Frontiers in Pharmacology
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2025
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IF 4.8
Qian Feng,Cai-Zhi Li,Yi-Hua Zou,Xue-Yu Wang,Xia Yang,Rong Zhang*,Zhong-Qiu Liu*,Rong-Rong Zhang
Introduction: Brain metastasis (BM) is the most common and serious complication of breast cancer (BC). There is significant interest in investigating the crosstalk between BC cells and immune cells. β-elemene is the main pharmacodynamic component of Curcumae Rhizoma, a traditional Chinese medicine that is commonly used for the clinical treatment and prevention of various tumors. However, the specific underlying mechanism of β-elemene in BC-BM is still unclear.Methods: An intracardiac (ICT) injection model was used to establish specific BC-BM cells, then an intracarotid (ICD) injection model was used to verify the inhibitory effect of β-elemene in BC-BM. Tumor-cell-conditioned media, a primary microglia co-culture model, and an in vitro recruitment experiment were used to explore crosstalk between BC cells and immune cells. TMT-based quantitative proteomic, ELISA, IF, and other molecular biotechnologies were used to investigate the mechanisms.Results: The BC-BM cells established in our study not only increased BM rates but also exhibit mesenchymal phenotype and activated the JAK–STAT signaling pathway. Microglia, particularly M2 microglia, were enriched in BM lesions and secreted high levels of both IL6 and CCL2. Hypersecretory IL6 reversed the MET process of BC cells by regulating the JAK2/STAT3 signaling pathway to promote colonization in the brain. Increased levels of CCL2 significantly recruited monocytic myeloid-derived suppressor cells (M-MDSCs) to induce an immunosuppressive brain microenvironment. β-elemene could significantly inhibit BC-BM in mice by regulating the IL6/STAT3 signaling pathway and suppressing the M-MDSC recruitment.Conclusion: Our work first demonstrated that β-elemene regulated the IL6/STAT3 axis and M-MDSC recruitment to reconstruct immunosuppressive brain microenvironment to suppress BC-BM.
研究领域:
肿瘤学
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免疫学
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药理学
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DOI
PubMed
高影响因子
INFLAMMATION RESEARCH
·
2014
·Vol. 63
·期 7
·597-608
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IF 2.143
Pan Xiaolong,Cao Xiang,Li Na,Xu Yimiao,Wu Qiuyue,Bai Jing,Yin Zhimin,Luo Lan,Lan Lei
Objective Forsythin (FOR) is an active ingredient extracted from the fruit of the medicinal plant Forsythia suspensa (Thunb.) Vahl. Here, we investigated the effect of FOR on LPS-induced inflammatory response and the underlying molecular mechanisms in RAW264.7 macrophages. Materials and methods RAW264.7 cells were pre-treated with or without FOR and then stimulated with or without LPS. The productions of TNF-α, IL-1β, IL-6, PGE 2 and NO were determined by ELISA and nitrite analysis, respectively. The expressions of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were measured by Western blotting and RT-PCR analysis. The activations of signaling molecules were detected by Western blotting using phosphorylation specific antibodies. Reactive oxygen species (ROS) production was determined by ROS assay. Results LPS-induced productions of IL-1β, IL-6, TNF-α, NO and PGE 2 were inhibited by FOR in a dose-dependent manner. FOR also suppressed the LPS-elevated expressions of iNOS and COX-2. Further investigations revealed that FOR significantly inhibited the LPS-induced activations of JAK-STATs and p38 MAPKs, but not of IKKα/β in LPS-stimulated RAW264.7 cells. Additionally, FOR interfered with both JAK-STATs and p38 MAPKs signaling pathways to modulate the expressions of IL-1β, IL-6, TNF-α, iNOS and COX-2. Furthermore, FOR reduced the LPS-induced ROS accumulation, validating that FOR serves as an antioxidant. Conclusions Our data suggested that FOR exerts anti-inflammatory action, at least in part, via suppressing LPS-induced activation of JAK-STATs and p38 MAPKs signalings and production of ROS in macrophage cells.
研究领域:
药理学
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免疫学
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细胞生物学
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分子生物学
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DOI
PubMed
高影响因子
Acta Pharmaceutica Sinica B
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2023
·
IF 14.5
Peng Hua,Ruifeng Liang,Yanbei Tu,Yuying Yin,Man-Kay Law,Meiwan Chen
Normalizing inflamed soils including reactive oxygen species (ROS), nitric oxide (NO), cell-free DNA, and regulating inflammation-related seeds such as macrophages, neutrophils, fibroblasts, represent a promising strategy to maintain synovial tissue homeostasis for rheumatoid arthritis (RA) treatment. Herein, ROS scavenging amphiphilic block copolymer PEGylated bilirubin and NO-scavenging PEGylated o-phenylenediamine were fabricated to self-assemble into a dually responsive nanoparticle loaded with JAK inhibitor notopterol ( [email protected] /oPDA-PEG, NBOP NPs). The simultaneous ROS and NO depletion combined with JAK-STAT pathway inhibition could not only promote M2 polarization to reduce further ROS and NO generation, but also decrease cytokines and chemokines to prevent immune cell recruitment. Specifically, NBOP NPs responded to high level ROS and NO, and disintegrated to release notopterol in inflamed joints as the hydrophobic heads BR and oPDA were transformed into hydrophilic ones. The released notopterol could inhibit the JAK-STAT pathway of inflammatory cells to reduce the secretion of pro-inflammatory cytokines and chemokines. This strategy represented an effective way to regulate RA soils and seeds through breaking the positive feedback loop of inflammation aggravation, achieving an excellent anti-RA efficacy in a collagen-induced arthritis rat model. Taken together, our work offered a reference to adjust RA soils and seeds for enhanced RA treatment.
研究领域:
纳米技术
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药理学
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风湿病学
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炎症生物学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2024
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IF 4.8
Jia-Wei Wu,Wei Gao,Li-Ping Shen,Yong-Lin Chen,Shi-Qing Du,Zhi-Yong Du,Xu-Dong Zhao,Xiao-Jie Lu
ABSTRACT Ethnopharmacological relevance Leonurus japonicus Houtt. (Labiatae), commonly known as Chinese motherwort, is a herbaceous flowering plant that is native to Asia. It is widely acknowledged in traditional medicine for its diuretic, hypoglycemic, antiepileptic properties and neuroprotection. Currently, Leonurus japonicus (Leo) is included in the Pharmacopoeia of the People's Republic of China. Traditional Chinese Medicine (TCM) recognizes Leo for its myriad pharmacological attributes, but its efficacy against ICH-induced neuronal apoptosis is unclear. Aims of the study This study aimed to identify the potential targets and regulatory mechanisms of Leo in alleviating neuronal apoptosis after ICH. Materials and methods The study employed network pharmacology, UPLC-Q-TOF-MS technique,molecular docking, pharmacodynamic studies, western blotting, and immunofluorescence techniques to explore its potential mechanisms. Results Leo was found to assist hematoma absorption, thus improving the neurological outlook in an ICH mouse model. Importantly, molecular docking highlighted JAK as Leo's potential therapeutic target in ICH scenarios. Further experimental evidence demonstrated that Leo adjusts JAK1 and STAT1 phosphorylation, curbing Bax while augmenting Bcl-2 expression. Conclusion Leo showcases potential in mitigating neuronal apoptosis post-ICH, predominantly via the JAK/STAT mechanism.
研究领域:
药理学
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神经科学
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传统中药
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分子生物学
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DOI
PubMed
高影响因子
PHYTOMEDICINE
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2023
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IF 7.9
Jiong Wang,Chenchen Qian,Yue Chen,Tianyang Jin,Yongsheng Jiang,Lijiang Huang,Xinyan Fu,Dong Yang,Leiming Jin,Bo Jin,Yi Wang
ABSTRACT Background Hyperglycemic induced cardiac hypertrophy and cardiac inflammation are important pathological processes in diabetic cardiomyopathy. β-elemene (Ele) is a natural compound extracted from Curcuma Rhizoma and has anti-tumor effects. It also has therapeutic effects in some inflammatory diseases. However, the therapeutic effect of Ele on diabetic cardiomyopathy is not clear. The purpose of this study was to evaluate the effect of Ele on hyperglycemia-caused cardiac remodeling and heart failure. Methods C57BL/6 mice were intraperitoneally injected with streptozotocin to induce DCM, and Ele was administered intragastric after 8 weeks to investigate the effect of Ele. RNA sequencing of cardiac tissue was performed to investigate the mechanism. Results Ele markedly inhibited cardiac inflammation, fibrosis and hypertrophy in diabetic mice, as well as in high glucose-induced H9c2 cells. RNA sequencing showed that cardioprotective effect of Ele involved the JAK/STAT3-NF-κB signaling pathway. Ele alleviated heart and cardiomyocyte inflammation in mice by blocking diabetes-induced JAK2 and STAT3 phosphorylation and NF-κB activation. Conclusions The study found that Ele preserved the hearts of diabetic mice by inhibiting JAK/STAT3 and NF-κB mediated inflammatory responses, suggesting that Ele is an effective therapy for DCM.
研究领域:
药理学
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心脏病学
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糖尿病
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DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2025
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IF 6.1
Jiaxiang Zhang,Haitao Ma,Yongjie Yang,Liyin Liu,Dasheng Luo,Defu Yu,Tao Chen
Excessive intake of essential and toxic metals affects the pathological process of osteoporosis. At present, the effects of single forms of iron (Fe), lead (Pb) and other metals on bone injury have been widely studied. However, these metal elements usually do not exist in the environment in a separate form. They are ingested in various ways and are often found together in the human body. However, the mechanism of bone damage caused by Fe and Pb mixed exposure is still unclear at this stage. At present, the combined analysis of multi-omics is the conventional method to explore the molecular mechanism behind the disease. Therefore, we attempted to combine proteomics and metabolomics to explain the mechanism of bone damage caused by mixed Fe and Pb exposure. Differential proteins and metabolites were found to be predominantly enriched in the JAK-STAT signalling pathway, inflammatory bowel disease (IBD), and osteoclast differentiation. Combined analysis showed that Fpr2, Lifr, Lisofylline, 7-Ketocholesterol, LacCer (d18: 1/14:0) and other substances may be involved in the process of bone injury mediated by mixed metal exposure. In summary, we hypothesise that mixed exposure to Fe and Pb leads to osteoclast activation via the JAK-STAT signalling pathway in situ and indirectly via the gut-bone axis, resulting in bone damage. In general, our study potentially suggests that bone injury induced by mixed exposure of Fe and Pb may be related to osteoclast proliferation mediated by changes in inflammatory levels in vivo .
研究领域:
分子生物学
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毒理学
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骨代谢研究
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
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2026
·Vol. 40
·期 1
·e70661
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IF 2.8
Li Yao,Xin-ze Qiu,Jun Zou,Jing-rong Liang,Meng-bin Qin,Jin-xiu Zhang,Peng Peng,Jie-an Huang
Metabolic dysfunction-associated steatotic liver disease (MASLD) has become a leading cause of chronic liver disease with no available therapies. Currently, the pathogenesis of MASLD remains to be further elucidated. Ferroptosis and ferroptosis-related genes may play a vital role in the development of MASLD. Thus, this study investigated the role of heme oxygenase-1 (HMOX1/HO-1) in ferroptosis associated with MASLD. Here, we applied bioinformatics to identify ferroptosis-related genes. HMOX1 expression was validated by immunohistochemistry. Mice fed a methionine-choline-deficient diet for 8 weeks were treated with hemin, followed by biochemical and histological analyses. HL7702 cells were transfected to overexpress HMOX1, exposed to oleic acid, and treated with erastin or AZD1480. Iron, ROS, lipid peroxidation, and mitochondrial damage were assessed by ELISA, flow cytometry, and electron microscopy. Western blotting explored molecular mechanisms. HMOX1 was identified as a ferroptosis-related hub gene in MASLD datasets and was decreased in patient liver tissues. MCD-fed mice developed hepatic steatosis with elevated ALT, AST, TG, LDL, Fe²⁺, MDA, and ROS, along with reduced HMOX1 and GSH. Hemin ameliorated MASLD and inhibited ferroptosis. Cell experiments showed JAK/STAT pathway activation in MASLD. HMOX1 upregulation reduced lipid peroxidation, inhibited ferroptosis, and downregulated JAK/STAT, whereas erastin reversed these effects. AZD1480 reversed the effects of erastin and improved MASLD. Collectively, our results suggest that HMOX1 protects against MASLD by suppressing ferroptosis through JAK/STAT pathway inhibition.
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DOI
PubMed
高影响因子
ACS Omega
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2023
·
IF 4.1
Zhihai Wu,Zhiqiang Luo,Wen Sun,Yuanyuan Shi,Qi Ding
Allergic asthma is a prevalent form of asthma that is characterized primarily by airway inflammation. Jiegeng decoction (JGT) is a traditional Chinese herbal formula known for its anti-inflammatory properties and has been used to treat respiratory diseases for centuries. This study aimed to investigate the biological effects and mechanisms of action of JGT in improving allergic asthma. An experimental allergic asthma mouse model was established using ovalbumin. The results showed that JGT significantly improved inflammation cell infiltration in the lung tissue of allergic asthmatic mice and the inflammatory environment of Th2 cells in the bronchoalveolar lavage fluid while also reducing serum IgE levels. Subsequently, 38 components of JGT were identified through liquid chromatography–mass spectrometry. Network pharmacology revealed that regulating inflammation and immune responses is the primary biological process by which JGT improves allergic asthma, with Th2 cell differentiation and the JAK-STAT signaling pathway being the key mechanisms of action. Finally, qPCR, flow cytometry, and Western blotting were used to validate that JGT inhibited Th2 cell differentiation by blocking the JAK1-STAT6 signaling pathway in CD4+ T cells, ultimately improving allergic asthma. This study provides a novel perspective on the therapeutic potential of JGT in the treatment of allergic asthma.
研究领域:
药理学
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免疫学
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中医
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分子生物学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2026
·
IF 6.8
Fuyu Xiong,Yuxin Bai,Shifei Wu,Yulu Wang,Xinjie Dai,Yang Yang,Jiyu Gong,Gaole Zhang,Tianzhu Zhang
Ethnopharmacological relevance Yupingfeng San (YPFS), a classic tonic formula in Traditional Chinese Medicine (TCM), has been extensively applied clinically for centuries. Originating from Jiuyuan Fang , its earliest extant record is Danxi Xinfa . YPFS is composed of Huangqi ( Astragalus membranaceus Bunge), Baizhu ( Atractylodes rubra Dekker), and Fangfeng ( Saposhnikovia divaricata (Turcz.) Schischk). Due to its traditional efficacy of " replenishing qi and consolidating the exterior," YPFS is commonly prescribed for allergic rhinitis, nephrotic syndrome, and chronic nephritis. Recent studies have confirmed that YPFS protects renal function and alleviates renal fibrosis in mice with diabetic nephropathy, while simultaneously improving lung function and reducing pulmonary fibrosis in bleomycin-induced rats. Taken together, these results suggest YPFS possesses substantial potential for mitigating organ fibrosis. Purpose This study investigated the renoprotective efficacy and underlying mechanism of YPFS extract in a cisplatin-induced mouse model of renal interstitial fibrosis. Using an integrated in vivo and in vitro approach, we sought to validate the therapeutic potential of this traditional formula against chemotherapy-induced nephrotoxicity. Methods The chemical components of YPFS extract were analyzed using UPLC-Q-TOF -MS. For the in vivo study, male BALB/c mice received YPFS extract (1, 1.95, or 3 g/kg) by oral administration once daily for 7 days after a single injection of cisplatin (20 mg/kg, i.p.). Renal function was assessed by measuring serum creatinine, plasma BUN, fasting blood glucose, and the urine protein-to-creatinine ratio. Kidney tissues were examined using H&E and Masson's trichrome staining for histopathological analysis, and the expression of fibrosis markers (α-SMA, collagen I, fibronectin) was measured by immunohistochemistry and western blotting. For the in vitro study, MPC-5 podocytes were treated with high glucose (25 mM) for 48 h to induce injury, and then intervened with YPFS extract at concentrations of 20, 40, or 80 μg/mL, along with JAK2 inhibitor AG490 and STAT3 agonist Colivelin for mechanism verification. Cell viability was measured by MTT assay, apoptosis was assessed by Hoechst 33342 staining, the expression of α-SMA was measured by cellular immunofluorescence, and mitochondrial morphology was observed using MitoTracker Red staining and TEM. Mitochondrial function was evaluated by Na + /K + -ATPase and Complex I activities, and oxidative stress levels were determined by T-SOD, GSH, and MDA assays. RNA-seq was conducted to identify DEGs in MPC-5 cells, and Western blotting was used to verify key protein expression in both cells and tissues. Results UPLC-Q-TOF-MS analysis identified 57 compounds in YPFS extract, predominantly flavonoids (40.35%) and saponins (21.05%). In cisplatin-treated mice, the extract dose-dependently reduced serum creatinine, blood urea nitrogen, Urine protein-to-creatinine ratio, and fasting blood glucose. It also decreased collagen deposition and α-SMA overexpression in kidney tissues. In MPC-5 cells, the extract restored cell viability, reduced apoptosis and α-SMA overexpression, improved mitochondrial membrane potential and redox balance, and restored mitochondrial fusion-fission balance by increasing Mfn1/2 and decreasing Drp1 expression. Transcriptomic analysis revealed that the extract reversed the high glucose-induced activation of gene pathways related to IL-6/JAK/STAT3 signaling, oxidative phosphorylation, and apoptosis, with findings confirmed at the protein level. Mechanistic investigations using the JAK2 inhibitor AG490 and STAT3 agonist Colivelin confirmed that the cytoprotective and anti-fibrotic effects of YPFS were primarily dependent on the IL-6/JAK/STAT3 signaling pathway. Conclusion YPFS extract ameliorates cisplatin-induced renal interstitial fibrosis by suppressing IL-6/JAK/STAT3 signaling and restoring mitochondrial homeostasis. These findings provide a pharmacological basis for the traditional use of this formula and highlight its potential as an adjunct therapy for reducing chemotherapy-related kidney injury.
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DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2026
·
IF 6.7
Donglei Zheng,Xiaojuan Xin,Hui Ouyang,Lulu Ma,Hao Wang,Xin Liu,Xiangxin Liao,Xinzi Chu,Ying Gao,Jiaying Huo,Shugang Li
Ovotransferrin (OVT) is a functionally active protein demonstrated to alleviate ulcerative colitis (UC), although its mechanism remains incompletely understood. Notably, UC is closely associated with dysbiosis of the gut microbiota. This study investigates the potential of OVT to alleviate colitis by reshaped gut microbiota composition in a DSS-induced UC mouse model. Specifically, Ligilactobacillus murinus (L. murinus) was isolated from the gut microbiota of OVT-treated UC mice and stimulated by OVT in vitro. Integrated whole-genome sequencing and targeted metabolomics revealed that L. murinus encodes bile salt hydrolase, thereby driving secondary bile acid biosynthesis. Mechanistically, fermentation products (FP) derived from coculture of L. murinus with bile exerts potent anti-inflammatory in both Caco-2 cells and a colitis model by Ptgs2 (COX-2) downregulation and the JAK-STAT signaling pathway inhibition. These results established the “OVT-L. murinus-bile acids-Ptgs2/JAK-STAT” axis as a novel mechanism for UC treatment, providing a foundation for high-value applications of OVT in functional foods.
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DOI
PubMed
高影响因子
PLoS Genetics
·
2021
·Vol. 17
·期 7
·e1009649
·
IF 5.917
Kun Wu,Yiming Tang,Qiaoqiao Zhang,Zhangpeng Zhuo,Xiao Sheng,Jingping Huang,Jie’er Ye,Xiaorong Li,Zhiming Liu,Haiyang Chen
The differentiation efficiency of adult stem cells undergoes a significant decline in aged animals, which is closely related to the decline in organ function and age-associated diseases. However, the underlying mechanisms that ultimately lead to this observed decline of the differentiation efficiency of stem cells remain largely unclear. This study investigated Drosophila midguts and identified an obvious upregulation of caudal ( cad ), which encodes a homeobox transcription factor. This factor is traditionally known as a central regulator of embryonic anterior-posterior body axis patterning. This study reports that depletion of cad in intestinal stem/progenitor cells promotes quiescent intestinal stem cells (ISCs) to become activate and produce enterocytes in the midgut under normal gut homeostasis conditions. However, overexpression of cad results in the failure of ISC differentiation and intestinal epithelial regeneration after injury. Moreover, this study suggests that cad prevents intestinal stem/progenitor cell differentiation by modulating the Janus kinase/signal transducers and activators of the transcription pathway and Sox21a-GATAe signaling cascade. Importantly, the reduction of cad expression in intestinal stem/progenitor cells restrained age-associated gut hyperplasia in Drosophila . This study identified a function of the homeobox gene cad in the modulation of adult stem cell differentiation and suggested a potential gene target for the treatment of age-related diseases induced by age-related stem cell dysfunction.
Adult stem cells undergo an aging-related decline of differentiation efficiency in aged animals. However, the underlying mechanisms that ultimately lead to this observed decline of differentiation efficiency in stem cells still remain largely unclear. By using the Drosophila midgut as a model system, this study identified the homeobox family transcription factor gene caudal ( cad ), the expression of which is significantly upregulated in intestinal stem cells (ISCs) and progenitor cells of aged Drosophila . Depletion of cad promoted quiescent ISCs to become activate and produce enterocytes (ECs) in midguts under normal gut homeostasis conditions; However, overexpression of cad resulted in the failure of ISC differentiation and intestinal epithelial regeneration after injury. Moreover, cad prevents ISC-to-EC differentiation by inhibiting JAK/STAT signaling, and the expressions of Sox21a and GATAe . Reduction of cad expression in intestinal stem/progenitor cells restrained age-associated gut hyperplasia in Drosophila . These findings enable a detailed understanding of the roles of homeobox genes in the modulation of adult stem cell aging in humans. This will be beneficial for the treatment of age-associated diseases that are caused by a functional decline of stem cells.
研究领域:
发育生物学
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干细胞生物学
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衰老研究
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分子遗传学
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DOI
PubMed
高影响因子
ENVIRONMENTAL RESEARCH
·
2026
·
IF 8.2
Jiawei Yang,Qiong Zhang,Haichen Zhang,Tao Zhou,Lening Chen,Qianqian Xiao,Qinghe Meng,Jianjun Jiang,Weidong Hao,Xuetao Wei
Bis(2-ethylhexyl) tetrabromophthalate (TBPH), an emerging brominated flame retardant, has raised environmental concern due to its endocrine-disrupting potential. While epidemiological evidence and our previous animal studies have linked TBPH to thyroid disruption, the molecular mechanisms remain unclear. This study aimed to identify potential molecular targets and downstream pathways involved in TBPH-induced effects on thyroid. We found that TBPH (100 nM) significantly upregulated the expression of key thyroid hormone synthesis markers PAX-8, TPO, and TG in human thyroid follicular cells (Nthy-ori 3-1). In silico docking identified S1PR3 as a potential interactor with moderate predicted affinity, and cellular thermal shift assay (CETSA) provided initial evidence of target engagement. S1 pr 3 knockdown partially attenuated TBPH-induced marker upregulation. Mechanistically, TBPH increased interleukin-10 (IL-10) in an S1PR3-dependent manner, coupled with activation of a non-canonical JAK-STAT pathway (JAK3, TYK2, STAT2, and STAT5). Further, overexpression of Il-10 enhanced downstream effector expression, whereas overexpression of Jak3 similarly promoted PAX-8 and TPO levels; conversely, Tyk2 knockdown reduced these markers, supporting a functional role for this alternative signaling cascade. Importantly, key elements of this pathway were recapitulated in thyroid tissues of TBPH-treated rats, providing in vivo corroboration for the cellular observations. Collectively, our results suggest a S1PR3/IL-10/non-canonical JAK-STAT axis as a candidate mechanism for TBPH-induced thyroid marker upregulation, providing a hypothesis-generating framework for future toxicological investigations of TBPH and related emerging brominated flame retardants.
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高影响因子
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