JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Yanjie Bai,Shuai Cheng,Hongwei Gao,Yaxin Yang,Haojia He,Zhibiao Tian,Yonghua Ji,Hongjie Wang,Zhiyong Tan,You Zhou
Ethnopharmacology relevance Fuyuan Huoxue Decoction (FYHX), originally documented in Yixue Faming , is traditional Chinese medicine used to promote blood circulation, remove blood stasis, and soothe liver meridians. It is mainly prescribed for traumatic injuries and blood stasis-related syndromes. In modern clinical practice, FYHX has been widely applied in the treatment of soft tissue injuries, neuropathic pain, and chondritis. However, its bioactive constituents and the multi-target mechanisms underlying its analgesic effects remain largely unclear. Aim of the study This study aimed to evaluate the analgesic effects of FYHX, identify its active small-molecule constituents, and elucidate the molecular mechanisms involved using a CFA-induced pain model. Materials and methods CFA was injected into the hind paw of rats. Pain behaviors were examined using von-Frey filaments and the Hargreaves’ test. High-performance liquid chromatography-mass spectrometry (HPLC-MS) was used to identify the circulating bioactive components and metabolites of FYHX. Network pharmacology, quantitative transcriptomics and molecular docking were integrated to explore potential mechanisms in the dorsal root ganglia (DRG) and spinal cord. Key molecular targets were validated using Quantitative Real-time PCR (qPCR) and Western blotting. Results FYHX significantly alleviated CFA-induced mechanical and thermal pain behaviors. A total of 42 molecules and metabolites were identified as the circulating components of FYHX. Integrated analysis revealed that FYHX primarily modulates the chemokine signaling pathway in the DRG and the IL-17 signaling pathway in the spinal cord. Validation experiments confirmed that downregulation of critical molecules in these pathways was associated with the analgesic of FYHX. Furthermore, four compounds—Scutellarein, 3,4′-Dibydroxyflavone, 5,6,7-Trimethoxyflavone and Armillarisin A—were shown to significantly reduce pain behaviors in the CFA model. Conclusion FYHX effectively alleviates CFA-induced chronic pain, potentially through the suppression of chemokine and IL-17 signaling pathways in the DRG and spinal cord, respectively. The identified bioactive compounds may contribute to its analgesic effects. Overall, FYHX and its active ingredients might be further developed to be new analgesic treatment for chronic pain.
研究领域:
民族药理学
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疼痛研究
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中医中药
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分子药理学
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神经炎症
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DOI
PubMed
高影响因子
IMMUNITY
·
2023
·
IF 32.4
Qiong Luo,Yijun Liu,Ke Shi,Xuecheng Shen,Yaqi Yang,Xuejiao Liang,Liangliang Lu,Wenxuan Qiao,Airu Chen,Dongmei Hong,Yang Sun,Qiang Xu
Anti-interleukin-17 (IL-17) therapy has been used in various autoimmune diseases. However, the efficacy is unexpectedly limited in several IL-17-associated diseases, and the mechanism of limited efficacy remains unclear. Here, we show that a molecular complex containing the adaptor molecule Act1 and tyrosine phosphatase SHP2 mediated autonomous IL-17R signaling that accelerated and sustained inflammation. SHP2, aberrantly augmented in various autoimmune diseases, was induced by IL-17A itself in astrocytes and keratinocytes, sustaining chemokine production even upon anti-IL-17 therapies. Mechanistically, SHP2 directly interacted with and dephosphorylated Act1, which replaced Act1-TRAF5 complexes and induced IL-17-independent activation of IL-17R signaling. Genetic or pharmacologic inactivation of SHP2, or blocking Act1-SHP2 interaction, paralyzed both IL-17-induced and IL-17-independent signaling and attenuated primary or relapsing experimental autoimmune encephalomyelitis. Therefore, Act1-SHP2 complexes mediate an alternative pathway for autonomous activation of IL-17R signaling, targeting which could be a therapeutic option for IL-17-related diseases in addition to current antibody therapies.
研究领域:
免疫学
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分子生物学
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自身免疫疾病
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药理学
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DOI
PubMed
高影响因子
Scientific Reports
·
2026
·
IF 4.9
Niu Jiale,Liu Guangxia,He Guangyao,Zhang Xiaomeng,Bai Huihui,Lu Yamin
To investigate the role of IL-17 in macrophage M1 polarization within a type 2 diabetic (T2DM) milieu and to evaluate the therapeutic potential of its neutralizing antibody. PMA-differentiated THP-1 macrophages were polarized to M1 state. Under high glucose, cells were treated with IL-17 and an IL-17 neutralizing antibody. Inflammatory cytokines (IL-1β, IL-6, TNF-α) were measured; mRNA levels of TNF-α, HIF-1α, and NLRP3 were assessed by qPCR; and protein expression related to the NF-κB, mTOR/HIF-1α axis and pyroptosis (NLRP3, Caspase-1, GSDMD) was analyzed by Western Blot. High glucose and IL-17 synergistically promoted M1 polarization, enhancing proinflammatory cytokine secretion. This was associated with activation of the NF-κB, mTOR/HIF-1α signaling axis and induction of pyroptosis, evidenced by NLRP3 inflammasome assembly, Caspase-1 activation, and GSDMD cleavage. The IL-17 neutralizing antibody effectively suppressed these pathological processes. IL-17 acts as a key immunological amplifier in diabetes, driving M1 polarization, oxidative stress, and pyroptosis via the NF-κB, mTOR/HIF-1α axis and NLRP3 inflammasome. Treatment with an αIL-17 effectively reversed the aberrant activation of the aforementioned cellular phenotypes and signaling pathways, partially restoring macrophage functional balance. This finding provides preliminary experimental support for further exploration of IL-17-targeted immunomodulatory strategies to ameliorate diabetes-associated metabolic inflammation.
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PubMed
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Zhongyuan Qu,Huimin Li,Fajing Qiang,Kaili Liu,Shuang Wu,Jianli Li,Xiang Zou
Background Breast cancer-related depression (BCRD) is one of the severest comorbidities, affecting the quality of life and the treatment efficacy in BC patients. Chaihu-Shugan-San (CSS), a traditional Chinese medicine presents a potential therapeutic method in BCRD. Purpose The main purpose of the research was to investigate the effects of CSS on BCRD in a mouse model and to elucidate its mechanisms, particularly its impact on microglial polarization through the IL-17/ NF-κB pathway. Methods A mouse BCRD model was constructed and treated with CSS. Behavioral testing, biochemical parameters, H&E staining, and small animal imaging were used to assess the depressive-like behaviors and tumor growth in mice. RNA sequencing analysis was performed, and the data were authenticated by Western blot as well as quantitative qRT-PCR to explore the mechanisms of CSS treatment in BCRD. The BV2 microglia were stimulated with LPS in vitro and intervened by IL-17 protein, IL-17 antagonist, IMD-0354, and CSS. In addition, western blot was utilized to confirm the expression of IL-17/ NF-κB pathway-related factors. Molecular docking technique and UPLC-Q-TOF/MS were used to find out the key active components of CSS. Results CSS treatment significantly improved depression-like behaviors and retarded tumor growth in mice. Through RNA sequencing analysis, it was indicated that the improvement of BCRD by CSS was highly associated with the regulation of the IL-17/ NF-κB pathway. Western blot and qRT-PCR outcomes suggested that CSS inhibited the IL-17/ NF-κB pathway, facilitating the transformation from pro-inflammatory M1 microglial phenotype to anti-inflammatory M2 phenotype, contributing to the reduction of neuroinflammation. In vitro experiments demonstrated that CSS modulated the immune reaction through the induction of phenotypic transformation of microglia from M1 toward M2 phenotype, hence reducing neuroinflammation. Notably, this therapeutic effect of CSS was highly similar to the effects of IL-17 antagonists, thus suggesting that CSS alleviates the symptoms of BCRD by targeting IL-17. Molecular docking revealed that the major bioactive compounds in CSS were Saikosaponin A, Saikosaponin C, and Saikosaponin D. Conclusion This study systematically demonstrates that CSS ameliorates BCRD by suppressing the IL-17/ NF-κB pathway as well as modulating microglial polarization and elucidates the dual function of IL-17. These results point to a new multi-target intervention strategy for BCRD treatment and fully reflect the holistic effects of CSS by its multi-component as well as multi-target actions.
研究领域:
药理学
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神经科学
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肿瘤学
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免疫学
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中医中药
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Science Advances
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2026
·Vol. 12
·期 20
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IF 13.9
Xuhong Yang,Hui Yang,Nuo Xu,Yini Zhu,Zhengcheng Yun,Haoge Zhang,Jia Miao,Yinzhuo Xie,Lin Gao,Leqian Ying,Lei Dong,Yuqi Wang,Yicheng Ni,Jinbing Xie
Immune checkpoint inhibitors show promise in the treatment of melanoma brain metastases but are limited by CD73/adenosine axis-mediated immune evasion. Directly targeting CD73 with antibodies faces challenges due to poor blood-brain barrier permeability and metabolic regulators within the tumor microenvironment (IL-17-driven HIF-1α/VEGF-A). To overcome these barriers, we developed a nose-to-brain delivery platform using glycerol as a mucosal penetration enhancer to codeliver anti–IL-17 and anti-CD73 antibodies. Glycerol reversibly opened nasal epithelial tight junction proteins, enhancing the brain delivery of anti–IL-17 and anti-CD73 antibodies by 19.4- and 17.1-fold, respectively, while minimizing systemic exposure. Critically, anti–IL-17 attenuated CD73/adenosine axis-mediated immune evasion, significantly boosting anti-CD73 targeting efficacy. Ultimately, this combination promoted CD8 + T cell activation and residency, pro-inflammatory macrophage polarization, and reduced T reg cell infiltration, thereby eliciting a strong antitumor effect. Our results establish an efficient nose-to-brain delivery platform for macromolecules and propose a therapeutic strategy for tumors using anti–IL-17 to overcome TME-imposed limitations in CD73-targeted immunotherapy.
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2026
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IF 5.6
Ruo-Xuan Li,Rui-Ze Wang,Jia-Yu Tian,Zi-Hao Wang,Xiao-Nan Ye,Li-Li Huang,Yan-Yan Wang
Depression is a prevalent and severe mental disorder. Recently, the “Gut-Brain Axis” theory has offered a novel perspective on its pathophysiological mechanisms. As a major bioactive constituent isolated from Rhodiola rosea L., Salidroside (SAL) possesses well-documented anti-stress, antioxidant, and neuroprotective activities. Based on the gut-brain axis hypothesis, the present work evaluated whether SAL exerts antidepressant-like actions in a murine model of chronic unpredictable mild stress (CUMS) and further clarified its potential molecular mechanisms. During the establishment of the CUMS model, mice received intragastric SAL at doses of 25 mg·kg −1 and 50 mg·kg −1 daily for 4 weeks. Behavioral experiments evaluated anxiety and depressive-like behaviors, while gastrointestinal function changes were monitored. Results indicated that SAL significantly alleviated depressive-like behaviors, restored gastrointestinal function and structure, increased serotonin expression in the gut-brain axis, and repaired hippocampal neural damage. RNA sequencing of hippocampal tissue suggested that SAL inhibited abnormal IL-17 signaling pathway activation. Western blot analysis confirmed that SAL reduced IL-17 levels in hippocampal tissue and inhibited excessive phosphorylation of downstream p-MAPK and p-NF-κB. Additionally, SAL intervention restored the disrupted intestinal flora in depressed mice. Spearman correlation analysis showed that changes in bacterial genera such as Rikenella , Oscillibacter , and Barnesiella might be crucial in SAL's regulation of the gut-brain axis and its antidepressant effects. In summary, this study documented the ameliorative effects of SAL on depressive-like behaviors in CUMS model mice, as well as its impact on the gut-brain axis and the IL-17 signaling pathway. These observations may serve as a reference for future research on SAL as a functional food ingredient.
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Lisha Song,Jiaqing Shen,Huiying Wu,Yi Liu
Background Psoriasis is a chronic inflammatory disease often accompanied by metabolic syndrome. The function of AKR1B10 in the “metabolism-immune” interplay remains unclear. This study aimed to identify the role of AKR1B10 in pathogenesis and evaluate its inhibitor, Epalrestat, for psoriasis treatment via drug repurposing. Methods Integrating GEO transcriptomic data, we screened for key metabolic signature genes. An imiquimod (IMQ)-induced murine psoriasis model was established to evaluate the efficacy and safety of intragastric and topical epalrestat, as assessed by PASI scores, histopathology, spleen index and body weight monitoring. Furthermore, RNA sequencing, functional enrichment analysis, protein–protein interaction analysis, immunofluorescence and RT-qPCR were performed to explore the underlying mechanisms. Results AKR1B10 was identified as a key differentially expressed gene positively correlating with activated DCs, neutrophils and Th17 cells (AUC = 0.970). In vivo, Epalrestat significantly ameliorated skin lesions, reduced PASI scores, and exhibited a safety profile superior to methotrexate(MTX). Mechanistically, Epalrestat treatment upregulated retinol metabolism while markedly suppressing the IL-17 signaling pathway. Conclusions Epalrestat alleviates skin inflammation by inhibiting AKR1B10 activity, thereby restoring retinol homeostasis. The subsequent suppression of the IL-17 signaling axis is more likely a downstream consequence of improved metabolic status and a remodeled inflammatory microenvironment, rather than a direct effect. These findings support Epalrestat as a potential therapeutic agent for psoriasis that concurrently modulates metabolic and inflammatory pathways.
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DOI
PubMed
高影响因子
PATHOLOGY RESEARCH AND PRACTICE
·
2026
·
IF 3.7
Wei Chen,Lin Xu,Meng Wang,Yan Li,Zhilin He,Pei Zhu
Background Dihydroartemisinin (DHA), a sesquiterpene lactone derived from artemisinin, exhibits well-documented anti-inflammatory and anti-cancer properties. However, the precise mechanisms through which DHA alleviates ulcerative colitis (UC) remain incompletely understood. Purpose This study aimed to investigate the effects and underlying mechanisms of DHA on dextran sulfate sodium (DSS)-induced colitis in mice using a multi-omics approach, including 16S rRNA microbiomics, non-targeted and targeted metabolomics, RNA-seq transcriptomics and network pharmacology analysis. Methods A DSS-induced murine colitis model was established and treated with DHA. Disease activity, colonic pathology, and intestinal barrier function were assessed. Gut microbiota composition was analyzed via 16S rRNA sequencing, while colonic metabolites were profiled using non-targeted metabolomics. Key signaling pathways associated with DHA treatment were predicted through RNA-seq and network pharmacology, and further validated by qRT-PCR and flow cytometry. Antibiotic depletion experiments were performed to evaluate the role of the gut microbiota. Intestinal barrier integrity was examined by immunofluorescence, western blot, and AB/PAS staining. Targeted metabolomic analysis of specific colonic metabolites was conducted using the Q300 kit. Results DHA treatment significantly ameliorated colitis symptoms, as indicated by reduced body weight loss, lower disease activity index (DAI) scores, attenuated colon shortening, and improved histopathology. DHA treatment correlated with restored intestinal barrier function including increased goblet cell numbers, enhanced mucin-2 expression, and upregulating tight junction proteins. It was also associated with mitigated gut microbiota dysbiosis, notably including restored abundance of Bifidobacterium and suppressed opportunistic pathogens. Non-targeted metabolomics revealed that DHA treatment was associated with significant changes in arachidonic acid metabolism. Integrated transcriptomics and network pharmacology analysis indicated that DHA treatment was correlated with suppression of the IL-17 signaling pathway and restoration of Th17/Treg balance in colonic tissues. Crucially, the therapeutic benefits of DHA were abolished in microbiota-depleted mice, manifested as loss of mucosal protection, absence of IL-17 pathway and Th17/Treg balance modulation, and no significant alteration in arachidonic acid levels as detected by targeted metabolomics. Conclusion Our findings highlight the multifaceted therapeutic potential of DHA in colitis treatment, and suggest that the gut microbiota is associated with its protective effects. The beneficial effects observed with DHA treatment are correlated with preservation of intestinal barrier integrity, restoration of microbial homeostasis, changes in arachidonic acid metabolism, and modulation of the IL-17 pathway and Th17/Treg balance. These insights provide promising directions for novel UC therapeutic strategies.
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DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
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2021
·
IF 13.273
Xinyu Jiang,Qing Yao,Xing Xia,Yingying Tang,Meng Sun,Yingtao Li,Hailun Zheng,Aimin Cai,Hailin Zhang,Vadivel Ganapathy,Ruijie Chen,Longfa Kou
Psoriasis is a chronic inflammatory skin disease with dysregulation of the immune system, which usually manifests as erythematous scleroma with hyperplasia of the epidermis. Although the pathogenesis remains unclear, oxidative stress and inflammation are inextricably linked during the development of psoriasis. Therefore, scavenging of ROS and suppression of inflammation may be a rational and effective strategy to ameliorate psoriasis and delay its further development. Here, a “Tanghulu”-like nanoplatform (BJN) is developed using the endogenous antioxidant bilirubin and a specific inhibitor (JPH203) of LAT1, an amino acid transporter involved in the activation of mTOR, for treatment of psoriasis by scavenging ROS and interfering with mTOR signaling, consequently blocking Th17 and IL-17 release. The nanoparticles show increased uptake in inflamed keratinocytes and display an efficient ROS scavenging capability. In an in vivo psoriasis model, BJN effectively permeate into the inflamed skin and be retained there, thereby reversing the psoriasis-specific changes in the imiquimod-induced mice as evident from suppression of keratinocyte hyperplasia and decrease in immune cell infiltration. This study shows that BJN can exert a superior anti-psoriasis effect by scavenging ROS, blocking the LAT1-mTOR pathway, inactivating immune reaction, restricting Th17 differentiation, and decreasing IL-17A secretion, offering a promising strategy for psoriasis treatment.
研究领域:
药学
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免疫学
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皮肤病学
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纳米技术
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分子生物学
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DOI
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
·
IF 5.4
Qinfeng Lu,Zhu Chen,Bai-Xiang Mu,Bo-Han Wang,Fanchao Feng,Jun Zhao,Hailang He,Yu Wei
Ethnopharmacological relevance COPD, marked by coughing, sputum production, and wheezing, is categorized as "Lung Distension" in Traditional Chinese Medicine (TCM). The combined use of Suzi Jiangqi Decoction and Sanzi Yangqin Decoction, known as Jia Wei Su Zi Jiang Qi Formula (JWSZJQF), is a common treatment for Lung Distension with phlegm accumulation in the lungs. It is particularly effective for symptoms like excessive phlegm and chest tightness. However, the specific active components of JWSZJQF and their molecular mechanisms in addressing mucus hypersecretion in COPD remain unclear, requiring further investigation and validation. Aim of the study This study aims to identify the potential targets and signaling pathways of JWSZJQF in treating COPD-associated mucus hypersecretion using UHPLC-Q-Orbitrap MS/MS, network pharmacology, and in vitro experimental verification. Materials and methods All plant names were verified through WorldFloraOnline ( www.worldFloraonline.org ) and MPNs ( http://mpns.kew.org ). First, the effective components of JWSZJQF were identified and analyzed using UHPLC-Q-Orbitrap MS/MS, supplemented by data from TCMSP. Network pharmacology analysis was used to determine the potential targets and pathways of JWSZJQF in COPD treatment. A mucus hypersecretion cell model was created using IL-17 cytokine, and the effectiveness of JWSZJQF in reducing mucus hypersecretion was assessed through immunofluorescence assay, Western blotting, and quantitative real-time polymerase chain reaction (qPCR). Lastly, a prospective study was conducted to collect data from 30 inpatients with AECOPD between September 2023 and July 2024. Serum samples before and after treatment were analyzed to validate the findings. Results A total of 864 active components were identified, with 79 potential COPD therapeutic targets confirmed based on the top 30 active components, including TNF, IL-6, and AKT1. The involved KEGG pathways included the IL-17 and NF-κB signaling pathways. In vitro experiments showed that JWSZJQF inhibited mucin (MUC5AC) secretion at both mRNA and protein levels. Additionally, JWSZJQF modulated i-κBα and p65 expression in the NF-κB pathway. Compared to the control group, patients treated with JWSZJQF exhibited lower levels of IL-17 and MUC5AC in their serum. Conclusion This study preliminarily explored the mechanisms of JWSZJQF in treating COPD-associated mucus hypersecretion through UHPLC-Q-Orbitrap MS/MS, network pharmacology, in vitro experiments, and clinical observation. The main active components and potential targets were identified, laying a scientific foundation for further research.
研究领域:
药理学
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民族药理学
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呼吸病学
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分子生物学
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网络药理学
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临床研究
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Shangping Xing,Xue Cheng,Shiyu Hou,Lidan Qin,Juan Wang,Yue Ding,Zhangyang Shen,Ziteng Dai,Xiaoming Huang,Yanying Liu,Dan Zhu
Novel therapeutic agents with improved safety and efficacy are urgently required for ulcerative colitis (UC), a refractory inflammatory bowel disease. Mangrove-derived natural products represent a promising reservoir for drug discovery. Monomethylsulochrin (MMSC) is a type II polyketide isolated from the endophytic fungus Aspergillus fumigatus of the mangrove plant Aegiceras corniculatum . However, its therapeutic effects on UC and the underlying mechanisms remain unclear. Herein, we evaluated the efficacy of MMSC by using a dextran sodium sulfate (DSS)-induced colitis mouse model and elucidated the underlying mechanisms by proteomics analyses, molecular biology techniques, and 16S rDNA gene sequencing. Our results demonstrated that MMSC significantly ameliorated DSS-induced colitis, as evidenced by reduced disease activity index, preserved colon length, and attenuated histopathological damage. Mechanistically, proteomics profiling and subsequent validation confirmed that MMSC concurrently suppressed the interleukin (IL)-17 and tumor necrosis factor (TNF) signaling pathways by downregulating key nodes (matrix metalloproteinase [MMP]-9, S100 calcium-binding protein A8 [S100a8], CCAAT/enhancer-binding protein beta [Cebpb], cAMP responsive element binding protein 1 [Creb1], and Fas) and related pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-17, TNF-α) in both colonic tissues and lipopolysaccharide (LPS)-stimulated NCM460 cells. Furthermore, MMSC restored gut microbial diversity and composition in mice with colitis, reversing DSS-induced dysbiosis. Spearman correlation analysis revealed that the IL-17/TNF pathway exhibited a notable correlation with MMSC-mediated restoration of the gut microbiota. In conclusion, MMSC alleviates UC through a dual mechanism integrating suppression of IL-17/TNF signaling and restoration of gut microbiota homeostasis, highlighting it as a promising candidate for developing novel therapies against UC.
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产品关联
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高影响因子
ACS Applied Nano Materials
·
2025
·
IF 5.5
Hao Sun,Hui Yuan,Jiangshan Hu,Jiayu Chen,Jie Han,Peiyuan Wang,Can-zhong Lu,Ting Hu,Yuhang Li
Psoriasis is a prevalent chronic inflammatory disorder affecting approximately 0.72% of the Chinese population. Currently, available treatments cannot completely cure this disease. The excessive production of reactive oxygen species (ROS) has been considered to be a key contributor to the progression of psoriasis. In this study, Ce and Mn were doped into mesoporous silicon nanomaterials with optimized ratios that could form uniform and well-dispersed CM@MSNs particles, which were able to effectively remove a wide range of ROS. As a result, treatment with CM@MSNs could reduce epidermal hyperplasia and prevent inflammatory reactions in the imiquimod (IMQ)-induced psoriasis-like model in mice. Mechanistically, CM@MSNs might prevent the inflammation by repressing the IL-17 and NF-κB signaling pathways and ameliorating epidermal hyperplasia through the activation of both canonical and noncanonical Wnt signaling pathways. In conclusion, this research could lead to a promising treatment method for psoriasis. This work provides an example of nanoenzymes for effectively scavenging ROS of diseases.
研究领域:
皮肤病学
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纳米医学
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免疫学
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产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）