Pharmacological inhibition of TLR4/NF‐κB with TLR4‐IN‐C34 attenuated microcystin‐leucine arginine toxicity in bovine Sertoli cells

This study investigated the pharmacological inhibition of the toll‐like receptor 4 (TLR4) genes as a measure to attenuate microcystin‐LR (MC‐LR) reproductive toxicity. Bovine Sertoli cells were pretreated with TLR4‐IN‐C34 (C34) for 1 hour. Thereafter the pretreated and non‐pretreated Sertoli cells were cultured in medium containing 10% heat‐activated fetal bovine serum + 80 μg/L MC‐LR for 24 hours to assess the ability of TLR4‐IN‐C34 to attenuate the toxic effects of MC‐LR. The results showed that TLR4‐IN‐C34 inhibited MC‐LR‐induced mitochondria membrane damage, mitophagy and downregulation of blood‐testis barrier constituent proteins via TLR4/nuclear factor‐kappaB and mitochondria‐mediated apoptosis signaling pathway blockage. The downregulation of the mitochondria electron transport chain, energy production and DNA replication related genes (mt‐ND2, COX‐1, COX‐2, ACAT, mtTFA) and upregulation of inflammatory cytokines (interleukin [IL]‐6, tumor necrosis factor‐α, IL‐1β, interferon‐γ, IL‐4, IL‐10, IL‐13 and transforming growth factor β1) were modulated by TLR4‐IN‐C34. Taken together, we conclude that TLR4‐IN‐C34 inhibits MC‐LR‐related disruption of mitochondria membrane, mitophagy and downregulation of blood‐testis barrier proteins of the bovine Sertoli cell via cytochrome c release and TLR4 signaling blockage.     

Physiological Effects of a Novel Immune Stimulator Drug, (1,4)‐α‐d‐Glucan,in Rats

Abstract: The (1,4)‐α‐d ‐glucan (α‐d ‐glucan), derived from medicinal plant, Tinospora cordifolia, activates human lymphocytes with downstream synthesis of the pro‐ and anti‐inflammatory cytokines, in vitro. We investigated physiological and immunological effects of a low and a high dose of α‐d ‐glucan (0.5 and 10 mg/kg), in vivo, testing the hypothesis that intravenous administration of α‐d ‐glucan does not affect haemodynamic, respiratory, haematological, and immune responses in normal rats. Male rats (300–400 g) were anaesthetized, tracheostomized, and catheterized in one femoral artery and vein. The mean arterial blood pressure and heart rate were continuously recorded. The baselines for gas exchange, differential blood cell count, and plasma concentration of TNF‐α, IL‐1β, IL‐4, IL‐6, and IFN‐γ were determined. Rats were then randomly assigned to controls (n = 7), a low dose (0.5 mg/kg; n = 10), and a high dose (10 mg/kg; n = 7) of α‐d ‐glucan for a six 6 hr study period. Gas exchange, differential cell count, plasma concentration of TNF‐α, IL‐1β, IL‐4, IL‐6, and IFN‐γ, and mean arterial blood pressure values remained within physiological range. Intravenous administration of 10 mg/kg α‐d ‐glucan created tachycardia, associated with hyperventilation, and significant reductions in the blood haemoglobin and haematocrit concentrations. We suggest that these in vivo effects of α‐d ‐glucan should be considered for future clinical and/or experimental trials.     

Toxicity of cobalt–chromium nanoparticles released from a resurfacing hip implant and cobalt ions on primary human lymphocytes in vitro

Adverse tissue responses to prostheses wear particles and released ions are important contributors to hip implant failure. In implant‐related adverse reactions T‐lymphocytes play a prominent role in sustaining the chronic inflammatory response. To further understand the involvement of lymphocytes in metal‐on‐metal (MoM) implant failure, primary human lymphocytes were isolated and treated with cobalt–chromium (Co‐Cr) wear debris and Co ions, individually, and in combination, for 24, 48 and 120 h. There was a significant increase in cell number where debris was present, as measured by the Neutral Red assay. Interleukin‐6 (IL‐6), interferon‐γ (IFN‐γ) and tumour necrosis factor‐α (TNF‐α) secretion levels significantly decreased in the presence of metal particles, as measured by ELISA. Interleukin‐2 (IL‐2) secretion levels were significantly decreased by both debris and Co ions. Flow cytometry analysis showed that the metal nanoparticles induced a significant increase in apoptosis after 48‐h exposure. This investigation showed that prolonged exposure (120 h) to metal debris induces lymphocyte proliferation, suggesting that activation of resting lymphocytes may have occurred. Although cytokine production was affected mainly by metal debris, cobalt toxicity may also modulate IL‐2 secretion, and even Co ion concentrations below the MHRA guideline levels (7 ppb) may contribute to the impairment of immune regulation in vivo in patients with MoM implants. Copyright © 2015 John Wiley & Sons, Ltd.     

Long‐term exposure to high levels of decabrominated diphenyl ether inhibits CD4 T‐cell functions in C57Bl/6 mice

In recent years, the adverse health effects of decabrominated diphenyl ether (BDE‐209) have raised more concerns as a growing number of studies reported its persistence in the environment and abundance in the human population, especially in occupational environmental compartments and exposed personnel. This study applies our previous animal model simulating occupational exposure to BDE‐209 to investigate its potential adverse effects on CD4 T cells. Female C57Bl/6 mice were orally gavaged with BDE‐209 at a dose of 800 mg kg^?1 every 2 days for 10 months and the blood of each mouse was collected for analysis. Kinetic changes of the peripheral immune system were investigated from 1 to 5 months of exposure. The chronic effects on cytokine production, proliferation and the antigen‐specific responses of CD4 T cells were evaluated at 7, 9 and 10 months, respectively. The results have shown that impaired proliferation and cytokine (IFN‐γ, IL‐2 or TNF‐α) production of CD4 T cells were observed in BDE‐209‐exposed mice, accompanied by increased T regulatory cells in the blood. BDE‐209 exposure in vitro also suppressed the reactivity of CD4 T cells at concentrations of 0.01, 0.1, 1 and 10 μM. Furthermore, we observed weaker antigen‐specific CD4 T‐cell responses to Listeria monocytogenes infection in the mice exposed to BDE‐209, suggesting decreased resistance to exogenous pathogens. Taken together, these observations indicate an impaired cellular immunity after long‐term and relative high‐dose exposure to BDE‐209 in adult mice. Copyright © 2015 John Wiley & Sons, Ltd.     

Regulatory B cell is critical in bone union process through suppressing proinflammatory cytokines and stimulating Foxp3 in Treg cells

Bone fractures may result in delayed union (DU) or non‐union (NU) in some patients. Evidence suggests that the skewing of the immune system toward the proinflammatory type is a contributing factor. Because B cells were previously found to infiltrate the fracture healing site at abundant levels, we examined the regulatory B cells (Bregs) in DU/NU patients. In bone fracture patients with normal healing, the frequency of interleukin (IL)‐10‐expressing B cells was significantly upregulated in the early healing process (6 weeks post‐surgery) and was downregulated later on (18 weeks post‐surgery), whereas in DU/NU patients, the early upregulation of IL‐10‐expressing B cells was missing. The majority of IL‐10‐expressing B cells were concentrated in the IgM⁺CD27⁺ fraction in both controls and patients. IgM⁺CD27⁺ B cells effectively suppressed interferon gamma (IFN‐γ), tumor necrosis factor alpha (TNF‐α), and IL‐2 expression from CD4⁺ T cells, as well as IFN‐γ and TNF‐α expression from CD8⁺ T cells. The IgM⁺CD27⁺ B cell‐mediated suppression was restricted to the sample from the early healing time point in controls, as the IgM⁺CD27⁺ B cells from normal healing patients later on or from DU/NU patients did not present significant regulatory function. In addition, culturing of CD4⁺CD25⁺ Tregs with IgM⁺CD27⁺ B cells from controls at early healing time point resulted in higher Foxp3 expression, a function absent in controls at later time point, or in DU/NU patients. In conclusion, our results support a role of B cell‐mediated regulation early during the bone healing process.     

Toxic effects of microcystin‐LR on the HepG2 cell line under hypoxic and normoxic conditions

Microcystins (MCs) are highly liver‐specific and evidenced as a liver tumor promoter. Oxidative stress is one of the most important toxicity mechanisms of MCs, which is tightly related to oxygen concentration. The effects of MCs on animals and cell lines in normoxia and the mechanisms have been well studied, but such effects in different oxygen conditions were still unclear. The aim of the present study was to explore the cellular response of the human hepatocellular carcinoma cell line (HepG2) to MC‐LR exposure under hypoxic (1% O₂) and normoxic (21% O₂) conditions. We examined cell viability, mitochondrial membrane potential (MMP), superoxide dismutase (SOD) activity and gene expression posttoxin exposure. Cell viability was increased by MC‐LR in normoxia although decreased in hypoxia. MC‐LR markedly induced MMP loss under hypoxic condition but only slightly MMP loss under normoxic condition. SOD activity was significantly induced by MC‐LR in hypoxia, indicating prolonged oxidative stress. Inhibitory apoptosis protein (c‐IAP2) was significantly up‐regulated by MC‐LR under normoxic condition, suggesting that c‐IAP2 played an important role in the promotion of cell proliferation by MC‐LR. These results indicate that MC‐LR promotes cell proliferation under normoxic condition whereas induces cell apoptosis under hypoxic condition. Copyright © 2012 John Wiley & Sons, Ltd.     

紫杉醇化疗方案对乳腺癌患者血清Th1/Th2细胞因子水平的影响

目的探讨紫杉醇化疗方案对乳腺癌患者血清Th1/Th2细胞因子水平的影响。方法将100例乳腺癌术后辅助化疗患者随机(1︰1)分为2组,常规组行AC(阿霉素-环磷酰胺,每3周1次)-P(紫杉醇80mg·m~(-2),每周1次)方案化疗,剂量密集组,行AC(阿霉素-环磷酰胺每2周1次)-P(紫杉醇175mg·m~(-2),每2周1次)方案化疗,化疗前后观察患者血清细胞因子水平变化。结果常规组及剂量密集组化疗后患者血清IL-2、TNF-α及IFN-γ浓度均显著增高(P<0.05),血清IL-4、IL-6及IL-10水平显著降低(P<0.05)。结论常规组及剂量密集组均能够改善乳腺癌患者细胞免疫功能;剂量密集组较常规组具有更强的恢复细胞免疫为主的抗肿瘤免疫能力,且未显著增加毒性和不良反应。     

In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

Radiation‐induced manifestations like free radical burst, oxidative damage and apoptosis leading to cell death. In present study, N‐acetyl tryptophan glucopyranoside (NATG) was assessed for its immune‐radioprotective activities using J774A.1 cells. Clonogenic cell survival, cell cycle progression and cytokines i.e. IFN‐γ, TNF‐α, IL‐2, IL‐10, IL‐12, IL‐13 and IL‐17A expression were evaluated in irradiated and NATG pretreated cells using clonogenic formation ability, flow cytometry and ELISA assay. Results indicated that 0.25μg/ml NATG exhibited maximum radioprotection against gamma‐radiation (2Gy) without intervening in cell cycle progression. NATG pretreated (−2 h) plus irradiated cells showed significant elevation in IFN‐γ (∼38.2%), IL‐17A (∼53.7%) and IL‐12 (∼58.8%) expression as compared to only irradiated cells. Conversely, significant decrease in TNF‐α (∼21.6%), IL‐10 (∼31.2%), IL‐2 (∼23.7%) and IL‐13 expression (∼17.8%) were observed in NATG pretreated plus irradiated cells as compared to irradiated cells. Conclusively, NATG pretreatment to irradiated J774A.1 cells, stimulate Th₁ while diminish Th₂ cytokines that contributes to radioprotection.     

Aflatoxin B1 modulates the expression of phenotypic markers and cytokines by splenic lymphocytes of male F344 rats

Aflatoxin B₁ (AFB₁) is immunotoxic to animals and a suspected immunosuppressant in humans. In this study, we investigated the effects of AFB₁ on splenic lymphocyte phenotypes and the inflammatory cytokine expression in male F344 rats. Exposure of animals to AFB₁ [5–75 µg kg^–1 body weight (BW)] for 1 week showed dose‐dependent decreases in the percentage of splenic CD8⁺ T cells and CD3^‐CD8a⁺ NK cells. A general inhibition of the expression of interleukin (IL)‐4 and interferon (IFN)‐γ by CD4⁺ T cells, IL‐4 and IFN‐γ by CD8a⁺ cells, and tumor necrosis factor (TNF)‐α expression by natural killer (NK) cells was also found; however, no concurrent histological changes in spleen tissue were present, suggesting acute immunosuppression without overt toxicity. Five‐week exposure with AFB₁ significantly increased the percentages of CD3⁺ and CD8⁺ T cells, especially at low doses (≤ 25 µg kg^–1). AFB₁ treatment significantly decreased the anti‐inflammatory cytokine IL‐4 expression by CD4⁺ T cells and significantly increased the pro‐inflammatory cytokine IFN‐γ expression by CD4⁺ T cells and TNF‐α expression by NK cells. These results indicated that repeated AFB₁ exposure promotes inflammatory responses by regulating cytokine expression. Our data provides novel insights into the mechanisms by which AFB₁ exposure differentially modulates the cell‐mediated immune responses and suggests the involvement of an inflammatory response upon repeated exposure. Copyright © 2013 John Wiley & Sons, Ltd.     

α‐Lipoic acid protects against microcystin‐LR induced hepatotoxicity through regeneration of glutathione via activation of Nrf2

Microcystins (MCs), as the most dominant bloom‐forming strains in eutrophic surface water, can induce hepatotoxicity by oxidative stress. Alpha‐lipoic acid (α‐LA) is a super antioxidant that can induce the synthesis of antioxidants, such as glutathione (GSH), by nuclear factor erythroid 2‐related factor 2 (Nrf2). However, the potential molecular mechanism of α‐LA regeneration of GSH remains unclear. The present study aimed to investigate whether α‐LA could reduce the toxicity of MCs induced in human hepatoma (HepG2), Bel7420 cells, and BALB/c mice by activating Nrf2 to regenerate GSH. Results showed that exposure to 10 μM microcystin‐leucine arginine (MC‐LR) reduced viability of HepG2 and Bel7402 cells and promoted the formation of reactive oxygen species (ROS) compared with untreated cells. Moreover, the protection of α‐LA included reducing the level of ROS, increasing superoxide dismutase activity, and decreasing malondialdehyde. Levels of reduced glutathione (rGSH) and rGSH/oxidized glutathione were significantly increased in cells cotreated with α‐LA and MC‐LR compared to those treated with MC‐LR alone, indicating an ability of α‐LA to attenuate oxidative stress and MC‐LR‐induced cytotoxicity by increasing the amount of rGSH. α‐LA can mediate GSH regeneration through the Nrf2 pathway under the action of glutathione reductase in MC‐LR cell lines. Furthermore, the data also showed that α‐LA‐induced cytoprotection against MC‐LR is associated with Nrf2 mediate pathway in vivo. These findings demonstrated the potential of α‐LA to resist MC‐LR‐induced oxidative damage of liver.     

Role of microRNA‐122 in microcystin‐leucine arginine‐induced dysregulation of hepatic iron homeostasis in mice

Microcystin‐leucine arginine (MC‐LR) is a cyclic heptapeptide hepatotoxin produced by cyanobacteria. MicroRNA‐122 (miR‐122) is specifically expressed in the liver. This study focuses on the role of miR‐122 in MC‐LR‐induced dysregulation of hepatic iron homeostasis in C57BL/6 mice. The thirty mice were randomly divided into five groups (Control, 12.5 μg/kg·BW MC‐LR, 25 μg/kg·BW MC‐LR, Negative control agomir and 25 μg/kg·BW MC‐LR + miR‐122 agomir). The results show that MC‐LR decreases the expressions of miR‐122, Hamp, and its related regulators, while increasing the content of hepatic iron and the expressions of FPN1 and Tmprss6. Furthermore, miR‐122 agomir pretreatment improves MC‐LR induced dysregulation of hepatic iron homeostasis by arousing the related regulators and reducing the expression of Tmprss6. These results suggest that miR‐122 agomir can prevent the accumulation of hepatic iron induced by MC‐LR, which may be related to the regulation of hepcidin by BMP/SMAD and IL‐6/STAT signaling pathways.     

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Acute kidney injury (AKI) represents a group of complicated syndromes with a high mortality rate. The administration of adipose‐derived mesenchymal stem cells (ADMSCs) has been tested as a possible treatment method for AKI. The long‐term evaluation of AKI induced by ischemia/reperfusion (IR) and the probable renal protection of ADMSCs are limited. In this study we have established a rat AKI model induced by IR and investigated the possible protective effects of ADMSCs. Adult Sprague‐Dawley (SD) rats were divided into three groups (n = 6/each group). The MOCK group was as the normal control. Rats in the IR‐AKI and IR‐AKI+ADMSCs groups were subjected to IR injury by clamping both renal pedicles for 40 minutes. Rats in the MOCK and IR‐AKI groups were injected with PBS via the tail vein as negative treatment controls. Rats in the IR‐AKI+ADMSCs group received ADMSCs therapy (2 × 10⁶ cells were injected into the rats via the tail vein). We found that ADMSC transplantation restored the pathologic morphology induced by IR‐AKI to normal compared with the MOCK group, suggesting the reparative function of ADMSCs in kidney tissues. Compared with IR‐induced AKI alone, ADMSC treatment significantly decreased the number of apoptotic cells, the level of total urinary protein and serum creatinine, the expression of pro‐inflammatory cytokines (IL‐6, TNF‐α, IL‐1β, IFN‐γ, TNF‐α, IFN‐γ, and TGF‐β), and the inflammation‐associated proteins (HGF and SDF1), but increased the expression of the anti‐inflammatory cytokine, IL‐10, and the anti‐apoptotic regulator, Bcl‐2. Our data have indicated that ADMSC transplantation may protect against IR‐induced AKI by anti‐apoptotic and anti‐inflammatory effects.     

Anti‐viral activity of jatrophone against RSV‐induced respiratory infection via increase in interferon‐γ generating dendritic cells

Respiratory syncytial virus (RSV), a member of Paramyxoviridae family is responsible for bronchiolitis and pneumonia. The present study investigated anti‐viral and anti‐inflammatory activities of jatrophone against RSV‐infection in pulmonary epithelial cells in vitro and in mice model in vivo. The changes in viabilities of RSV infected cells by jatrophone treatment were determined by MTT assay. The fluorescence associated with production of ROS was evaluated by fluorescence microscopy using H2DCFDA dye. The IFN‐γ secreting cells were detected in mice BALF by stimulation with phorbol myristate acetate and ionomycin. The reduction of BEAS‐2B cell viability by RSV was alleviated on treatment with jatrophone in dose based manner. The cytopathogenic changes by RSV infection were prevented and viral growth inhibited by jatrophone in BEAS‐2B cells. Jatrophone treatment significantly alleviated RSV mediated overproduction of IL‐6/‐8 and suppressed ROS generation in the cells. The pulmonary viral titers were found to be markedly lower in mice treated with jatrophone relative to untreated group. The jatrophone treated mice also showed reduced IL‐4/‐5/‐13 levels and elevated IFN‐γ level in BALF relative to untreated RSV infected mice. Flow cytometry revealed elevated count of IFN‐γ generating cells in RSV infected mice on treatment with jatrophone. Thus jatrophone inhibits viral growth and oxidative damage by RSV in pulmonary epithelial cells. In RSV infected mice jatrophone increased immunity for viral infection by modulating cell phenotype for promotion of anti‐viral IFN‐γ. Thus jatrophone acts as potential anti‐viral compound and may be developed for treatment of respiratory treat infection.     

Characterization of in vitro effects of microcystin‐LR on intestinal epithelial cells

The intestinal epithelium is a single‐cell layer that provides an important barrier against natural toxins. Microcystin‐LR (MC‐LR), a cyclic heptapeptide, is one of the best known toxins able to alter the functions of intestine. This study evaluated the toxic effects and the possible mechanisms of MC‐LR on barrier function of the intestinal epithelial cells. Intestinal epithelial cells (IEC‐6) were exposed to 0, 6.25, 12.5, 25 and 50 μM MC‐LR. Cell viability significantly decreased, while the ratio of apoptotic cells increased after exposure to 12.5μM and higer concentration of MC‐LR. As expected, the integrity of a polarized IEC‐6 monolayer was affected by MC‐LR exposure, as demonstrated by a decrease in the transepithelial electrical resistance (TEER) values, becoming most pronounced at 50μM, 24 h. No effects were detected on the protein expression levels of the tight junction protein claudin at 50μM. However, the expression of occludin and zonula occludens‐1 (ZO‐1) declined. Furthermore, MC‐LR can immigrate into IEC‐6 cells. The activity of protein phosphatases 2A (PP2A) decreased from the concentration of 12.5 μM, showing a dose‐dependent decline. These results provide new information that strengthens the concept that the intestinal epithelium is important targets for toxic effects of water contaminants like MC‐LR. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1539–1547, 2017.     

Immunological Response to (1,4)‐α‐d‐Glucan in the Lung and Spleen of Endotoxin‐Stimulated Juvenile Rats

Abstract: We investigated the effects of (1,4)‐α‐D‐glucan (α‐DG), a novel immune stimulatory drug from Tinospora cordifolia, on the concentration of pro‐ and anti‐inflammatory cytokines (interleukin [IL]‐1β, IL‐6, tumour necrosis factor‐α [TNF‐α], γ‐interferon [IFN‐γ] and IL‐10) in the lung and spleen of endotoxin‐stimulated juvenile rats. Experimental groups (n = 16/group) included controls with an intraperitoneal injection of saline, endotoxaemic rats with a non‐lethal dose of 10 mg/kg Escherichia coli endotoxin, and endotoxaemic rats treated with two doses of 10 mg/kg α‐DG, intraperitoneally, 2 and 4 hr after endotoxin injection. At 24 hr of treatment, rats were euthanized and lungs and spleen were removed for cytokines determination and lung injury. Endotoxaemia increased IL‐1β concentration by fivefold in both organs, while creating a moderate pulmonary hypercellularity (demonstrated by about 11% increase in the alveolar‐septal thickening and 11% decrease in the alveolar‐interstitial space ratio). In the lung, α‐DG treatment reduced concentrations of IL‐1β by 30% (p > 0.05), IL‐6 by 43% (p < 0.01), IFN‐γ by 46% (p < 0.01) and the anti‐inflammatory cytokine, IL‐10, by 31% (p > 0.05) compared to endotoxaemia. In the spleen, α‐DG treatment decreased the ratio of IL‐1β to IL‐10 by 55% (p < 0.05), demonstrating an anti‐inflammatory trend. These data suggest that α‐DG differentially modulates cytokine response in the lung and spleen and modifies the pro‐ and anti‐inflammatory balance during an early period of endotoxaemia in juvenile rats.     

Analysis of the roles of dietary protein and calcium in fluoride‐induced changes in T‐lymphocyte subsets in rat

The roles of dietary protein (Pr) and calcium (Ca) levels on the changes in T‐lymphocyte subsets induced by excessive fluoride (F) intake were assessed using rats that were malnourished for 120 days as a model. The CD⁴⁺ and CD⁸⁺ T‐lymphocytes in the spleen tissue were determined by flow cytometry and immunofluorescence assay. The percentages of CD³⁺, CD⁴⁺, and CD⁸⁺ T‐lymphocytes were reduced in the spleen of rats exposed to excessive F, and malnutrition aggravated these changes in the T‐lymphocytes. In addition, the mRNA expression levels of IL‐1β, IL‐2, IL‐6, TNF‐α, and IFN‐γ in the spleen were downregulated significantly. We also reported herein the increased apoptosis ratio following caspase‐9 and caspase‐3 upregulation in the spleen of rats exposed to excessive amount of F. Light and transmisison electron microscopy revealed the irregularly arranged lymphocytes, few lymph nodules and the apoptotic characteristic of lymphocytes, which are caused by the increased expression of caspase. In addition, Pr and Ca supplementation reversed the morphologic and T‐lymphocytic changes in spleen under malnutrition. Taken together, our results revealed an endogenous caspase‐mediated mechanism of regulating the apoptosis of the T‐lymphocyte subsets, as well as the immune‐related cytokine secretion, which reduces the immune function in F‐induced rats. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1587–1595, 2017.     

Cyanidin‐3‐glucoside inhibits inflammatory activities in human fibroblast‐like synoviocytes and in mice with collagen‐induced arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint tissue inflammation. Cyanidin‐3‐glucoside (C3G) is a major component in the flavonoid family and has shown anti‐inflammatory, anti‐oxidant and anti‐tumour activity. In this study, we investigated the effects of C3G on lipopolysaccharides (LPS)‐induced inflammation on human rheumatoid fibroblast‐like synoviocytes (FLS) and on collagen‐induced arthritis (CIA) mice model. We treated FLS with C3G followed by LPS induction, the expressions of tumour necrosis factor alpha (TNF‐α), interleukin 1 beta (IL‐1β) and IL‐6 and the activation of nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) and mitogen‐activated protein kinase (MAPK) signalling pathway were analyzed. CIA was induced in mice and the arthritic mice were treated with C3G for 3 weeks. The disease severity was compared between control and C3G treated mice. The serum levels of TNF‐α, IL‐1β and IL‐6 were analyzed by ELISA. C3G inhibited LPS‐induced TNF‐α, IL‐1β and IL‐6 expression in FLS. Moreover, C3G inhibited LPS‐induced p65 production and IκBa, p38, ERK and JNK phosphorylation. Administration of C3G significantly attenuated disease in mice with CIA and decreased the serum level of TNF‐α, IL‐1β and IL‐6. C3G inhibited LPS‐induced inflammation in human FLS by inhibiting activation of NF‐κB and MAPK signalling pathway. C3G exhibited therapeutic effects in mice with CIA.