Protective effect of cinnamic acid in endotoxin‐poisoned mice

In this work, we aimed to evaluate the protective effect of cinnamic acid (CD) on lipopolysaccharide (LPS; Escherichia coli 055:B5)‐induced endotoxin‐poisoned mice and clarify the underlying mechanisms. The mice were administrated CD 5 d before 15 mg/kg LPS challenge. 12 hr later, thymus was separated for determination of thymus indexes. Lung and spleen tissues were collected for histologic examination and the wet/dry weight ratio of lung was calculated, and serum was acquired for tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐18, and IL‐1β measurement. Moreover, the expression of NOD‐like receptor (NLR) family, pyrin domain‐containing 3 (NLRP3) inflammasome was determined in lung. CD increased the thymus indexes and decreased lung wet/dry weight ratio. In addition, CD improved the lung and spleen histopathological changes induced by LPS and decreased the number of neutrophils in lung tissues. CD also inhibited the pro‐inflammatory cytokines (TNF‐α, IL‐18, and IL‐1β) production in serum. Furthermore, CD suppressed the LPS‐induced NLRP3, Caspase‐1, and IL‐1β mRNA expression in lung, as well as the expression of NLRP3 and Caspase‐1 (p20) protein. CD may have protective effects in endotoxin‐poisoned mice via inhibiting the activation of NLRP3 inflammasome, and can be considered as a potential therapeutic candidate for diseases involved in endotoxin poisoning such as sepsis.     

Farrerol attenuates MPP+‐induced inflammatory response by TLR4 signaling in a microglia cell line

Farrerol was found to possess neuroprotective effect; however, the mechanism remains unknown. The aim of the present study was to explore the effect of farrerol on MPP⁺‐induced inflammation in mouse microglial BV‐2 cells and to elaborate the underlying mechanism. MTT assay was performed to measure the cell viability. The pro‐inflammatory mediators and cytokines including interleukin (IL)‐6, IL‐1β, and tumor necrosis factor‐α (TNF‐α); inducible nitric oxide synthase; and cyclooxygenase 2 were measured. The expression of p‐p65, p‐IκBα, toll‐like receptor 4 (TLR4), and myeloid differentiation primary response 88 were analyzed by western blot. We found that farrerol treatment improved cell viability in MPP⁺‐induced BV‐2 cells. MPP⁺‐induced upregulation of IL‐6, IL‐1β, and TNF‐α was inhibited by farrerol treatment. Farrerol treatment also attenuated MPP⁺‐induced expression of inducible nitric oxide synthase and cyclooxygenase 2 as well as the activation of NF‐κB in BV‐2 cells. MPP⁺‐induced TLR4 signaling was markedly diminished by farrerol treatment. Knockdown of TLR4 attenuated MPP⁺‐induced inflammatory response in BV‐2 cells. In conclusion, farrerol treatment attenuated MPP⁺‐induced inflammatory response by inhibiting the TLR4 signaling pathway in BV‐2 cells. The results indicated that farrerol could be used as a therapeutic agent for preventing or alleviating the neuroinflammation‐related diseases, such as Parkinson's disease.     

Isoforskolin and forskolin attenuate lipopolysaccharide‐induced inflammation through TLR4/MyD88/NF‐κB cascades in human mononuclear leukocytes

The principal active component of isoforskolin (ISOF) is from the plant Coleus forskohlii, native to China, which has attracted much attention for its biological effects. We hypothesize that ISOF and forskolin (FSK) pretreatment attenuates inflammation induced by lipopolysaccharide (LPS) related to toll‐like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa B (NF‐κB) signaling. Mononuclear leukocytes (MLs) from healthy donors' blood samples were separated by using density gradient centrifugation. Protein levels of TLR4, MyD88, and NF‐κB were detected using western blot and inflammatory cytokines interleukin (IL) 1β, IL‐2, IL‐6, IL‐21, IL‐23, tumor necrosis factor (TNF) α, and TNF‐β were tested by enzyme‐linked immunosorbent assay and Quantibody array in MLs. Our results showed that LPS augmented the protein levels of TLR4, MyD88, and NF‐κB in MLs and the production of IL‐1β, IL‐2, IL‐6, IL‐21, IL‐23, TNF‐α, and TNF‐β in supernatants of MLs. Despite treatment with ISOF and FSK prior to LPS, the protein levels of TLR4, MyD88, NF‐κB, IL‐1β, IL‐2, IL‐6, IL‐21, IL‐23, TNF‐α, and TNF‐β in MLs were apparently decreased. roflumilast (RF) and dexamethasone (DM) had a similar effect on MLs with ISOF and FSK. Our results, for the first time, have shown that ISOF and FSK attenuate inflammation in MLs induced by LPS through down‐regulating protein levels of IL‐1β and TNF‐α, in which TLR4/MyD88/NF‐κB signal pathway could be involved.     

The Effects of Propolis and its Isolated Compounds on Cytokine Production by Murine Macrophages

Since propolis and phenolic compounds, such as cinnamic and coumaric acids, have several biological properties, their immunomodulatory effect on cytokine production (IL‐1β, IL‐6 and IL‐10) was investigated. Peritoneal macrophages from BALB/c mice were incubated with propolis, coumaric and cinnamic acids in different concentrations and the concentrations that inhibited cytokine production were tested before or after macrophage challenge with LPS, to evaluate a possible immunomodulatory action. Propolis and the acids stimulated IL‐1β production, while IL‐6 production was significantly inhibited after incubation with propolis (5, 50 and 100 µg/well), coumaric and cinnamic acids (50 and 100 µg/well). In LPS‐challenge protocols, inhibitory concentrations of cinnamic and coumaric acids after LPS incubation prevented efficiently its effects on IL‐6 production, whereas propolis inhibited LPS effects both before and after its addition. Propolis, coumaric and cinnamic acids (50 and 100 µg/well) inhibited IL‐10 production as well. Both acids showed a similar inhibitory activity on IL‐10 production when added after LPS challenge, while propolis counteracted LPS action when added before and after LPS incubation. Propolis modulated the immune/inflammatory response, depending on the concentration. Its efficiency may occur due to the synergistic effect of its compounds, and cinnamic and coumaric acids may be involved in the action of propolis on cytokine production. Copyright © 2012 John Wiley & Sons, Ltd.     

Antipyretic and Anti‐inflammatory Effects of Asiaticoside in Lipopolysaccharide‐treated Rat through Up‐regulation of Heme Oxygenase‐1

Asiaticoside (AS), a triterpenoid isolated from Centella asiatica, has been found to exhibit antioxidant and anti‐inflammatory activities in several experimental animal models. However, the underlying mechanisms remain elusive. In this study, we provide experimental evidences that AS dose‐dependently inhibited lipopolysaccharide (LPS)‐induced fever and inflammatory response, including serum tumor necrosis factor (TNF)‐α and interleukin (IL)‐6 production, liver myeloperoxidase (MPO) activity, brain cyclooxygenase‐2 (COX‐2) protein expression and prostaglandin E₂ (PGE₂) production. Interestingly, AS increased serum IL‐10 level, liver heme oxygenase‐1 (HO‐1) protein expression and activity. Furthermore, we found that the suppressive effects of AS on LPS‐induced fever and inflammation were reversed by pretreatment with ZnPPIX, a HO‐1 activity inhibitor. In summary, our results suggest that AS has the antipyretic and anti‐inflammatory effects in LPS‐treated rat. These effects could be associated with the inhibition of pro‐inflammatory mediators, including TNF‐α and IL‐6 levels, COX‐2 expression and PGE₂ production, as well as MPO activity, which might be mediated by the up‐regulation of HO‐1. Copyright © 2012 John Wiley & Sons, Ltd.     

Effect of taxifolin glycoside on atopic dermatitis‐like skin lesions in NC/Nga mice

Increased levels of eosinphils, IgE, IL‐4, 5, and 13 and pro‐inflammatory factors (COX‐2, iNOS) are observed in patients with atopic dermatitis (AD). Taxifolin 3‐O‐β‐D‐glucopyranoside (TAX) from the roots of Rhododendron mucronulatum (RM) was examined to determine whether its immunomodulatory effect was applicable for treating atopic dermatitis. A total of 7 groups of NC/Nga mice with AD were treated by topical application or intraperitoneal injection of TAX for 4 weeks. Follow‐up evaluations were done to assess the changes in clinical observations, eosinophil counts, and levels of IgE, cytokines, COX‐2 and iNOS. In the clinical observation during the experimental period, TAX treatment significantly reduced the severity of AD‐like lesions induced in NC/Nga mice. Eosinophil and IgE levels decreased after treatment of the animals with TAX. TAX may thus be associated with improvement of eosinophil‐related allergic diseases. The expression of cytokines (IL‐4, 5 and 13) was significantly inhibited in the TAX‐treated group, suggesting that TAX might play an immunoregulatory role associated with AD. In RT‐PCR, iNOS and COX‐2 expression levels were reduced in the TAX‐treated group. In western blotting, the expression levels of iNOS and COX‐2 were also reduced in the TAX‐treated group. These findings suggest that TAX is effective for the treatment of AD by preventing the production of inflammatory cytokines and by reducing skin inflammation. Copyright © 2009 John Wiley & Sons, Ltd.     

Nerolidol Protects Against LPS‐induced Acute Kidney Injury via Inhibiting TLR4/NF‐κB Signaling

Acute kidney injury (AKI) is a critical care syndrome, resulting in acute reduction of renal function and up to 22% mortality of hospitalized patients. Nerolidol is a major component in several essential oils that possesses various pharmacological properties. The present study aimed to investigate the potential effect of nerolidol on lipopolysaccharide (LPS)‐induced AKI. Nerolidol dose‐dependently reduced the pathological injuries of kidney induced by LPS in rats. Nerolidol significantly decreased the levels of blood urea nitrogen and creatinine in LPS‐treated rats in a dose‐dependent manner. In addition, nerolidol inhibited LPS‐induced decrease of cell viability in NRK‐52E rat proximal tubular cells, which effect was concentration dependent. Nerolidol notably inhibited the increase of TNFα and IL‐1β in LPS‐treated rats and the mRNA expression of TNFα and IL‐1β in LPS‐treated NRK‐52E cells. Nerolidol suppressed the increase of toll‐like receptor 4 (TLR4) expression, phosphorylation and nuclear translocation of p65 NF‐κB in kidneys of LPS‐treated rats and LPS‐treated NRK‐52E cells. Overexpression of TLR4 and p65 NF‐κB significantly suppressed nerolidol‐induced inhibition of TNFα and IL‐1β expression and increase of cell viability in LPS‐treated cells. In summary, we found that nerolidol played a critical anti‐inflammatory effects through inhibition of TLR4/NF‐κB signaling and protected against LPS‐induced AKI. Copyright © 2017 John Wiley & Sons, Ltd.     

Evaluation of Anti‐atopic Dermatitis Activity of Hypsizigus marmoreus Extract

Hypsizigus marmoreus is an edible mushroom that is cultivated worldwide. In this study, we investigated antiinflammatory activities of H. marmoreus extract on atopic dermatitis (AD)‐like symptoms. Ethanol extract of H. marmoreus (HMEE) was administrated in powder to BALB/c mice in which AD was induced by 1‐chloro 2, 4, 6‐trinitrobenzene [picryl‐chloride, (PCL)]. The dermatitis severity score and the thickness of the epidermis were significantly decreased following daily intake of HMEE powder (1 g/kg/day) for 5 weeks compared with a PCL‐treated group. The mRNA expression of proinflammatory cytokines, such as interleukin‐1 beta (IL‐1β) and interferon‐gamma (IFN‐γ), was significantly attenuated in the dorsal skin of the HMEE‐fed mouse group compared with the PCL‐treated mouse group. In addition, in concanavalin A‐stimulated and lipopolysaccharide‐stimulated mouse splenocytes and macrophages, levels of IL‐1β and IFN‐γ production were attenuated following the addition of HMEE. Interestingly, the administration of HMEE to mouse splenocytes stimulated the production of an antiinflammatory cytokine, IL‐4. However, increases in the levels of proinflammatory cytokines and nitric oxide were attenuated by treating the mouse splenocytes, mouse macrophages, and Raw 264.7 cell line with HMEE. These results strongly suggest that HMEE exhibits anti‐AD activity via the regulation of inflammatory responses. Copyright © 2014 John Wiley & Sons, Ltd.     

Toll‐like receptor 4‐mediated immunoregulation by the aqueous extract of Mori Fructus

The aqueous extract of Mori Fructus (MF) exerts a change of phenotype and a cytoprotective effect in macrophages. The present study was carried out to investigate the immunomodulating activity of MF on the expression of nitric oxide (NO), tumor necrosis factor alpha (TNF‐α), co‐stimulatory molecules and also interferon‐gamma (IFN‐γ) in macrophages and splenocytes. Toll‐like receptor 4 (TLR4) is a promising molecular target for immune‐modulating drugs. It was hypothesized that one possible upstream signaling pathway leading to immunoregulation of MF may be mediated by TLRs. Multiple signaling molecules (NF‐κB, ERK1/2, p38 and JNK) of the TLR4 signaling pathway were also detected. It was found that MF increased NO production and TNF‐α secretion in RAW 264.7 and peritoneal macrophages, co‐stimulatory molecules expression in peritoneal macrophages and IFN‐γ expression in splenocytes. Further studies indicated that MF could significantly induce the phosphorylation of signal molecules of MAPKs and the degradation of IκBα which finally led to the activation and nuclear translocation of nuclear factor‐κB (NF‐κB) for the target gene expression. All those notions disclosed that the aqueous extract MF is a new TLR4 activator, which induces a Th1 immune response as a consequence of induction of cytokines secretion, especially TNF‐α and IFN‐γ. Copyright © 2009 John Wiley & Sons, Ltd.     

Tectorigenin protects against experimental fulminant hepatic failure by regulating the TLR4/mitogen‐activated protein kinase and TLR4/nuclear factor‐κB pathways and autophagy

Tectorigenin has received attention due to its antiproliferation, anti‐inflammatory, and antioxidant activities. In this study, we investigated the effects of tectorigenin on lipopolysaccharide (LPS)/D‐galactosamine(D‐GalN)‐induced fulminant hepatic failure (FHF) in mice and LPS‐stimulated macrophages (RAW 264.7 cells). Pretreatment with tectorigenin significantly reduced the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), histological injury, apoptosis, and the mortality of FHF mice, by suppressing the production of inflammatory cytokines such as TNF‐α and IL‐6. Tectorigenin also suppressed the activation of the inflammatory response in LPS‐stimulated RAW 264.7 cells. Tectorigenin‐induced protection is mediated through its mitigation of TLR4 expression, inhibition of mitogen‐activated protein kinase (MAPK) and nuclear factor‐κB (NF‐κB) pathway activation, and promotion of autophagy in FHF mice and LPS‐stimulated RAW 264.7 cells. Therefore, tectorigenin has therapeutic potential for FHF in mice via the regulation of TLR4/MAPK and TLR4/NF‐κB pathways and autophagy.     

Brassinin,a phytoalexin in cruciferous vegetables,suppresses obesity‐induced inflammatory responses through the Nrf2‐HO‐1 signaling pathway in an adipocyte‐macrophage co‐culture system

The aim of this study was to investigate the effect of brassinin (BR), a phytoalexin found in plants belonging to the Brassicaceae family, on the obesity‐induced inflammatory response and its molecular mechanism in co‐culture of 3T3‐L1 adipocytes and RAW264.7 macrophages. BR effectively suppressed lipid accumulation by down‐regulating the expression of adipogenic factors, which in turn, were regulated by early adipogenic factors such as CCAAT‐enhancer‐binding protein‐β and Kruppel‐like factor 2. Production of inflammatory cytokines and reactive oxygen species, induced by adipocyte‐conditioned medium, was significantly decreased in BR‐treated cells. This effect of BR was more prominent in contact co‐culture of adipocytes and macrophages with a 90% and 34% reduction in IL‐6 and MCP‐1 levels, respectively. BR also restored adiponectin expression, which was significantly reduced by culturing adipocytes in macrophage‐conditioned medium. In the transwell system, BR increased the protein levels of nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2) and its target molecule, hemoxygenase‐1 (HO‐1), by 55%–93% and 45%–48%, respectively, and also increased Nrf2 translocation into the nucleus. However, knockdown of Nrf2 or HO‐1 in RAW264.7 cells restored this BR‐mediated inhibition of IL‐6 and MCP‐1 production. These results indicated that BR inhibited obesity‐induced inflammation via the Nrf2‐HO‐1 pathway.     

Nimbolide Inhibits Nuclear Factor‐КB Pathway in Intestinal Epithelial Cells and Macrophages and Alleviates Experimental Colitis in Mice

Nimbolide is a limonoid extracted from neem tree (Azadirachta indica) that has antiinflammatory properties. The effect of nimbolide on the nuclear factor‐kappa B (NF‐κB) pathway in intestinal epithelial cells (IECs), macrophages and in murine colitis models was investigated. The IEC COLO 205, the murine macrophage cell line RAW 264.7, and peritoneal macrophages from interleukin‐10‐deficient (IL‐10^?/?) mice were preconditioned with nimbolide and then stimulated with tumor necrosis factor‐α (TNF‐α) or lipopolysaccharide. Dextran sulfate sodium‐induced acute colitis model and chronic colitis model in IL‐10^?/? mice were used for in vivo experiments. Nimbolide significantly suppressed the expression of inflammatory cytokines (IL‐6, IL‐8, IL‐12, and TNF‐α) and inhibited the phosphorylation of IκBα and the DNA‐binding affinity of NF‐κB in IECs and macrophages. Nimbolide ameliorated weight loss, colon shortening, disease activity index score, and histologic scores in dextran sulfate sodium colitis. It also improved histopathologic scores in the chronic colitis of IL‐10^?/? mice. Staining for phosphorylated IκBα was significantly decreased in the colon tissue after treatment with nimbolide in both models. Nimbolide inhibits NF‐κB signaling in IECs and macrophages and ameliorates experimental colitis in mice. These results suggest nimbolide could be a potentially new treatment for inflammatory bowel disease. Copyright © 2016 John Wiley & Sons, Ltd.     

Puerarin Exerts an Antiinflammatory Effect by Inhibiting NF‐kB and MAPK Activation in Staphylococcus aureus‐Induced Mastitis

Mastitis is defined as the inflammation of the mammary gland. There is generally no effective treatment for mastitis in animals. Puerarin, extracted from Radix puerariae, has been proven to possess many biological activities. The present study aims to reveal the potential mechanism that is responsible for the antiinflammatory action of puerarin in Staphylococcus aureus (S. aureus)‐induced mastitis in mice. Histopathological changes showed that puerarin ameliorated the inflammatory injury induced by S. aureus. Quantitative real‐time polymerase chain reaction and ELISA analysis indicated that puerarin not only suppressed the production of pro‐inflammatory cytokines such as TNF‐α, IL‐1β, and IL‐6 but also promoted the secretion of IL‐10. Toll‐like receptor 2 (TLR2) is important in the immune defense against S. aureus infection. Research in molecular biology has shown that the expression of TLR2 was inhibited with administration of puerarin. Further studies were performed on NF‐kB and mitogen‐activated protein kinase signaling pathways using western blot. The results demonstrated that puerarin suppressed phosphorylated IkBα, p65, p38, extracellular signal‐regulated kinase 1and 2 (ERK), and c‐Jun N‐terminal kinase (JNK) in a dose‐dependent manner. All of the results suggested that puerarin may be a potential therapy for treating mastitis. Copyright © 2016 John Wiley & Sons, Ltd.     

The Effect of propolis on Th1/Th2 cytokine expression and production by melanoma-bearing mice submitted to stress

Since propolis possesses immunomodulatory and antitumoral activities, this work aimed to evaluate its effect on Th1 (IL-2 and IFN-γ) and Th2 (IL-4 and IL-10) cytokines mRNA expression and production by melanoma-bearing mice submitted to immobilization stress. C57BL/6 male mice were inoculated with B16F10 cells, treated with propolis and submitted to stress for 14 days. Spleen cells were assessed for Th1/Th2 cytokine expression and production. Stress induced a higher tumor area, while propolis-treated mice, stressed or not, showed a melanoma development similar to the control. In groups without melanoma, stress or propolis treatment did not affect IL-2, IL-4 and IL-10 gene expression. On the other hand, IL-2 and IL-10 expression was inhibited in melanoma-bearing mice, stressed or not. Th1 cytokine production was also inhibited in melanoma-bearing mice. Propolis administration to melanoma-bearing mice submitted to stress stimulated IL-2 expression, as well as Th1 cytokine (IL-2 and IFN-γ) production, indicating the activation of antitumor cell-mediated immunity. Propolis also stimulated IL-10 expression and production, which may be related to immunoregulatory effects. The data indicate that propolis exerted an immunomodulatory activity in this assay, which may be related to its antitumoral action in vivo.     

Modulation of cerulein‐induced pancreatic inflammation by hydroalcoholic extract of curry leaf (Murraya koenigii)

This study was performed to study the in vitro and in vivo efficacy of hydroalcoholic extract of curry leaf (CLE) rich in carbazole alkaloids, against LPS‐induced inflammation in Raw 264.7 macrophages and cerulein‐induced acute pancreatitis, respectively. CLE was characterized by Fourier‐transform infrared (FTIR) and liquid chromatography–mass spectrometry. Raw 264.7 cells were stimulated with LPS (2 μg/ml) and treated with CLE. The animals were treated with two doses of CLE (100 and 300 mg/kg). Plasma biochemistry, tissue lipid peroxidation, cytokines, and histological examination were evaluated. CLE was found to decently scavenge the activity of DPPH radical. It dose dependently suppressed nitrite production and oxidative stress in macrophages. CLE alleviated LPS‐induced inflammation in macrophages as evident from the results of various inflammatory cytokines (IL‐1β, IL‐6, and TNF‐α). In vivo, CLE reduced cerulein‐induced pancreatic edema. CLE significantly abrogated the cerulein‐induced lipid peroxidation, nitrite, MPO, and GSH levels. The inflammatory cytokines and p65‐NFκB activity were significantly reduced by CLE. Mechanistically, CLE reduced the expression of NT, MPO, IL‐1β, ICAM‐1, and COX‐2, and increased the expression of Nrf2. It reduced distant organ damage markers as well. We report for the first time that CLE holds substantial potential for the prevention of acute pancreatitis.     

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

Acute lung injury (ALI) often leads to high mortality, and there is as yet no effective drug treatment. The present study aimed to investigate protective effects of mogroside IIIE (MGIIIE, a cucurbitane‐type triterpenoid from Siraitia grosvenorii Fruits) in experimental ALI and its underlying mechanism. MGIIIE (1, 10 0r 20 mg/kg) was orally administered for 1 h before a single intratracheal administration of lipopolysaccharide (LPS, 5 mg/kg). MGIIIE treatment dose‐dependently suppressed pulmonary oedema, pro‐inflammatory mediators (IL‐1β, IL‐6, TNF‐α and HMGB1) release and higher MPO activity in lung tissues induced by LPS challenge. Molecular researches showed that mogroside IIIE (20 mg/kg) not only increased the phosphorylation of adenosine 5′‐monophosphate‐activated protein kinase (AMPK) but suppressed the over‐expression of toll‐like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). In addition, MGIIIE also inhibited the activation of MAPKs and nuclear factor κB (NF‐κB) signalling in lung tissues from LPS‐challenged mice. Similar antiinflammatory effects of MGIIIE were obtained in LPS‐treated macrophages. Compound C (a pharmacological AMPK inhibitor) obviously reversed the antiinflammatory effect of MGIIIE in LPS‐induced ALI mice. Taken together, AMPK activation plays a crucial role in the antiinflammatory effects of MGIIIE in LPS‐induced ALI by down‐regulating TLR4/MAPK/NF‐κB signalling pathways. Copyright © 2017 John Wiley & Sons, Ltd.     

Zerumbone Suppresses IL‐1β‐induced Cell Migration and Invasion by Inhibiting IL‐8 and MMP‐3 Expression in Human Triple‐negative Breast Cancer Cells

Inflammation is a key regulatory process in cancer development. Prolonged exposure of breast tumor cells to inflammatory cytokines leads to epithelial‐mesenchymal transition, which is the principal mechanism involved in metastasis and tumor invasion. Interleukin (IL)‐1β is a major inflammatory cytokine in a variety of tumors. To date, the regulatory mechanism of IL‐1β‐induced cell migration and invasion has not been fully elucidated. Here, we investigated the effect of zerumbone (ZER) on IL‐1β‐induced cell migration and invasion in breast cancer cells. The levels of IL‐8 and matrix metalloproteinase (MMP)‐3 mRNA were analyzed by real‐time polymerase chain reaction. The levels of secreted IL‐8 and MMP‐3 protein were analyzed by enzyme‐linked immunosorbent assay and western blot analysis, respectively. Cell invasion and migration was detected by Boyden chamber assay. The levels of IL‐8 and MMP‐3 expression were significantly increased by IL‐1β treatment in Hs578T and MDA‐MB231 cells. On the other hand, IL‐1β‐induced IL‐8 and MMP‐3 expression was decreased by ZER. Finally, IL‐1β‐induced cell migration and invasion were decreased by ZER in Hs578T and MDA‐MB231 cells. ZER suppresses IL‐1β‐induced cell migration and invasion by inhibiting IL‐8 expression and MMP‐3 expression in TNBC cells. ZER could be a promising therapeutic drug for treatment of triple‐negative breast cancer patients. Copyright © 2014 John Wiley & Sons, Ltd.