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• Knockdown of IFIT3 represses M1 polarization. • IFIT3 does not affect IL-4 induced M2 polarization of microglia. • Knockdown of IFIT3 blocks the activation of STAT1 and NF-ĸB pathways. • IFIT3 regulates the polarization of microglia, thereby facilitating MS. The key to the treatment of multiple sclerosis (MS) is to promote the transition from inflammation-induced demyelination to remyelination. Polarization of microglia towards M1 or M2 phenotype is critical in this transition. Interferon induced protein with tetratricopeptide repeats 3 (IFIT3) is involved in inflammatory reaction and up-regulated in M1-polarized macrophages. However, its effect on microglia during MS has not been reported. In this paper, we demonstrated the important role of IFIT3 in selectively regulating microglia polarization. The expression of IFIT3 was increased when microglia were polarized towards M1, but did not change under M2 polarization. The knockdown of IFIT3 selectively inhibited M1 polarization, while M2 polarization was not affected by IFIT3 silencing. Furthermore, the activation of signal transducer and activator of transcription 1 (STAT1) and nuclear factor kappa-B (NF-ĸB) signaling in M1 polarized microglia was suppressed by downregulating IFIT3. In experimental autoimmune encephalitis (EAE) mice, an animal model of MS, IFIT3 expression was upregulated. The disease progression, inflammatory infiltration and demyelination in the EAE mice were alleviated by silencing IFIT3. The inhibitory effects of IFIT3 knockdown on M1 polarization and STAT1 and NF-ĸB pathways were also confirmed in the spinal cord of EAE mice. In summary, our findings suggest that IFIT3 selectively intensified microglia polarization towards the pro-inflammatory M1 phenotype, and may contribute to the progression of MS. [ABSTRACT FROM AUTHOR]

Abstract As antigen-presenting cells (APC), B cells exert a variety of immune regulatory functions mainly by presenting antigens, triggering immune response, and producing antibodies for immune regulation. Regulatory B cells (Bregs) are special subpopulations of B cells with immune-regulating or immune-suppressing properties and play a role in peripheral tolerance. Bregs suppress immune response through inhibiting the differentiation of dendritic cells (DCs), suppressing the proliferation of helper T1(TH1) cells and helper T17 (TH17) cells, inducing the differentiation of fork head transcription factor p3 positive regulatory T cells (FoxP3+ Tregs). Different subsets of Bregs have distinct phenotypes and markers. Different subsets of Bregs participate in immune modulation by different ways. The absence or loss of Bregs exacerbates the severity of many disease such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and graft-versus-host-disease (GVHD). Bregs are also involved in tumor immunosuppressive effect and inhibit the antitumor immune process. In this article, we review the research advances of Bregs in autoimmune diseases, GVHD and tumor. Highlights • Previous studies have shown that regulatory B cells play important roles in inflammatory diseases and tumor. • There is no systematic review of the role of regulatory B cells in inflammatory diseases and tumor. • In this paper, the role of regulatory B cells in inflammatory diseases and tumors is systematically reviewed. • This article provides researchers with the latest systematic research of regulatory B cells. [ABSTRACT FROM AUTHOR]

Sepsis is characterized by the extensive release of cytokines and other mediators. It results in a dysregulated immune response and can lead to organ damage and death. Curcumin has anti-inflammatory properties and immunoregulation functions in various disorders such as sepsis, cancer, rheumatoid arthritis, cardiovascular diseases, lung fibrosis, gallstone formation, and diabetes. This paper investigates the effects of curcumin on immune status and inflammatory response in mice subjected to cecal ligation and puncture (CLP). Inflammatory tissue injury was evaluated by histological observation. Magnetic microbeads were used to isolate splenic CD4 + CD25 + regulatory T cells (Tregs), and phenotypes were then analyzed by flow cytometry. The levels of Foxp3 were detected by Western blot and real-time PCR and cytokine levels were determined by enzyme-linked immunosorbent assay. We found that the administration of curcumin significantly alleviated inflammatory injury of the lung and kidney in septic mice. The suppressive function of Treg cells was enhanced and the plasma levels of IL-10 increased after treatment with curcumin. Furthermore, the secretion of plasma TNF-α and IL-6 was notably inhibited in septic mice treated with curcumin and administration with curcumin could improve survival after CLP. These data suggest that curcumin could be used as a potential therapeutic agent for sepsis. [ABSTRACT FROM AUTHOR]

• This paper describes the basic structure of CXCL1 and CXCR2 and the combination between them. CXCL1/CXCR2 is widely expressed in central and peripheral systems. • CXCL1/CXCR2 recruits inflammatory cells to the lesion site, causing an inflammatory response at the lesion site. • CXCL1/CXCR2 in the central nervous system can cause the development of inflammation, pain, depression, and Alzheimer's disease, but it can also inhibit the development of Alzheimer's disease in certain ways. • CXCL1/CXCR2 causes pain in the peripheral nervous system through multiple pathways. • CXCL1/CXCR2 are involved in cancer metastasis through the peripheral nervous system. The C-X-C chemokine ligand (CXCL) 1 and its receptor C-X-C chemokine receptor (CXCR) 2 are widely expressed in the peripheral nervous systems (PNS) and central nervous systems (CNS) and are involved in the development of inflammation and pain after various nerve injuries. Once a nerve is damaged, it affects not only the neuron itself but also lesions elsewhere in its dominant site. After the CXCL1/CXCR2 axis is activated, multiple downstream pathways can be activated, such as c-Raf/MAPK/AP-1, p-PKC-μ/p-ILK/NLRP3, JAK2/STAT3, TAK1/NF-κB, etc. These pathways in turn mediate cellular motility state or cell migration. CXCR2 is expressed on the surface of neutrophils and monocytes/macrophages. These cells can be recruited to the lesion through the CXCL1/CXCR2 axis to participate in the inflammatory response. The expression of CXCR2 in neurons can activate some pathways in neurons through the CXCL1/CXCR2 axis, thereby causing damage to neurons. CXCR2 is also expressed in astrocytes, and when CXCR2 activated, it increases the number of astrocytes but impairs their function. Since inflammation can occur at almost any site of injury, elucidating the mechanism o f CXCL1/CXCR2 axis' influence on inflammation may provide a favorable target for clinical treatment. Therefore, this article reviews the research progress of the CXCL1/CXCR2 axis in neurological diseases, aiming to provide a more meaningful theoretical basis for the treatment of neurological diseases. [ABSTRACT FROM AUTHOR]

• The OVA sensitized AR mouse model and EOL-1 cells model are established. • The level of miR-223-3p is up-regulated in AR patients and AR mice. • MiR-223-3p affects AR inflammatory response by promoting eosinophil degranulation. • FBXW7 is a target gene of miR-223-3p, and its expression is low in AR group. • MiR-223-3p affects eosinophil degranulation and AR inflammation by targeting FBXW7. MiR-223-3p is a multifunctional microRNA regulated by multiple transcription factors and plays a critical role in inflammation. This paper was designed to investigate the regulatory role and mechanism of miR-223-3p in eosinophils degranulation and allergic rhinitis (AR) inflammation. OVA sensitized AR mouse model and EOL-1 cells model were established. RT-qPCR and FISH were performed to detect the miR-223-3p expression. ELISA and WB were utilized to evaluate mRNA and protein expression. HE staining and transmission electron microscopy were applied to observe the morphological changes in nasal mucosa. Flow cytometry and immunofluorescence staining were performed to measure the proportion of eosinophils and eosinophilic major basic protein expression. The targeting relationship between miR-223-3p and FBXW7 was verified by bioinformatic analysis and dual-luciferase reporter gene assay. The expression of FBXW7 was detected by immunohistochemistry. The level of miR-223-3p in nasal mucosa was significantly up-regulated in AR group. The expression of miR-223-3p, ECP, MBP, and EPO were increased in EOL-1 cells, further increasing the miR-223-3p level could promote the ECP and EPO mRNA expression. Upregulation of miR-223-3p increased eosinophils granule protein expression, aggravated mucosal destruction and enhanced AR inflammation. Luciferase assay verified miR-223-3p directly target the 3ʹ-UTR of FBXW7. In vitro, overexpression of FBXW7 could reverse the increase in MBP expression caused by the up-regulation of miR-223-3p. In vivo, knockdown of FBXW7 could reverse the down-regulation in granule protein level caused by the down-regulation of miR-223-3p, thereby aggravating AR inflammation. Collected evidence elucidated that miR-223-3p could regulate the eosinophil degranulation and enhances the inflammation in AR by targeting FBXW7. The miR-223-3p/FBXW7 axis may provide a novel approach for AR treatment. [ABSTRACT FROM AUTHOR]

In this paper, we investigate the effect of glabridin (Glab) on psoriasis. We observed that Glab significantly suppressed the levels of nitric oxide (NO), NF-κB subunit p65, interleukin (IL)-6, and IL-1β in lipopolysaccharide (LPS)-stimulated HaCaT cells. In addition, Glab treatment reduced the expression of IL-17A, IL-22, and IL-23 in TNF- α- stimulated-HaCaT cells. These findings prompted us to test whether Glab could be used to treat psoriasis in vivo. The effects of Glab on PASI scores, histopathological changes, oxidative/anti-oxidative indexes and pro-inflammatory cytokines in IMQ-induced mice were investigated. The results indicated that Glab could reduce the PASI scores and ameliorate the deteriorating histopathology. Interestingly, RT-PCR revealed that Glab significantly decreased the mRNA expression of p65, IL-6, IL-1β, IL-17A, IL-22, and IL-23. These results were confirmed by Western blot analysis and immunohistochemistry staining. In conclusion, our present study revealed that Glab had beneficial effects on psoriasis, and the underlying mechanism may be associated with the downregulation of pro-inflammatory cytokines and the improvement of antioxidant status. Hence, Glab is a promising candidate molecule for development of effective psoriasis therapies. [ABSTRACT FROM AUTHOR]

[Display omitted] • SARS-CoV-2 promotes an inflammatory phenotype in human monocytes. • In SARS-CoV-2 stimulated PBMC Tα1 mitigates monocyte and myeloid DC activation. • Tα1 dampens SARS-CoV-2 mediated induction of pro-inflammatory cytokines. • Tα1 promotes release of the anti-inflammatory factors IL-10 from SARS-CoV- 2-stimulated PBMC. The peculiar property of Thymosin alpha 1 (Tα1) to act as master regulator of immune homeostasis has been successfully defined in different physiological and pathological contexts ranging from cancer to infection. Interestingly, recent papers also demonstrated its mitigating effect on the "cytokine storm" as well as on the T-cell exhaustion/activation in SARS-CoV-2 infected individuals. Nevertheless, in spite of the increasing knowledge on Tα1-induced effects on T cell response confirming the distinctive features of this multifaceted peptide, little is known on its effects on innate immunity during SARS-CoV-2 infection. Here, we interrogated peripheral blood mononuclear cell (PBMC) cultures stimulated with SARS-CoV-2 to disclose Tα1 properties on the main cell players of early response to infection, namely monocytes and myeloid dendritic cells (mDC). Moving from ex vivo data showing an enhancement in the frequency of inflammatory monocytes and activated mDC in COVID-19 patients, a PBMC-based experimental setting reproduced in vitro a similar profile with an increased percentage of CD16+ inflammatory monocytes and mDC expressing CD86 and HLA-DR activation markers in response to SARS-CoV-2 stimulation. Interestingly, the treatment of SARS-CoV-2-stimulated PBMC with Tα1 dampened the inflammatory/activation status of both monocytes and mDC by reducing the release of pro-inflammatory mediators, including TNF-α, IL-6 and IL-8, while promoting the production of the anti-inflammatory cytokine IL-10. This study further clarifies the working hypothesis on Tα1 mitigating action on COVID-19 inflammatory condition. Moreover, these evidence shed light on inflammatory pathways and cell types involved in acute SARS-CoV-2 infection and likely targetable by newly immune-regulating therapeutic approaches. [ABSTRACT FROM AUTHOR]

B7-H3, a recently discovered B7 family member, is documented as a regulator in the inflammatory response as well as T cell-mediated immune responses. In this paper, we find that patients with acute pancreatitis revealed overwhelming levels of serum soluble B7-H3 (sB7-H3) associated with the clinical outcomes. Furthermore, B7-H3 protein was marked increased in l -arginine-induced acute experimental pancreatitis. Anti-B7-H3 monoclonal antibody treatment attenuated the proinflammatory cytokine production, downregulated the activation of the NF-κB signaling pathway, and ameliorated the pancreas disruption in l -arginine-induced pancreatitis. In addition, although l -arginine alone failed to induce the production of proinflammatory cytokine and anti-B7-H3 mAb had no effect on the proinflammatory cytokine production of acinar cells, administration of anti-B7-H3 mAb in the coculture model of acinar cells and macrophages stimulated by l -arginine displayed the similar effects. On the whole, B7-H3 participates in the development of acute pancreatitis, and anti-B7-H3 monoclonal antibody ameliorates severity of acute experimental pancreatitis via attenuation of the inflammatory response. [ABSTRACT FROM AUTHOR]

α7 nicotinic acetylcholine receptors (α7 nAChRs) are involved in regulating inflammatory reactions, as well as the cell viability. They are expressed in both the plasma membrane and mitochondria of eukaryotic cells. Previously we found that neuroinflammation resulted in the decrease of α7 nAChR density in the brain of mice and was accompanied by accumulation of amyloid-beta (Aβ) peptides and memory impairment. In the present paper, it is shown that inflammation induced by either regular bacterial lipopolysaccharide (LPS) injections or immunizations with α7 nAChR extracellular domain (1–208) affected also the brain cell mitochondria. Using various modifications of sandwich ELISA, we observed the decrease of α7 nAChRs and accumulation of Aβ(1–40) and Aβ(1–42) in mitochondria of immunized or LPS-treated mice compared to control ones. Mitochondria of treated mice responded with cytochrome c release to lower Ca 2 + concentrations than mitochondria of control mice and were less sensitive to its attenuation with α7 nAChR agonist PNU282987. It is concluded that inflammation decreases α7 nAChR expression in both mitochondria and cell plasma membrane and makes mitochondria more susceptible to apoptosis induction. [ABSTRACT FROM AUTHOR]

Gangliosides, sialic acid-containing glycosphingolipids, have been considered to be involved in the development, differentiation, and function of nervous systems in vertebrates. However, the mechanisms for anti-inflammation caused by gangliosides are not clear. In this paper, we investigated the anti-inflammation effects of ganglioside GD1a by using RAW264.7 macrophages. Our data demonstrated that treatment of macrophages with lipopolysaccharide significantly increased the production of NO and pro-inflammatory cytokines. GD1a suppressed the induction of iNOS and COX-2 mRNA and protein expression and secretory pro-inflammatory cytokines in culture medium, such as TNFα, IL-1α and IL-1β. In addition, LPS-induced phosphorylation of mitogen-activating protein kinases and IκBα degradation followed by translocation of the NF-κB from the cytoplasm to the nucleus were attenuated after GD1a treatment. Furthermore, GD1a probably inhibited LPS binding to macrophages and LPS-induced accumulation between TLR4 and MyD88. Taken together, the results demonstrated that ganglioside GD1a inhibited LPS-induced inflammation in RAW 264.7 macrophages by suppressing phosphorylation of mitogen-activating protein kinases and activation of NF-κB through repressing the Toll-like receptor 4 signaling pathway. [ABSTRACT FROM AUTHOR]

[Display omitted] • Quinolone antibiotics, as commonly used human and animal antibiotics, are widely residual in the environment, and the immunotoxicity study for quinolones is of great importance. • Quinolone antibiotics acting on RAW264.7 macrophages at concentrations of 0.01, 0.1, 1, 10, 100, and 1000 μg/L exhibited a low-dose excitatory hormesis effect, which was demonstrated by activity assays, migration assays, and phagocytosis assays. • The dose that exerts excitatory effect was found to induce macrophage polarization of M1 type by ELISA and Western blot assay, and 0.1 μg/L was selected for mechanism study to explore the relationship between hormesis effect and polarization. • Mechanistic studies have confirmed that when quinolone antibiotics at 0.1 μg/L induce the release of inflammatory factors through PI3K/Akt, Notch1, JNK and JAK2/STAT3 signaling pathways, leading to inflammation. In order to eliminate inflammation, macrophages increase the number of feedback and enhance the migration and phagocytosis functions. • Environmental residual doses of quinolone antibiotics have immunotoxicity. Widespread use of quinolone antibiotics leads to serious residues in the environment and toxicity effects. This paper studied the effects of three typical quinolone antibiotics ciprofloxacin, norfloxacin and pipemidic acid on the polarization of macrophages RAW264.7 cells. The experimental concentrations were 0.01, 0.1, 1, 10, 100 and 1000 μg/L according to the environmental residual level. By MTT assay, phagocytosis assay and migration assay, macrophages were found to exhibit hormesis effect of low dose promotion and high dose inhibition. The detection of macrophages surface markers showed that 0.1 μg/L antibiotics increased the secretion of pro-inflammatory cytokines and induced macrophages to be M1-type, and 1000 μg/L antibiotics significantly increased the secretion of anti-inflammatory cytokines and induced macrophages to be M2-type. In order to explore the relationship between low-dose excitatory effects and polarization, the mechanism of 0.1 μg/L antibiotics inducing macrophages to M1-type was further studied. Results showed that 0.1 μg/L quinolone antibiotics activated the key proteins in the PI3K/Akt, Notch1, JNK and JAK2/STAT3 signaling pathways to cause the secretion of pro-inflammatory cytokines and induce inflammation. In order to eliminate inflammation, macrophages number feedback increased, phagocytosis and migration function enhanced, showing hormesis effect. In vitro macrophages experiment confirmed that quinolone antibiotics with environmental residual concentration had immunotoxicity. [ABSTRACT FROM AUTHOR]

The development of agents that can modulate microglial activation has been suggested as one potential strategy for the treatment or prevention of neurodegenerative diseases. Among these agents, resveratrol, with its anti-inflammatory action, has been described to have neuroprotective effects. In this paper we demonstrate that in LPS-stimulated microglia resveratrol pretreatment reduced, in a dose-dependent manner, pro-inflammatory cytokines IL-1β, TNF-α and IL-6 mRNA expression and increased the release of anti-inflammatory interleukin (IL)-10. Moreover, resveratrol pretreatment up-regulated the phosphorylated forms of JAK1 and STAT3, as well as suppressor of cytokine signaling (SOCS)3 protein expression in LPS activated cells, demonstrating that the JAK–STAT signaling pathway is involved in the anti-inflammatory effect exerted by resveratrol. By supplementing the cultures with an IL-10 neutralizing antibody (IL-10NA) we obtained the opposite effect. Taken together, these data allow us to conclude that the LPS-induced pro-inflammatory response in microglial cells can be markedly reduced by resveratrol, through IL-10 dependent up-regulation of SOCS3, requiring the JAK–STAT signaling pathway. [ABSTRACT FROM AUTHOR]

α7 Nicotinic acetylcholine receptors (α7 nAChRs) are involved in regulating inflammatory cytokine production in macrophages and astrocytes. In the present paper, it is shown that α7-specific agonists PNU282987 (130 nM) or choline (1.6 mM) attenuated the interleukin-6 (IL-6) production stimulated by bacterial lipopolysaccharide in monocyte-derived U937 and astrocyte-derived U373 cell lines. In contrast, α7(179–190)-specific antibody, which bound to and was internalized by U373 cells, stimulated IL-6 production in p38 kinase-dependent manner in the absence of lipopolysaccharide. The antibody effect was not due to its Fc-fragment because similar capacity was found for recombinant single-chain (scFv) α7(179–190)-specific antibody selected from the gene library of healthy human subject. The data obtained allow suggesting that α7-specific antibody can provoke neuroinflammation within the brain by inducing IL-6 production in astrocytes. [ABSTRACT FROM AUTHOR]

Abstract: Background: 2,3,5,6-Tetramethylpyrazine (TMP) is known as a composition of Ephedra sinica and it has been used in the treatment of several disorders such as asthma, heart failure, rhinitis, and urinary incontinence. It has been reported that TMP inhibits melanoma metastasis and suppression angiogenesis by VEGF. Objective: The inhibitory activity of melanogenic proteins by TMP was confirmed in UVA-induced melanoma/keratinocyte co-culture system in this paper. Methods: The melanin content, cell viability and cytokines release such as TNFα, IL-1β, IL-8 and GM-CSF were measured by ELISA assay. In addition, TRP1, MITF and MAPK signaling protein expression were also evaluated by Western blotting analysis. Results: Decreasing melanogenic factors (TRP1, MITF, and MAPK) and factors (TNFα, IL-1β, IL-8, and GM-CSF) improving skin cancer and inflammation were identified. Conclusion: It suggests that TMP can serve as a potent candidate for regulation of melanogenesis. [Copyright &y& Elsevier]

Abstract: The pro-inflammatory cytokine, macrophage migration inhibitory factor (MIF), is currently enjoying a renewed interest owing to its recently revealed functions. Among these its enzymatic tautomerase activity remains the most perplexing. There is a notion that some aspects of MIF signaling might involve its catalytic action. Though a true in vivo substrate for MIF has not been identified yet small molecule inhibitors of MIF are sought currently as potential anti-inflammatory agents. We have reported earlier that ketone bodies and some plant phenols feature acidic CH groups that appear to be good markers of their inhibitor potency toward MIF phenylpyruvate tautomerase. These molecules, like phenylpyruvate itself, belong to the keto-carboxylic acids or to the α,β-unsaturated ketones. Some ketones of similar structure have earlier been reported to have anti-inflammatory effect. In this paper we report tautomerase inhibition by certain synthetic α,β-unsaturated cyclic ketones, a novel class of small molecule MIF inhibitors. [Copyright &y& Elsevier]

Abstract: There is a great interest in the pharmacological properties of cannabinoid like compounds that are not linked to the adverse effects of Δ9-tetrahydrocannabinol (THC), e.g. psychoactive properties. The present paper describes the potential immuno-modulating activity of unheated Cannabis sativa extracts and its main non-psychoactive constituent Δ9-tetrahydrocanabinoid acid (THCa). By heating Cannabis extracts, THCa was shown to be converted into THC. Unheated Cannabis extract and THCa were able to inhibit the tumor necrosis factor alpha (TNF-α) levels in culture supernatants from U937 macrophages and peripheral blood macrophages after stimulation with LPS in a dose-dependent manner. This inhibition persisted over a longer period of time, whereas after prolonged exposure time THC and heated Cannabis extract tend to induce the TNF-α level. Furthermore we demonstrated that THCa and THC show distinct effects on phosphatidylcholine specific phospholipase C (PC-PLC) activity. Unheated Cannabis extract and THCa inhibit the PC-PLC activity in a dose-dependent manner, while THC induced PC-PLC activity at high concentrations. These results suggest that THCa and THC exert their immuno-modulating effects via different metabolic pathways. [Copyright &y& Elsevier]

Abstract: In the present paper, the effect of Fumigaclavine C, a fungal metabolite, on experimental colitis was examined. Fumigaclavine C, when administered intraperitoneally once a day, significantly reduced the weight loss and mortality rate of mice with experimental colitis induced by intrarectally injection of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). This compound also markedly alleviated the macroscopic and microscopic appearances of colitis. Furthermore, Fumigaclavine C, given both in vivo and in vitro, showed a marked inhibition on the expression of several inflammatory cytokines, including IL-1β, IL-2, IL-12α, IFN-γ, TNF-α as well as MMP-9 in sacral lymph node cells, colonic patch lymphocytes and colitis tissues from the TNBS colitis mice. Meanwhile, the compound caused a dose-dependent reduction in IL-2 and IFN-γ from the lymphocytes at the protein level and MMP-9 activity. These results suggest that Fumigaclavine C may alleviate experimental colitis mainly via down-regulating the production of Th1 cytokines and the activity of matrix metalloproteinase. [Copyright &y& Elsevier]

Intracranial hemorrhage (ICH) is one of the most common brain traumas, and inflammation caused by ICH seriously affects the quality of life and prognosis of patients. Eupatilin has been shown to have anti-inflammatory effects in various diseases. However, only one paper has reported that Eupatilin has a therapeutic effect on the inflammatory response caused by ICH and the underlying mechanism needs to be studied. We used erythrocyte lysis stimulation (ELS) to induce mouse microglia BV2 as the inflammation model. CCK-8 and Transwell assays were used to detect cell viability and migration. RT-PCR, western blotting, and ELISA were used to detect the secretion of inflammatory factors and the expression of related mechanism proteins. HE staining was used to detect cell edema and death. We found that ELS significantly increased protein and mRNA levels and secretion of inflammatory factors IL-1β and TNF-α, which Eupatilin attenuated through the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) pathway. The anti-inflammatory effect of Eupatilin was significantly attenuated after siRNA was used to reduce TLR4 expression. The experimental results and mechanism were also verified in TLR4 knockout mice in vivo. Eupatilin has a therapeutic effect on inflammation caused by ICH. The underlying mechanism may be related to TLR4/MyD88, which brings new hope for clinical patients to improve symptoms and prognosis. • Eupatilin attenuated ELS-induced BV2 inflammation model in vitro. • Eupatilin had a therapeutic effect on inflammation via the TLR4/MyD88 pathway in vitro. • Eupatilin had a therapeutic effect on ICH-induced inflammation in vivo. [ABSTRACT FROM AUTHOR]