Combining Network Pharmacology and Experimental Verification to Ascertain the Mechanism of Action of Asparagus officinalis Against the Brain Damage Caused by Fluorosis.

Asparagus officinalis (ASP) has antioxidation, anti-inflammatory, antiaging, and immune system-enhancing effects. We explored the preventive and therapeutic consequences of ASP on the brain damage elicited by fluorosis through network pharmacology and in vivo experimental validation. We ascertained the pharmaceutically active ingredients and drug targets of ASP from the Traditional Chinese Medicine Systems Pharmacology database, predicted the disease targets of fluorosis-induced brain injury using GeneCards and Online Mendelian Inheritance in Man databases, obtained target protein-protein interaction networks in the Search Tool for the Retrieval of Interacting Genes/Proteins database, used Cytoscape to obtain key targets and active ingredients, and conducted enrichment analyses of key targets in the Database for Annotation, Visualization and Integrated Discovery. Enrichment analyses showed that "mitogen-activated protein kinase" (MAPK), "phosphoinositide 3-kinase/protein kinase B" (PI3K-Akt), "nuclear factor-kappa B" (NF-κB), and the "neurotrophin signaling pathway" were the most enriched biological processes and signaling pathways. ASP could alleviate fluorosis-based injury, improve brain-tissue damage, increase urinary fluoride content, and improve oxidation levels and inflammatory-factor levels in the body. ASP could also reduce dental fluorosis, bone damage, fluoride concentrations in blood and bone, and accumulation of lipid peroxide. Upon ASP treatment, expression of silent information regulator (SIRT)1, brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), MAPK, NF-κB, PI3K, Akt, and B-cell lymphoma-2 in rat brain tissue increased gradually, whereas that of Bax, caspase-3, and p53 decreased gradually. We demonstrated that ASP could regulate the brain damage caused by fluorosis through the SIRT1/BDNF/TrkB signaling pathway, and reported the possible part played by ASP in preventing and treating fluorosis.

Chanling Gao suppresses colorectal cancer via PI3K/Akt/mTOR pathway modulation and enhances quality of survival.

The Chinese medicine formula Chanling Gao (CLG) exhibits significant tumor inhibitory effects in colorectal cancer (CRC) nude mice. However, the detailed mechanisms remain elusive. CRC in situ nude mouse models were treated with CLG. Small animal magnetic resonance imaging (MRI) tracked tumor progression, and overall health metrics such as food and water intake, body weight, and survival were monitored. Posttreatment, tissues and blood were analyzed for indicators of tumor inhibition and systemic effects. Changes in vital organs were observed via stereoscope and hematoxylin-eosin staining. Immunohistochemistry quantified HIF-1α and P70S6K1 protein expression in xenografts. Double labeling was used to statistically analyze vascular endothelial growth factor (VEGF) and CD31 neovascularization. Enzyme-linked immunosorbent assay was used to determine the levels of VEGF, MMP-2, MMP-9, IL-6, and IL-10 in serum, tumors, and liver. Western blotting was used to assess the expression of the PI3K/Akt/mTOR signaling pathway-related factors TGF-ß1 and smad4 in liver tissues. CLG inhibited tumor growth, improved overall health metrics, and ameliorated abnormal blood cell counts in CRC nude mice. CLG significantly reduced tumor neovascularization and VEGF expression in tumors and blood. It also suppressed HIF-1α, EGFR, p-PI3K, Akt, p-Akt, and p-mTOR expression in tumors while enhancing PTEN oncogene expression. Systemic improvements were noted, with CLG limiting liver metastasis, reducing pro-inflammatory cytokines IL-6 and IL-10 in liver tissues, decreasing MMP-2 in blood and MMP-2 and MMP-9 in tumors, and inhibiting TGF-ß1 expression in liver tissues. CLG can enhance survival quality and inhibit tumor growth in CRC nude mice, likely through the regulation of the PI3K/Akt/mTOR signaling pathway.

The colonic metabolism differences of main alkaloids in normal and colitis mice treated with Coptis chinensis Franch. and Sophora flavescens Ait. herbal pair using liquid chromatography-high resolution mass spectrometry method combined with chemometrics.

Coptis chinensis Franch. and Sophora flavescens Ait. is a herbal pair frequently used in treating ulcerative colitis. However, the bio-disposition profile of the major components in the inflamed gut remains unclear, which is essential to understand the pharmacological material basis of this herb pair. Here we established an integral quantitative and chemometric method to deduce the colonic metabolism differences of this herbal pair in normal and colitis mice. With this LC-MS method, a total of 41 components have been found in the Coptis chinensis Franch. and Sophora flavescens Ait. extract, and 28 metabolites were found in the colon after oral administration. Alkaloid and its phase I metabolites were the main components in the colon of normal and colitis mice. The results of principal component analysis at 6 h after oral administration showed significant colonic metabolism differences between normal and colitis mice. Heamap results showed that colitis induced significant changes in the colonic bio-disposition of this herbal pair extract. In particular, in the context of colitis, the phase I metabolism of berberine, coptisine, jatrorrhizine, palmatine,and epiberberine has been inhibited. These results may provide a basis for understanding the pharmacological material basis of Coptis chinensis Franch. and Sophora flavescens Ait. in treating ulcerative colitis.

Epidemiological analysis of drinking water-type fluorosis areas and the impact of fluorosis on children's health in the past 40 years in China.

This study analyzed the effect of China's fluorosis prevention and control program, which has been in effect for more than 40 years, and the impact of fluorosis on children's health. Relevant research studies were retrieved from the following online databases from the time of their inception to May 2022: PubMed, ScienceDirect, Embase, Cochrane, China National Knowledge Infrastructure, and Wanfang. The Review Manager 5.3 software was used in statistical analyses. This article included seventy studies: Thirty-eight studies reported the effect of improving water quality and reducing fluoride content, the incidence rate of dental fluorosis in children, and the level of urinary fluoride, and thirty-two studies reported the intelligence quotient (IQ) and health status of children. Following water improvement strategies, the fluoride levels in drinking water decreased significantly; urinary fluoride levels and dental fluorosis decreased significantly in children. With regard to the effect of fluorosis on the IQ of children, the results showed that the IQ of children in areas with a high fluoride of fluorosis was lesser than that in areas with a low fluoride, and this difference was significant. Based on the prevalence of dental fluorosis and its effect on the intelligence of children, it appears that reducing fluoride levels in drinking water and monitoring water quality are important strategies for the prevention and treatment of fluorosis.

Characterization of the chemical constituents and in vivo metabolic profile of Scutellaria barbata D. Don by ultra high performance liquid chromatography with high-resolution mass spectrometry.

Scutellaria barbata D. Don (S. barbata) is one of the most frequently used anticancer herb medicine in China. Mechanistic understanding of the biological activities of S. barbata is hindered by limited knowledge regarding its components and metabolic profile. In this study, ultra-high-performance liquid chromatography coupled with high resolution mass spectrometry (quadrupole time-of-flight mass spectrometry) was used to identify the chemical constituents in S. barbata and their metabolic profiles in rats. By applying cleavage rules and comparison with reference substances, 89 components were identified in S. barbata, which included 45 flavonoids, 28 diterpenoids, 10 phenolics, and 6 others. A total of 110 compounds, including 32 prototype compounds and 78 metabolites, were identified or tentatively characterized in vivo. Methylation, sulfonation, and glucuronidation were the main metabolic pathways, which could be attributed to the fact that several of the compounds in S. barbata have phenolic hydroxyl groups. This is the first systematic study on the chemical constituents and in vivo metabolic profile of S. barbata. The analytical method features a quick and comprehensive dissection of the chemical composition and metabolic profile of S. barbata and provides a basis for exploring its various biological activities.

Identification and validation of 12 immune-related genes as a prognostic signature for colon adenocarcinoma.

Colon adenocarcinoma (COAD) is a common malignant tumor of the digestive tract that threatens human health seriously. Thus, it is urgent to explore biomarkers that can be used to evaluate a patient's survival prognosis overall as a supplementary treatment. RNA-seq expression profiles were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus, and Lasso and multivariate Cox regression analyses were used for developing the prognostic model. Finally, a nomogram comprising the prognostic model was established to evaluate survival overall. A risk model comprised of a total of 12 immune-related gene pairs was constructed. Further analysis revealed the model's independent prognostic ability in relation to other clinical characteristics. This model's nomogram could help clinicians choose personalized treatment for COAD patients. This model has significant potential to complement COAD's clinical identifying characteristics, and also provide new insights into the identification of colon cancer patients with a high risk of death.

Two immune-enhanced molecular subtypes differ in inflammation, immune checkpoints, mutations, and prognostic outcome in stage I-II colonic carcinoma.

The purpose of this paper is to investigate the immune function of the tumor microenvironment and its clinical correlation with colonic carcinoma. Immune genes were downloaded from the The Cancer Genome Atlas database. Five subtypes are obtained by cluster screening based on immune gene expression data. The C3 and C4 subtypes show stronger immune activity. In addition, the C4 subtype has the largest number of gene mutations and the worst prognosis. Most of the immune signatures are upregulated in the C4 subtype, while most of the immune infiltration-related cells are upregulated in the C3 and C4 subtypes. The different immune microenvironments between these subtypes may provide new ideas for immunotherapy strategies in colon carcinoma.

SNHG17 promotes the proliferation and migration of colorectal adenocarcinoma cells by modulating CXCL12-mediated angiogenesis.

BACKGROUND: Colorectal adenocarcinoma (CRA) is one of the leading causes of cancer-related deaths in the world. Long non-coding RNAs (lncRNAs) have been implicated to be effective regulators in the disease course of human cancers, including CRA. Small nucleolar RNA host gene 17 (SNHG17) belongs to lncRNAs, and it has been reported in breast cancer and gastric cancer. However, the function of SNHG17 and its mechanism in CRA progression remain largely unknown. In this study, we attended to shedding some light on the role of SNHG17 in CRA. METHODS: RT-qPCR was used to assess SNHG17 expression in CRA cells. CCK-8 assay, colony formation and transwell assay were carried out to detect the regulatory effect of SNHG17 silencing on CRA cell proliferation and migration. The angiogenesis of SNHG7-downregulated CRA cells was analyzed by tube formation assay. Mechanism experiments were conducted to identify the interaction between miR-23a-3p and SNHG17 or C-X-C motif chemokine ligand 12 (CXCL12). RESULTS: SNHG17 possessed with high expression in CRA cells. Knockdown of SNHG17 caused the inhibition on CRA cell proliferation and migration. SNHG17 promoted CRA cell proliferation and migration by sponging miR-23a-3p to upregulate CXCL12. CONCLUSION: SNHG17 promotes the proliferation and migration of CRA cells by inhibiting miR-23a-3p to modulate CXCL12-mediated angiogenesis.

COL1A1 and MZB1 as the hub genes influenced the proliferation, invasion, migration and apoptosis of rectum adenocarcinoma cells by weighted correlation network analysis.

OBJECTIVES: The influences of COL1A1 and MZB1 on the proliferation, migration, invasion and apoptosis abilities of rectum adenocarcinoma was aimed to explore in this study. METHODS: Gene expression levels in rectum adenocarcinoma and adjacent tissues were analyzed by differential analysis. Weighted gene correlation network analysis (WGCNA) was employed to investigate rectal adenocarcinoma (READ) hub genes. MCODE was performed to screen the modules of protein-protein interaction network in Cytoscape software. Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool is considered to be the most effective tool in gene ontology (GO) enrichment and Kyoto Gene and Genomics Encyclopedia (KEGG) pathway analysis. Survival analysis was performed using READ patient information from TCGA-READ project database. Quantitative Real-time Polymerase Chain Reaction (qRT-PCR) and western blot were employedto examinemRNA and protein expressions of COL1A1 and MZB1 in tumor tissues and cell lines. After transfecting various interference sequences by liposome-mediated transfection, the influence of COL1A1 and MZB1 on the proliferation, apoptosis, migration and invasion of rectal cancer cells were observed by plate clone formation assay, flow cytometry, wound healing assay and transwell assay respectively. Moreover, xenograft tumor growth assay in vivo validated the results. RESULTS: Higher expression levels of COL1A1 and lower expression levels of MZB1 were discovered in tumor tissues of patients with colorectal adenocarcinoma. Overexpression of MZB1 and silencing COL1A1 significantly inhibited proliferation, migration and invasion, while cell apoptosis was promoted. Overexpression of MZB1 and silencing COL1A1 inhibited the orthotopic growth of tumor in vivo. CONCLUSION: COL1A1 promoted proliferation, migration and invasion but inhibited apoptosis of rectal adenocarcinoma cells while MZB1 was totally on the contrary.

Effective Chemotherapy of Lung Cancer Using Bovine Serum Albumin-Coated Hydroxyapatite Nanoparticles.

BACKGROUND Successful chemotherapy of lung cancer relies largely on the use of a good drug delivery system (DDS). We successfully constructed a hybrid DDS comprised of hydroxyapatite (HAP) nanoparticles and bovine serum albumin (BSA). MATERIAL AND METHODS The HAP nanoparticles were selected as the core to encapsulate the anticancer drug doxorubicin (DOX), followed by surface modification of BSA as a stabilizer and shielding corona to finally prepare the hybrid DDS (BSA/HAP/DOX). RESULTS The following characterizations revealed that BSA/HAP nanoparticles have high stability, high biocompatibility, and good DOX-loading capability to meet in vivo applications. Moreover, BSA/HAP/DOX can enhance the cellular uptake of drug in A549 cells (lung cancer cells). Most importantly, BSA/HAP had better in vivo tumor targetability than bare HAP nanoparticles, which resulted in stronger anticancer efficacy both in vitro and in vivo than free DOX or HAP/DOX, and greatly decreased the adverse effects of free DOX. CONCLUSIONS Our hybrid DDS shows potential to be applied in more advanced application of cancer therapy.

Long noncoding RNA MALAT1 mediates stem cell-like properties in human colorectal cancer cells by regulating miR-20b-5p/Oct4 axis.

Cancer stem cells (CSCs) are crucial components of the tumor microenvironment that take part in tumor initiation, progression, recurrence, metastasis, and resistance to chemotherapy. This study explores the mechanisms through which CSCs maintain their stemness, especially in tumors of colorectal cancer (CRC), which thus far remain uncertain. Our findings indicated that the expression of miR-20b-5p is negatively correlated with that of metastasis-associated lung adenocarcinoma transcript-1 (MALAT1, r = -0.928, p = 0.023) and Oct4 (r = -0.894, p = 0.041) in CRC cells. We hypothesized that there may be some targeted regulatory relationships among MALAT1, miR-20b-5p, and Oct4. We proceeded to show that both si-MALAT1 and miR-20b-5p-mimic attenuated microsphere formation and self-renewal capacity, decreased the proportion of CSCs, and downregulated the expression of proteins associated with tumor cell stemness maintenance (Oct4, Nanog, sex-determining region Y-box 2, and Notch1) and cellular metabolism (glucose transporter 1, lactate dehydrogenase B, hexokinase 2, and pyruvate kinase isozyme M2) in HCT-116 cells in vitro. In addition, a xenograft model based on Balb/c mice demonstrated that the administration of either si-MALAT1 or miR-20b-5p-mimic suppressed the tumorigenicity of HCT-116 cells in vivo. The underlying mechanisms may involve the targeting of the tumor cell stemness maintenance-related factor Oct4 by miR-20b-5p. For the first time, we present the possible underlying effects of MALAT1 in influencing the stem cell-like properties of CRC cells. We propose that microRNAs and long noncoding RNAs have vital functions in mediating tumor stemness, which remain to be fully elucidated.

LncRNA LUADT1 sponges miR-15a-3p to upregulate Twist1 in small cell lung cancer.

Lung adenocarcinoma associated transcript 1 (LUADT1) has been reported as an oncogenic long non-coding RNA (lncRNA) in lung adenocarcinoma, while its roles in small cell lung cancer (SCLC) are unknown. Our RNA interaction bioinformatics prediction showed that LUADT1 could form strong base pairing with miR-15a-3p, which is a tumor-suppressive miRNA that can target Twist1. We found that LUADT1 and Twist1 were upregulated in SCLC, while miR-15a-3p was downregulated in SCLC. However, LUADT1 was posively correlated with Twist1 but was not significnatly correlated with miR-15a-3p. Overexpression experiments showed that and LUADT1 and miR-15a-3p did not significantly affect the expression of each other. Moreover, LUADT1 overexpression mediated the upregualtion of Twist1, and miR-15a-3p overexpression played an oppsoite role. Transwell assays showed that LUADT1 and Twist1 overexpression mediated the increased rate of cell invasion and migration, while miR-15a-3p overexpression mediated the decreased rate of cell invasion and migration. In addition, miR-15a-3p overexpression played an oppsoite role and attenuated the effects of LUADT1 overexpression. Therefore, LUADT1 may sponge miR-15a-3p to upregulate Twist1 in SCLC, thereby promoting cancer cell invasion and migration. TRIAL REGISTRATION: 2017GZH-1-201,746,382, registered at Jan 02,2017.

Combination adjuvant chemotherapy with targeted drugs for treatment of colorectal cancer: A network meta-analysis.

Colorectal cancer (CRC) is one of the most fatal diseases in the world. The efficacy of present chemotherapy treatments are limited and the addition of targeted drugs have been put into practice. However, the preferred treatments among adjuvant chemotherapies still remain controversial and uncertain. To evaluate the efficacy of different adjuvant chemotherapies combined with or without targeted drugs to determine the optimal treatment for patients with CRC in clinical practice. PubMed and Embase were searched for eligible articles and only randomized controlled trials (RCTs) were included. R (Version 3.2.5) software was utilized to conduct the Bayesian network meta-analysis (NMA). Outcomes including overall survival (OS) and progression-free survival (PFS) were displayed using hazard ratios. And the rank probabilities of each treatment were evaluated using the surface under cumulative ranking curve. A total of 75 RCTs published after 1997 were included in the data analysis. Overall, FOLFIRI+ cetuximab was found to be the most effective treatment in terms of long-term survival and FOLFOX was the most effective pure chemotherapy treatment. The addition of targeted drugs will greatly improve the efficacy of chemotherapy. Targeted drug cetuximab combined with the chemotherapy regiment FOLFIRI is the preferable treatment for patients with CRC in clinical practice.

Study on the Mechanism of Cell Cycle Checkpoint Kinase 2 (CHEK2) Gene Dysfunction in Chemotherapeutic Drug Resistance of Triple Negative Breast Cancer Cells.

BACKGROUND This study aimed to investigate the mechanism of CHEK2 gene dysfunction in drug resistance of triple negative breast cancer (TNBC) cells. MATERIAL AND METHODS To perform our study, a stable CHEK2 wild type (CHEK2 WT) or CHEK2 Y390C mutation (CHEK2 Y390C) expressed MDA-MB-231 cell line was established. MTT assay, cell apoptosis assay and cell cycle assay were carried out to analyze the cell viability, apoptosis, and cell cycle respectively. Western blotting and qRT-PCR were applied for related protein and gene expression detection. RESULTS We found that the IC50 value of DDP (Cisplatin) to CHEK2 Y390C expressed MDA-MB-231 cells was significantly higher than that of the CHEK2 WT expressed cells and the control cells. After treatment with DDP for 48 h, cells expressing CHEK2 WT showed lower cell viability than that of the CHEK2 Y390C expressed cells and the control cells; compared with the CHEK2 Y390C expressed cells and the control cells, cells expressing CHEK2 WT showed significant G1/S arrest. Meanwhile, we found that compared with the CHEK2 Y390C expressed cells and the control cells, cell apoptosis was significantly increased in CHEK2 WT expressed cells. Moreover, our results suggested that cells expressing CHEK2 WT showed higher level of p-CDC25A, p-p53, p21, Bax, PUMA, and Noxa than that of the CHEK2 Y390C expressed cells and the control cells. CONCLUSIONS Our findings indicated that CHEK2 Y390C mutation induced the drug resistance of TNBC cells to chemotherapeutic drugs through administrating cell apoptosis and cell cycle arrest via regulating p53 activation and CHEK2-p53 apoptosis pathway.

Tryptanthrin Protects Mice against Dextran Sulfate Sodium-Induced Colitis through Inhibition of TNF-α/NF-κB and IL-6/STAT3 Pathways.

Inflammatory bowel disease (IBD) is a notable health problem and may considerably affect the quality of human life. Previously, the protective roles of tryptanthrin (TRYP) against dextran sulfate sodium (DSS) induced colitis has been proved, but the concrete mechanism remained elusive. It has been suggested that TRYP could diminish the weight loss and improve the health conditions of mice with DSS induced colitis. Hematoxylin and eosin staining revealed that TRYP could improve the histopathological structure of the colon tissue. Two signaling pathways (TNF-α/NF-κBp65 and IL-6/STAT3) were investigated using immunochemistry and western blot. The detected concentrations of the two cytokines TNF-α and IL-6 showed that their levels decreased after TRYP treatment of the colitis. The protein expression level of NF-κBp65 in cytoplasm increased after TRYP treatment of the induced colitis. However, the protein level of NF-κBp65 in the nucleus decreased after administration of TRYP. The expression level of IκBα, the inhibitory protein of NF-κBp65, was tested and the results suggested that TRYP could inhibit the degradation of IκBα. The phosphorylation level of STAT3 was inhibited by TRYP and the expression level of STAT3 and p-STAT3 decreased after administration of TRYP. We conclude that TRYP improves the health condition of mice with DSS induced colitis by regulating the TNF-α/NF-κBp65 and IL-6/STAT3 signaling pathways via inhibiting the degradation of IκBα and the phosphorylation of STAT3.

[Overview of research projects funding in traditional Chinese medicine oncology field supported by National Natural Science Foundation of China].

In this paper, the funding situation of traditional Chinese medicine oncology research projects supported by National Natural Science Fund from 1986-2016 was reviewed. The characteristics of funded projects were summarized from funding amount, funding expenses, funding category, and the main research contents of projects, etc. At the same time, the main problems in the projects were analyzed in this paper, in order to provide reference for the relevant fund applicants.

Synthesis and Photoluminescent Properties of Eu²âº-Doped BaSiF6 Nanoparticles.

By adjusting the molar ratio of oleic acid (OA), oleylamine (OM), and 1-octadecene (OD) ligands in reaction solution, Eu²âº-doped BaSiF6 nanoparticles were synthesized using a thermal decomposition synthesis route. Eu²âº ions have been successfully doped into BaSiF6 host lattice and strong 4f-4f line emission of the Eu²âº in BaSiF6 matrix is observed. Meanwhile, the photoluminescent (PL) properties of BaSiF6:Eu²âº nanoparticles doping Eu²âº ions at different concentrations were also studied.

Hydrothermal Synthesis and Luminescence Properties of Eu²âº- and Eu³âº-Doped SrAIF5 Nanorods.

Eu²âº- and Eu³âº-doped SrAIF5 nanorods were synthesized via a hydrothermal process. The crystal structure and morphology of the final products were characterized by X-ray diffraction (XRD) and field emission scanning electron microscopy (FESEM). The prepared nanorods' diameters range from 40 to 50 nm, and lengths range from 400 nm to 2 µm along with the doped concentration of rare earth. The f-f transitions of Eu²âº can be observed in the SrAlF5:Eu²âº nanorods at room temperature, and the photo-luminescent (PL) properties of SrAlF5:Eu³âº nanorods are also described.

Preparation, Energy Transfer Characteristics and Colorimetric Properties of Na2Dy4(WO4)7:Eu³âº Nanophosphors.

Eu³âº-doped Na2Dy4(WO4)7 nanophosphors were synthesized via a co-precipitation method. The crystal structure and morphology of the nanophosphors were characterized by X-ray diffraction analysis and field emission scanning electron microscopy, respectively. For all Eu³âº doping concentrations, spherical particles with an average diameter of about 40 nm and consisting of a pure Na2Dy4(WO4)7 phase were obtained. The excitation and emission properties of the nanophosphors were examined by fluorescence spectroscopy and the energy transfer between Eu³âº and Dy³âº was studied. Furthermore, the influence of the Eu³âº concentration on the color coordinates and luminescence intensity is discussed. The nanophosphors could easily be excited by ultraviolet (UV) and near-UV light corresponding to the f-f transitions of Dy³âº. The color coordinates of the nanophosphors light emission are in the white light region and the Commission Internationale de l'Éclairage (CIE) coordinates of the nanophosphors light emission varied between (0.331, 0.354) and (0.405, 0.368) depending on the Eu³âº doping concentration.

Anti-inflammatory effects and related mechanisms in vitro and in vivo of Hedychium coccineum rhizome essential oil.

ETHNOPHARMACOLOGICAL RELEVANCE: Hedychium coccineum rhizome is an anti-inflammatory ethnomedicine used to remedy inflammation-related swelling and bronchial asthma. AIM OF THE STUDY: The study aimed to analyze the phytochemical constituents of H. coccineum rhizome essential oil (EO) and evaluate its in vitro and in vivo anti-inflammatory effects and underlying mechanisms. MATERIALS AND METHODS: Phytochemical constituents of H. coccineum rhizome EO were analyzed using GC-FID/MS. In RAW264.7 macrophages induced by LPS, blockade of PGE2, NO, IL-1ß, IL-6, and TNF-α secretion by H. coccineum rhizome EO was measured, and then Western blot, qRT-PCR, and immunofluorescent staining were used to evaluate its underlying mechanisms. Moreover, we used the xylene-induced ear edema model for testing anti-inflammatory potential in vivo and examined auricular swelling as well as tissue and serum contents of IL-1ß, IL-6, and TNF-α. RESULTS: EO's main components were E-nerolidol (40.5%), borneol acetate (24.8%), spathulenol (4.5%), linalool (3.8%), elemol (3.5%), and borneol (3.4%). In RAW264.7 cells stimulated by LPS, EO downregulated the expression of pro-inflammatory enzyme (iNOS and COX-2) genes and proteins, thereby suppressing pro-inflammatory mediators (NO and PGE2) secretion. Simultaneously, it reduced TNF-α, IL-1ß, and IL-6 release by downregulating their mRNA expression. Besides, H. coccineum EO attenuated LPS-stimulated activation of NF-κB (by reducing IκBα phosphorylation and degradation to inhibit NF-κB nuclear translocation) and MAPK (by downregulating JNK, p38, and ERK phosphorylation). In xylene-induced mouse ear edema, EO relieved auricular swelling and lowered serum and tissue levels of TNF-α, IL-1ß, and IL-6. CONCLUSIONS: H. coccineum EO had powerful in vivo and in vitro anti-inflammatory effects by inhibiting MAPK and NF-κB activation. Hence, H. coccineum EO should have great potential for application in the pharmaceutical field as a novel anti-inflammatory agent.