INTERNATIONAL IMMUNOPHARMACOLOGY
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2017
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IF 2.956
Jia-Ying Zhang,Zheng Yang,Kun Fang,Zhan-Li Shi,Dan-Hong Ren,Jing Sun
Oleuropein (OLE) is a natural secoiridoid that is derived from Olea europaea . OLE possesses cardioprotective effects in experimental models of hypertension, myocardial infarction, atherosclerosis and hyperlipidaemia . In the present study, the effects of OLE on experimental autoimmune myocarditis (EAM) were evaluated. EAM in rats were induced by subcutaneous injections of porcine cardiac myosin . Cardiac function parameters, myocardial pathology, myocardial inflammatory cell infiltration and nuclear factor kappa-B (NF-κB) expression were measured. Our data showed that the postmyocarditis rats exhibited increased left ventricular end systolic diameters, left ventricular end diastolic diameters, left ventricular end-diastolic pressures (LVEDP), and decreased ejection fractions . However, OLE significantly suppressed these changes in EAM rats. Histological analysis revealed that myosin induced miliary foci of discolouration on endocardial surfaces and extensive myocardial injuries with inflammatory cell infiltration were significantly improved by OLE therapy. A definitive positive correlation between the histological scores and LVEDP was observed. Moreover, OLE inhibited CD4 + , CD8 + cells and macrophage infiltration in myocardium and decreased the serum production of tumour necrosis factor-a (TNF-a), interleukin-1β (IL-1β) and IL-6 in EAM rats. Expectedly, the myocardial levels of NF-κB p65, p-IκBa, IKKa were significantly attenuated by OLE, indicating the inhibitory effects of OLE on the NF-κB pathway. Furthermore, OLE decreased the myocardial expressions of phosphorylated-p38 MAPK , phosphorylated-ERK, and did not change the levels of p38 MAPK and ERK in EAM rats. Collectively, our results suggest that OLE effectively prevents the development of myocarditis , at least in part, by inhibiting the MAPKs and NF-κB mediated inflammatory responses.
研究领域:
药理学
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免疫学
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心脏病学
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DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
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2022
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IF 7.419
Yuanqiao Ma,Xiaoxiao Xu,Hang Wu,Changbo Li,Peijie Zhong,Zejin Liu,Chuang Ma,Wenhua Liu,Chenyu Wang,Yijie Zhang,Junpeng Wang
Ivermectin has been proposed as a potential anti-inflammatory drug in addition to its antiparasitic activity. Here we investigated the potential role of ivermectin in the pathogenesis of acute lung injury (ALI) using the lipopolysaccharide (LPS)- or bleomycin (BLM)-induced mice models. Male C57BL/6 mice were given ivermectin orally every day for the remainder of the experiment at doses of 1 or 2 mg/kg after 24 h of LPS or BLM treatment. Ivermectin reversed severe lung injury caused by LPS or BLM challenge, including mortality, changes in diffuse ground-glass and consolidation shadows on lung CT imaging, lung histopathological scores, lung wet/dry ratio, and protein content in the bronchoalveolar lavage fluid (BALF). Furthermore, ivermectin also reduced total lung BALF inflammatory cells, infiltrating neutrophils, myeloperoxidase activity, and plasma TNF-α and IL-6 levels in mice treated with LPS or BLM. Finally, the mechanism study showed that LPS or BLM administration increased JNK, Erk1/2, and p38 MAPK phosphorylation while decreasing IκBα expression, an inhibitor of NF-κB. However, ivermectin increased IκBα expression but blocked elevated phosphorylated JNK and p38 MAPK, not Erk1/2, in both ALI mice. These findings suggested that ivermectin may alleviate ALI caused by LPS or BLM in mice, partly via lowering the inflammatory response, which is mediated at least by the inhibition of MAPK and NF-κB signaling. Collectively, ivermectin might be used to treat acute lung injury/acute respiratory distress syndrome.
研究领域:
药理学
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免疫学
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呼吸病学
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DOI
PubMed
高影响因子
Human Cell
·
2025
·Vol. 39
·期 1
·20
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IF 3.1
Tian Tian,Luan Xiaona,Wang Lingzhi,Kong Yan,Huang Liying,Wang Yan
Ovarian cancer is one of the most lethal gynecologic malignancies contributing to cancer-related deaths among women. However, the mechanisms underlying its development remain poorly understood. This study aimed to investigate the role of STARD7 in tumorigenesis and its potential molecular mechanisms in ovarian cancer. Cell proliferation was assessed using the Cell Count Kit-8 and colony formation assays. The migration and invasion capabilities of ovarian cancer cells were evaluated through wound healing and Transwell invasion assays. A xenograft tumor model was established in nude mice to examine the role of STARD7 in tumor growth in vivo. The results demonstrated that the knockdown of STARD7 in A2780 and SK-OV-3 cells inhibited cell proliferation, invasion, and migration, while overexpression of STARD7 yielded opposing results. Furthermore, STARD7 was found to enhance the levels of phosphorylated p65 proteins and nuclear protein p65. Treatment with the NF-κB inhibitor PDTC inhibited STARD7 overexpression-induced cell proliferation, invasion, and migration. These results suggest that the activation of the NF-κB pathway is involved in STARD7-mediated ovarian cancer progression. Consistent with the in vitro findings, similar results were observed in in vivo ovarian cancer xenograft models. Additionally, dual luciferase reporter assays indicated that STARD7 was regulated by RUNX1-IT1, which acted as a sponge for miR-377-3p. Collectively, these findings suggest that STARD7 may serve as an independent prognostic indicator, promoting ovarian cancer development by activating the NF-κB pathway. This research expands the current understanding of NF-κB regulatory networks and positions STARD7 as a promising therapeutic target for developing pathway-specific interventions. Graphical abstract
研究领域:
肿瘤学
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分子生物学
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信号转导
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癌症研究
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DOI
PubMed
高影响因子
Evidence-based Complementary and Alternative Medicine
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2022
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IF 2.65
Ying-Ying Wu,Yi-Lin Huang,Bin Dai,Jian-Wei Liu,Xu Han
Background/Aim. Abnormal proliferation and migration of vascular smooth muscle cells is one of the main causes of atherosclerosis (AS). Therefore, the suppression of abnormal proliferation and migration of smooth muscle cells are the important means for the prevention and inhibition of AS. The clinical effects of Guanxinping (GXP) tablets and preliminary clinical research on the topic have proved that GXP can effectively treat coronary heart disease, but its underlying mechanism remains unclear. This study aimed to confirm the inhibitory effect of GXP on the abnormal proliferation of mouse aortic vascular smooth muscle (MOVAS) cells and to explore the underlying mechanism. Methods. MOVAS cells were divided into two major groups: physiological and pathological groups. In the physiological group, MOVAS cells were directly stimulated with GXP, whereas in the pathological group, the cells were stimulated by endothelin-1 (ET-1) before intervention by GXP. At the same time, atorvastatin calcium, which effectively inhibits the abnormal proliferation of MOVAS cells, was used in the negative control group. CCK8 assay, scratch test, ELISA, Western blotting, and immunofluorescence staining were performed to observe the proliferation and migration of MOVAS cells and the expression levels of related factors after drug intervention in each group. Results. In the physiological group, GXP had no significant effect on the proliferation and migration of MOVAS cells and the related factors. In the pathological group, a high dose of GXP reduced the abnormal proliferation and migration of MOVAS cells. Further, it reduced the expression levels of PI3K; inhibited the phosphorylation of Akt (protein kinase B); upregulated IκB-α levels; prevented nuclear factor kappa B (NF-κB) from entering the nucleus; downregulated the expression of interleukin 6 (IL6), IL-1β, and iNOS; and upregulated the ratio of apoptosis-related factor Bax/Bcl-2. There was no significant difference between the high-dose GXP group and the atorvastatin calcium group (negative control group). Conclusion. Our findings revealed that GXP was able to inhibit the proliferation and migration of MOVAS cells by regulating the PI3K/Akt/NF-κB pathway.
研究领域:
心脏病学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
Food & Function
·
2019
·Vol. 11
·期 1
·456-471
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IF 3.241
Manling Hu,Jing Yang,Linlin Qu,Xuqian Deng,Zhiguang Duan,Rongzhan Fu,Lihua Liang,Daidi Fan
Ginsenoside Rk1 is a substance derived from ginseng and exhibits various activities such as anti-diabetic, anti-inflammatory and anti-cancer effects; however, its anti-tumor effect and target signaling mechanism in lung adenocarcinoma are not well understood. Here, we show that Rk1, a natural drug product, can function as an antitumor modulator that induces apoptosis in lung adenocarcinoma cells by inhibiting NF-κB transcription and triggering cell cycle arrest. Mechanistically, Rk1 suppressed the proliferation and clonal formation of two lung adenocarcinoma cell lines (A549 and PC9) in vitro and caused G1 phase cell arrest. In the A549 xenograft model, Rk1 significantly inhibited tumor growth and had few toxic side effects on normal organs. Western blotting results showed that Rk1 increased the protein expression of Bax, cleaved caspase-3, -8, and -9, and PARP, decreased the expression of Bcl-2 and blocked the NF-κB signaling pathway. Furthermore, ginsenoside Rk1 also reduced the high expression of PD-L1 in lung adenocarcinoma cells by inhibiting NF-κB signaling. These data revealed a previously unreported antitumor mechanism of Rk1, providing new ideas and an experimental basis for further study of the mechanism of action of Rk1 in lung adenocarcinoma.
研究领域:
肿瘤学
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药理学
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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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2025
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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
Cell Communication and Signaling
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2025
·Vol. 24
·期 1
·6
·
IF 8.9
Yang Xinyi,Ning Tingting,Zhang Wanru,Hou Songyuan,Su Jiayi,Li Wenkun,Wu Jing
Background Gastric microbiota dysbiosis is closely linked to chronic inflammation and carcinogenesis. Fusobacterium nucleatum ( Fn ), an opportunistic gastrointestinal pathogen, is implicated in perturbing the immune system and form an inflammatory microenvironment that fuels the occurrence and progression of gastric cancer (GC). However, the underlying mechanisms remain elusive. We aimd to investigate the impacts of Fn on GC cells and the crosstalk between GC cells and mast cells (MCs). Methods Fn abundance and MC infiltration were assessed in clinical GC tissues. Cell-based functional experiments, including wound healing, transwell, and ELISA, were performed using conditioned medium-based co-culture systems to explore how Fn influenced GC cell migration and the crosstalk with MC. A murine lung metastasis model was employed to evaluate Fn -driven metastasis and the effects of metronidazole and Reparixin. Results We showed that Fn and MCs were enriched and positively correlated in clinical GC tissues compared to paracancerous tissues. Fn and MCs exhibited tumor-promoting properties by facilitating GC cell migration. Besides, Fn and GC cells can recruit MCs and facilitate its activation. This crosstalk between GC cells and MCs was further enhanced by Fn , thereby amplifying this positive feedback loop between them. The production of CXCL8 in response to Fn stimulation was a significant mediator. Suppression of CXCL8 in GC cells weakened Fn ’s promoting effects on GC cell migration, MC recruitment and activation. Similarly, knocking down CXCL8 in MCs reversed the Fn -induced feedback effect of MCs on the highly invasive phenotype of GC cells. Mechanistically, the exoprotein Gbp of Fn activated CypA-NF-κB pathway in both GC cells and MCs, leading to the upregulation of CXCL8 expression. In addition, the in vivo assays substantiated Fn ’s ability to enhance tumor progression by facilitating cell migration, upregulating CXCL8 expression, and inducing MC infiltration and activation. However, these effects were reversed by metronidazole, a highly Fn -susceptible antibiotic, and Reparixin. Conclusions In summary, this study suggests that Fn contributes to GC progression by promoting tumor cell migration, MCs recruitment and activation. Simultaneously, the enhanced CXCL8-mediated crosstalk between GC cells and MCs plays a vital role in the pro-cancer effect of Fn.
研究领域:
肿瘤学
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微生物组学
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免疫肿瘤学
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分子肿瘤学
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炎症与癌症
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信号转导
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产品关联
DOI
PubMed
高影响因子
Food Frontiers
·
2026
·Vol. 7
·期 1
·e70225
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IF 6.9
Qiaoyu Sun,Qingqing Zhou,Sitong Ge,Danli Wu,Ping Li,Qing Gu
Impairment of intestinal barrier function is intricately linked to intestinal inflammation. Emerging evidence highlights that tryptophan-derived metabolites from the intestinal microbiota play a crucial role in maintaining the homeostasis of intestinal barrier function. In this study, a Caco-2/HT29 co-culture model was applied to evaluate the effects of indole-3-acetic acid (IAA) on the intestinal barrier and explore its underlying mechanism of action. Results demonstrated that lipopolysaccharide (LPS) caused the transepithelial resistance to drop to 387.5 ± 30.41 Ω·cm 2 , while IAA was able to increase it to 542 ± 31.11 Ω·cm 2 . At the same time, it reduced the paracellular permeability and restored the FITC-Dextran 4 (FD-4) permeability to 108.01%. This phenomenon was accompanied by an upregulation in the expression of tight junction (TJ) proteins. Concurrently, after IAA intervention, aryl hydrocarbon receptor (AHR) pathway was activated, while nuclear factor kappa-B (NF-κB) pathway was significantly inhibited. Furthermore, IAA exerted an inhibitory effect on the LPS-triggered upregulation of inflammatory factors (TNF-α, IL-6, IL-8) in RAW264.7 cells. These findings provide novel insights into the enhancement of intestinal barrier function and the in vitro anti-inflammatory properties of gut microbiota-derived metabolites.
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高影响因子
Food Science & Nutrition
·
2026
·Vol. 14
·期 1
·e71438
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IF 3.8
Ziyue Wang,Jianxiong Hao,Junye Yin,Huan Rao,Xia Zhao,Lulu Yu,Dandan Zhao
Acute lung injury (ALI) is a life‐threatening condition characterized by acute inflammatory damage to the alveolar epithelium and capillary endothelium, triggered by various pathological factors. Our previous study demonstrated the anti‐inflammatory and anti‐oxidative effects of Lycium barbarum polysaccharide (LBP) and chlorogenic acid (CA) against lipopolysaccharides (LPS)‐induced inflammatory response of NR8383 cells, while the current study further investigated the alleviating effect of LBP and CA against ALI through in‐depth experiments. In vitro experiments identified potential targets ( CASP3 , KDR ) and related pathways, while in mice with ALI induced by 5 mg/kg LPS, CA‐LBP (CA:LBP = 1:7, L/M/H dose: 25/50/100 mg/kg) was administered for 14 consecutive days, which reversed weight loss, alleviated lung injury, suppressed MPO activity, reduced TNF‐α, IL‐1β, IL‐6 and MDA levels, enhanced SOD and GSH‐Px activities, and mitigated NF‐κB activation significantly. Data of molecular docking further confirmed that the CA‐LBP complex can exert alleviating effects through suppressing the NF‐κB signaling pathway. Taken together, the present work sheds light on the multi‐target regulatory mechanism of CA‐LBP against ALI. Lycium barbarum polysaccharide (LBP) and chlorogenic acid (CA) ameliorate LPS‐induced acute lung injury (ALI) through a multi‐target regulatory mechanism, which involves suppression of the NF‐κB signaling pathway.
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PubMed
高影响因子
Algal Research-Biomass Biofuels and Bioproducts
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2026
·
IF 5
Yunmei Yin,Pei Wang,Zhen Zhang,Hongxiang Zhao,Meicong Xiao,Ran Chen,Kun Li,Shiqi Zhou,Rongqing Zhang
Astaxanthin's anti-atherosclerotic targets/pathways identified via network pharmacology and cellular assays. • Astaxanthin alleviates endothelial injury via dual anti-inflammatory and antioxidant effects. • Astaxanthin acts through PPARγ/NF-κB axis, with GW9662 reversing its regulatory effect. Astaxanthin, a lipophilic carotenoid predominantly derived from microalgae such as Haematococcus pluvialis , exhibits potent anti-inflammatory and antioxidant properties. Despite previous reports of its anti-atherosclerotic effects, the underlying molecular mechanisms of astaxanthin remain unclear. This study aimed to elucidate the pharmacological mechanisms of astaxanthin in alleviating atherosclerosis progression via an integrated approach of network pharmacology, molecular docking, and in vitro experimental validation. Molecular docking revealed strong binding affinities between astaxanthin and core targets including TNF, IL-6, and PPARγ. In vitro experiments demonstrated that astaxanthin attenuated oxidative stress and suppressed the secretion of pro-inflammatory cytokines in oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs). Mechanistically, astaxanthin upregulated PPARγ expression and reduced the phosphorylation of p65 and IκBα, two key components of the NF-κB pathway. Co-treatment with the specific PPARγ antagonist GW9662 abrogated these protective effects, confirming a PPARγ-dependent regulatory mechanism. These findings indicate that astaxanthin exerts anti-atherosclerotic effects by modulating the PPARγ/NF-κB signaling axis, highlighting its potential as a functional food ingredient for cardiovascular protection.
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高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2026
·
IF 3.2
Lili Liu,Zhengyao Li,Xinlei Peng,Hongli Zhang,Yuying Yang,Jun Liu,Min Liu
TPs reduced oxidative stress in PFOA-exposed mice. • TPs reduced intestinal permeability and ERK/NF-κB pathway in the ileal tissue. • TPs reduced harmful bacteria and increased beneficial bacteria in PFOA-exposed mice. • TPs as a potential dietary intervention alleviate pollutant-induced enterotoxicity. Perfluorooctanoic acid (PFOA), a persistent environmental contaminant, has been found to induce intestinal damage. Dietary tea polyphenols (TPs) have been reported to alleviate gastrointestinal diseases, however, the underlying mechanism through which TPs alleviate PFOA-induced ileal barrier injury remains unclear. Here, the effects of TPs on oxidative stress, intestinal permeability, extracellular signal-regulated kinase (ERK)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway, and gut microbiota in mice were evaluated. The results showed that TPs alleviated oxidative stress by elevating the serum GSH and CAT activities, and reducing MDA levels. Moreover, TPs decreased intestinal permeability by reducing serum DAO and LPS levels, upregulating the expression of claudin-1 and occludin, and inhibiting the phosphorylation of ERK and NF-κB in the ileum. Additionally, 16S rRNA gene sequence analysis revealed that TPs reversed PFOA-induced gut dysbiosis by decreasing harmful bacteria of Desulfovibrio and Ileibacterium , and increasing beneficial bacteria of Lachnospiraceae_NK4A136_grou p and Ligilactobacillus . This study reveals positive effects of TPs as a potential dietary intervention against pollutant-induced enterotoxicity. Download: Download high-res image (250KB) Download: Download full-size image
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高影响因子
Frontiers in Immunology
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2026
·
IF 7
Jiquan Shen,Changjian Zhou,Xinggao Wang,Yuxuan Chen,Run Liu,Liang Hong,Weiping Ji,Bo Wang
BackgroundRheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by severe synovial inflammation, joint deformities, and progressive tissue destruction. Celastrol (Cel), a natural triterpenoid with anti-inflammatory and antioxidant activity, is a promising therapeutic candidate for RA; however, its application is limited by poor aqueous solubility, low bioavailability, and systemic toxicity.PurposeThis study aimed to develop folate-modified liposomes encapsulating Cel (FA-Cel-LPs) to improve its solubility, stability, and joint accumulation, and to evaluate their anti-inflammatory efficacy and associated molecular changes in LPS-activated RAW264.7 macrophages and collagen-induced arthritis (CIA) rats.MethodsFA-Cel-LPs were prepared by thin-film hydration followed by extrusion and characterized for particle size, morphology, polydispersity index (PDI), encapsulation efficiency (EE), and in vitro release behavior. In LPS-activated RAW264.7 cells, cellular uptake, intracellular ROS levels, NF-κB nuclear translocation, COX-2/iNOS expression, and cytokine secretion were evaluated. In CIA rats, therapeutic efficacy was assessed by paw swelling, arthritis scores, in vivo fluorescence imaging, MRI, histological analysis, and micro-CT-based bone parameters. Safety was evaluated using hemolysis, serum biochemical analysis, and organ histology.ResultsFA-Cel-LPs showed a mean particle size of 110.65 ± 1.24 nm, an EE of 84.67 ± 2.55%, a PDI of 0.230 ± 0.018, and a sustained release profile with pH-dependent differences in vitro. In RAW264.7 cells, folate-modified liposomes showed greater cellular uptake and were associated with reduced ROS levels, attenuated NF-κB activation, and decreased COX-2, iNOS, and pro-inflammatory cytokine expression, with low cytotoxicity. In CIA rats, in vivo imaging suggested greater accumulation of FA-Cel-LPs in inflamed joints. Compared with free Cel and Cel-LPs, FA-Cel-LPs more effectively reduced paw swelling and joint inflammation while attenuating bone erosion and preserving joint architecture. Serum ALT and AST levels in the FA-Cel-LPs group remained within physiological ranges and were significantly lower than those in the free Cel group. Organ histology showed no obvious treatment-related injury, suggesting acceptable preliminary safety.ConclusionFA-Cel-LPs improved the solubility, formulation stability, and apparent joint accumulation of Cel and enhanced its anti-inflammatory and bone-protective effects in experimental RA. These effects were associated with reduced ROS/NF-κB/COX-2-related inflammatory changes, suggesting FA-Cel-LPs may represent a promising liposomal strategy for RA.
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高影响因子
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