, and effectively inhibited Cd-induced apoptosis and pyroptosis in the spleen. Shortly, the results verified that serine had an ameliorating toxicity effect and restored the M1/M2 and Th1/Th2 balance, restrained apoptosis and pyroptosis induced by Cd.
研究领域:
毒理学
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免疫学
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营养科学
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产品关联
DOI
PubMed
高影响因子
Food Frontiers
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2024
·
IF 7.4
Ying Yang,Mengfan Luo,Wanyi Zhou,Wenyang Tao,Jingrui Li,Jianrong Xing,Quanqin Tan,Yuxing Guo
In recent years, the development of immunosuppression has become common, and probiotics are a vital immunomodulatory strategy. This study evaluated the alleviating effect of Lactiplantibacillus plantarum ( L. plantarum ) YY-112 on cyclophosphamide-induced immune imbalance and resolved the possible mechanism of action. L. plantarum YY-112 at 10 9 CFU/mL lowered loss of body weight and alleviated splenic injury, intestinal injury, and inflammation, according to the hematoxylin and eosin staining. Biochemical results showed that 10 9 CFU/mL L. plantarum YY-112 increased interleukin-10 and immunoglobulin M levels and decreased interferon-γ levels. Additionally, the immunoregulatory effect at the molecular levels of L. plantarum YY-112 was analyzed by transcriptome sequencing. L. plantarum YY-112 significantly upregulated Cr2 and downregulated C5aR1 to regulate the complement system; downregulated S100a8 , S100a9 , and Mmp9 to inhibit neutrophil aggregation; upregulated Cd19 , Cd72 , Cd3e , Cd28 , Cd80 , Cd8a , and histocompatibility-2-related genes to regulate B- and T-cell activation; and upregulated Xiap , Malt1 , Ikbkb , Mapk11 , Mef2c , Mapk12 , Ras , and Myc to activate immune signaling pathways. Furthermore, L. plantarum YY-112 improved intestinal microbial structure and reduced enrichment of Lachnospiraceae_NK4A136_group , norank_f_Lachnospiraceae , Desulfovibrio , Colidextribacter , and Helicobacter . In conclusion, these findings offer valuable insights into the potential mechanisms through which L. plantarum YY-112 regulates immune imbalance.
研究领域:
免疫学
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微生物学
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分子生物学
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药理学
✓ 已验证
产品关联
DOI
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2025
·Vol. 26
·期 17
·8678
·
IF 4.9
Yamin Zhang,Jiajia Lin,Xiaomei Xu,Xuehua Lu,Lisha Li,Yuezhen Yang,Wenjin Lin
This study aimed to compare the therapeutic effects of fresh (CMF) and dried (CMD) Centipeda minima against allergic rhinitis (AR), elucidate their underlying molecular mechanisms, and identify the bioactive compounds responsible for their immunomodulatory actions. An ovalbumin-induced AR mouse model was treated with CMF or CMD extracts, followed by evaluation of nasal symptoms, serum biomarkers (IgE, histamine, cytokines), and nasal mucosa histopathology. Transcriptomics and widely targeted metabolomics were integrated with network pharmacology to identify differentially expressed genes and bioactive components, which were further validated in RAW264.7 and RBL-2H3 cells. CMF and CMD exhibited distinct anti-AR mechanisms: CMF predominantly suppressed Th2 responses (reducing IgE, IL-6, and histamine while elevating IL-10), whereas CMD enhanced Th1 activity (increasing IFN-γ). Metabolomic analysis revealed CMF was rich in amino acids while CMD contained higher flavonoids, with neocnidilide and 6-gingerol identified as key bioactive compounds that modulated TNF-α, IL-6, and IL-10 via NF-κB and JAK-STAT pathways. These findings demonstrate that CMF and CMD exert complementary anti-inflammatory effects through Th2 inhibition and Th1 activation, respectively, providing a molecular basis for the traditional use of Centipeda minima and highlighting its bioactive compounds as potential therapeutics for inflammatory diseases.
研究领域:
药理学
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免疫学
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民族药理学
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分子生物学
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植物学
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生物医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Molecular Medicine Reports
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2018
·Vol. 18
·期 1
·622-626
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IF 1.922
Qin Zhu,Peifen Zheng,Jianying Zhou,Xinyu Chen,Yuliang Feng,Weifeng Wang,Feng Zhou,Qiaona He
Ulcerative colitis (UC) is a chronic, idiopathic, inflammatory bowel disease of the colon. T cell responses have been associated with the pathology of UC. Andrographis paniculata (AP) extract has been previously reported as an effective treatment of UC. The present study aimed to explore the effects of andrographolide, the primary active component of AP, on the T cell responses of patients with UC. Peripheral blood mononuclear cells (PBMCs) were isolated from patients with UC and treated with various concentrations of andrographolide (0, 10, 20 and 30 µg/ml). Andrographolide decreased interferon γ, interleukin (IL)‑23 and IL‑17A, however it increased IL‑4 in a dose‑dependent manner, as indicated by ELISA assay. Andrographolide treatment resulted in a decreased percentage of T helper (Th)1 and Th17 cells and an increased proportion of Th2 cells, as demonstrated by flow cytometry analysis. T‑bet (a Th1‑specific transcription factor) and RAR‑related orphan receptor γt (key transcription factor of Th17 cells) expression was decreased, but GATA‑3 (Th2 lineage‑specific transcription factor) expression was increased following andrographolide treatment as indicated by western blot analysis. These results demonstrated the inhibitory effects on Th1/Th17 responses and the promoting effects on Th2 responses of andrographolide. Experiments on IL‑23‑treated PBMCs from healthy donors revealed similar effects of andrographolide on Th1/Th2/Th17 responses. In summary, these results suggest that andrographolide may be an effective candidate for the treatment of IL‑23‑mediated diseases.
研究领域:
免疫学
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药理学
·
炎症性肠病
✓ 已验证
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2024
·
IF 4.8
Meng-Ke Liu,Juan-Juan Tang,Hao Li,Xu-Yang Chen,Jun-Ling Cai,Gui-Ying Lin,Kan-Yao Chen,Zhi-Peng Liu,Xiao-Fang Ji,Zhong-Jin Yang,Zi Li
Artemisitene (ATT), an artemisinin (ART) analog retaining the endoperoxide moiety and incorporating an additional α, β-unsaturated carbonyl structure, exhibits enhanced biological activities. However, its therapeutic effects on liver fibrosis remain unclear. In this study, we demonstrated that ATT significantly alleviated liver inflammation and fibrosis induced by carbon tetrachloride (CCL 4 ) in mice. ATT treatment markedly reduced the count of neutrophils in the liver, as well as macrophages in both the liver and spleen. Additionally, the frequencies of Th2 and Th17 cells were significantly lowered, while Th1 cells frequency and the Th1/Th2 index were notably increased. The frequency of ILC2 cells, correlated with ST2 and IL-33 expression levels, was also significantly lowered. Consistently, ATT inhibited NLRP3 inflammasome activation, which was positively associated with AST and ALT levels, and with the count of Neutrophils, macrophages, and ILC2 cells, but negatively correlated with Th1frequeny. Furthermore, liver fibrosis severity showed a significant positive correlation with neutrophil and Th17 cell counts in the liver, and a negative correlation with Th1 cell count and the Th1/Th2 index. Therefore, ATT alleviated CCL 4 -induced mice liver fibrosis through NLRP3 inflammasome inhibition and immunomodulation.
研究领域:
药理学
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免疫学
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肝病学
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）