beta-elemene and Disease-Models--Animal

This study aims to investigate the effects of β-elemene on a mouse model of heart failure (HF) and to elucidate the underlying mechanisms in vitro approaches. In this study, left anterior descending (LAD)-induced HF mouse model and oxygen-glucose deprivation/recovery (OGD/R)-induced H9C2 model were leveraged to assess the therapeutic effects of β-elemene. Histological examination, western blot and quantitative real-time PCR analysis (RT-qPCR) and immunofluorescence staining was utilized to elucidate mechanism of β-elemene in lipid-induced inflammation. Results showed that β-elemene improved heart function in HF mice evidenced by the increase of cardiac ejection fraction (EF) and fractional shortening (FS) values. Furthermore, β-elemene administration rescued ventricular dilation, lipid accumulation, and inflammatory infiltration in arginal areas of mice myocardial infarction. At transcription level, β-elemene augmented the mRNA expression of fatty acid oxidation-associated genes, such as peroxisome proliferator-activated receptor-β (PPARβ). In vitro, treatment of β-elemene increased carnitine palmitoyltransferase 1A (CPT1A) and sirtuin 3 (SIRT3). Hallmarks of inflammation including the nuclear translocation of nuclear factor κB (NF-κB) and the degradation of inhibitory κBα (IκBα) were significantly suppressed. Consistently, we observed down-regulation of interleukin-6 (IL-6) and pro-inflammatory cytokines (such as TNFα) in β-elemene treated H9C2 cells. Finally, molecular docking model predicted an interaction between β-elemene and PPARβ protein. Furthermore, β-elemene increased the expression of PPARβ, which was validated by antagonist of PPARβ and siRNA for PPARβ.

Topics: Animals; Anti-Inflammatory Agents; Cardiotonic Agents; Cell Line; Cell Survival; Disease Models, Animal; Endoribonucleases; Heart Failure; Inflammation; Lipids; Male; Mice; Mitochondria; Molecular Docking Simulation; Multienzyme Complexes; NF-kappa B; NF-KappaB Inhibitor alpha; PPAR-beta; Protein Serine-Threonine Kinases; Rats; Sesquiterpenes

β-Elemene (1-methyl-1-vinyl-2,4-diisopropenyl-cyclohexane), a natural sesquiterpene-derived curcumae radix, exhibits a variety of pharmacologic properties including anticancer. However, the molecular action of β-elemene in chemical-induced skin carcinogenesis remains unclear. Therefore, the present study executes to investigate a possible effect of β-elemene in the 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin tumor model. The experimental mice were subjected to execute two-stage skin carcinogenesis and it has been initiated by the addition of DMBA on the dorsal portion of the mouse skin. One week after, for chemical carcinogen of mice, topical exposure of DMBA has been induced following with TPA (5 nmol) in acetone (200 μL) given weekly twice for 20 weeks respectively. After completion of the experimental period, we noticed that 100% of tumor incidence, histopathological changes, decreased lipid peroxidation (LPO), and decreased antioxidant levels in DMBA/TPA-promoted skin carcinogenesis. Furthermore, enhanced activity of inflammatory protein markers (nuclear factor [NF]-κB, tumor necrosis factor-α, interleukin-6, cyclooxygenase-2, and nitric oxide synthase) and cell-proliferative messenger RNA markers (PCNA, cyclin D1), and increased antiapoptotic protein Bcl-2; decreased proapoptotic protein marker events Bax and caspase 3 and 9 expressions were noticed in DMBA/TPA promoted skin tissue. In this study, we noticed that β-elemene noticeably reversed the histopathological changes and antioxidant levels in tumor-bearing mice. Conversely, β-elemene effectively inhibits inflammation, cell proliferation events, and enhances proapoptotic factors, by suppression of NF-κB transcriptional activation in DMBA/TPA animals. Thus, we concluded that β-elemene prevents DMBA/TPA promoted skin carcinogenesis through its antioxidant and abate inflammation markers and cell-proliferative markers also activating proapoptotic molecules.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Carcinogenesis; Carcinogens; Disease Models, Animal; Mice; NF-kappa B; Sesquiterpenes; Signal Transduction; Skin Neoplasms; Tetradecanoylphorbol Acetate

The present study aimed to investigate the significant role of β-elemene in mouse models of oxygen-induced retinopathy (OIR). C57BL/6J neonatal mice were used to establish OIR models. They were divided into four groups: Normoxia, OIR, OIR control and OIR‑treated. Mice in the OIR group were exposed to 75±5% oxygen for 5 days and returned to a normal oxygen environment on postnatal day 12 (P12). The OIR treated group was intravitreally injected with 1 µl β‑elemene on P12 and subsequently returned to a normal oxygen environment for 5 days (P12‑P17). Retinas were obtained on P17. Retinal neovascularization (RNV) was detected using adenosine diphosphatase staining and analyzed by counting the nuclei of neovascular endothelial cells. Vascular endothelial growth factor (VEGF) expression was determined by reverse transcription‑quantitative polymerase chain reaction, immunohistochemistry and western blot analysis. MicroRNA (miRNA/miR) microarrays were used to screen out differentially expressed miRNAs between the OIR and β‑elemene‑treated groups. Binding the 3'‑untranslated region (UTR) of VEGF and miR‑27a was confirmed using luciferase assays. It was found that high oxygen concentrations accelerated RNV and increased the number of preretinal neovascular cells; β‑elemene treatment reduced these effects. VEGF mRNA and protein expression was higher in the OIR and OIR control groups, compared with the normoxia and OIR‑treated groups. Further, it was shown that miR‑22, miR‑181a‑1, miR‑335‑5p, miR‑669n, miR‑190b, miR‑27a and miR‑93 were upregulated in the OIR‑treated group, and downregulated in the OIR group. The prediction websites TargetScan and miRanda revealed that VEGF contained a potential miR‑27a binding site in its 3'‑untranslated region (UTR). Luciferase assays demonstrated that miR‑27a directly bound to the 3'‑UTR of VEGF. In vitro experiments demonstrated that miR‑27a inhibited VEGF expression. In addition, β‑elemene treatment upregulate miR‑27a expression in vivo and in vitro. When miR‑27a expression was depleted by miR‑27a inhibitor, the protective effect of β‑elemene on RNV was eliminated. The present study demonstrated that β‑elemene reduced RNV in mouse OIR models via miR‑27a upregulation, leading to reduced VEGF expression. This finding may contribute to the development of novel therapeutic strategies for human retinopathy.

Topics: Animals; Animals, Newborn; Disease Models, Animal; Endothelial Cells; Gene Expression Regulation; Humans; Infant, Newborn; MicroRNAs; Oxygen; Retina; Retinal Neovascularization; Retinopathy of Prematurity; Sesquiterpenes; Vascular Endothelial Growth Factor A

Paclitaxel is highly effective at killing many malignant tumors; however, the development of drug resistance is common in clinical applications. The issue of overcoming paclitaxel resistance is a difficult challenge at present. In this study, we developed nano drugs to treat paclitaxel-resistant lung adenocarcinoma. We selected cabazitaxel and β-elemene, which have fewer issues with drug resistance, and successfully prepared cabazitaxel liposome, β-elemene liposome and cabazitaxel-β-elemene complex liposome with good flexibility. The encapsulation efficiencies of cabazitaxel and β-elemene in these liposomes were detected by precipitation microfiltration and microfiltration centrifugation methods, respectively. Their encapsulation efficiencies were all above 95%. The release rates were detected by a dialysis method. The release profiles of cabazitaxel and β-elemene in these liposomes conformed to the Weibull equation. The release of cabazitaxel and β-elemene in the complex liposome were almost synchronous. The pharmacodynamics study showed that cabazitaxel flexible liposome and β-elemene flexible liposome were relatively good at overcoming paclitaxel resistance on paclitaxel-resistant lung adenocarcinoma. As the flexible complex liposome, the dosage of cabazitaxel could be reduced to 25% that of the cabazitaxel injection while retaining a similar therapeutic effect. It showed that β-elemene can replace some of the cabazitaxel, allowing the dosage of cabazitaxel to be reduced, thereby reducing the drug toxicity.

Topics: Adenocarcinoma of Lung; Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Disease Models, Animal; Drug Resistance, Neoplasm; Humans; Liposomes; Mice; Molecular Structure; Paclitaxel; Particle Size; Sesquiterpenes; Taxoids; Tumor Burden; Xenograft Model Antitumor Assays

β-elemene, a compound extracted from Curcuma wenyujin plant, exhibits anticancer activity in many cancer types. However, the detailed mechanism by which β-elemene inhibits growth of nasopharyngeal carcinoma (NPC) cells remains unknown. We showed that β-elemene reduced phosphorylation of signal transducer and activator of transcription 3 (Stat3), and protein expressions of DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2). Exogenously expressed Stat3 antagonized the effect of β-elemene on DNMT1 and EZH2 expressions. Furthermore, overexpressions of DNMT1 and EZH2 reversed the effect of β-elemene on phosphorylation of Stat3 and cell growth inhibition. Intriguingly, exogenously expressed DNMT1 overcame β-elemene-inhibited EZH2 protein expression and promoter activity. On the contrary, silencing of EZH2 and DNMT1 genes feedback strengthened the effect of β-elemene on phosphorylation of Stat3. Consistent with this, β-elemene inhibited tumor growth, phosphorylation of Stat3, expressions of DNMT1 and EZH2 in a mouse xenograft model. Collectively, this study shows that β-elemene inhibits NPC cell growth via inactivation of Stat3, and reduces DNMT1 and EZH2 expressions. The interplay of DNMT1 and EZH2, and the mutual regulations among Stat3, EZH2 and DNMT1 contribute to the overall responses of β-elemene. This study uncovers a novel mechanism by which β-elemene inhibits growth of NPC cells.

Topics: Animals; Carcinoma; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferation; Disease Models, Animal; DNA (Cytosine-5-)-Methyltransferase 1; Enhancer of Zeste Homolog 2 Protein; Feedback, Physiological; Female; Humans; Mice, Nude; Nasopharyngeal Carcinoma; Nasopharyngeal Neoplasms; Phosphorylation; Promoter Regions, Genetic; Sesquiterpenes; STAT3 Transcription Factor

Glioma is the most frequent primary central nervous system tumor. Although the current first-line medicine, temozolomide (TMZ), promotes patient survival, drug resistance develops easily. Thus, it is important to investigate novel therapeutic reagents to solidify the treatment effect. β-Elemene (bELE) is a compound from a Chinese herb whose anticancer effect has been shown in various types of cancer. However, its role in the inhibition of glioma stem-like cells (GSLCs) has not yet been reported. We studied both the in vitro and the in vivo inhibitory effect of bELE and TMZ in GSLCs and parental cells and their combined effects. The molecular mechanisms were also investigated. We also optimized the delivery methods of bELE. We found that bELE selectively inhibits the proliferation and sphere formation of GSLCs, other than parental glioma cells, and TMZ exerts its effects on parental cells instead of GSLCs. The in vivo data confirmed that the combination of bELE and TMZ worked better in the xenografts of GSLCs, mimicking the situation of tumorigenesis of human cancer. Notch1 was downregulated with bELE treatment. Our data also demonstrated that the continuous administration of bELE produces an ideal effect to control tumor progression. Our findings have demonstrated, for the first time, that bELE could compensate for TMZ to kill both GSLCs and nonstem-like cancer cells, probably improving the prognosis of glioma patients tremendously. Notch1 might be a downstream target of bELE. Therefore, our data shed light on improving the outcomes of glioma patients by combining bELE and TMZ. Stem Cells Translational Medicine 2017;6:830-839.

Topics: Animals; Carcinogenesis; Cell Line, Tumor; Cell Proliferation; Disease Models, Animal; Down-Regulation; Drug Synergism; Glioma; Humans; Male; Mice, Nude; Neoplastic Stem Cells; Receptor, Notch1; Sesquiterpenes; Spheroids, Cellular; Temozolomide

Inflammation is part of the non-specific immune response that occurs in reaction to any type of bodily injury. In some disorders the inflammatory process, which under normal conditions is self-limiting, becomes continuous and chronic inflammatory diseases develop subsequently including cardiovascular diseases, diabetes, cancer etc. Barks of Delonix regia is used traditionally in the treatment of inflammatory diseases. Therefore, in this study we evaluated the therapeutic potential of D. regia ethanol extract and its active constituent β-Elemene with special interest in inflammation model using standard in vivo anti-inflammatory models: Carrageenan-induced paw edema, Cotton pellet granuloma, and Acetic acid-induced vascular permeability. To explicate the mechanism of action for the possible anti-inflammatory activity, we determined the level of major inflammatory mediators (NO, iNOS, COX-2-dependent prostaglandin E2 or PGE2), and pro-inflammatory cytokines (TNF-a, IL-1b, IL-6, and IL-12). Additionally, we determined the toll-like receptor 4 (TLR4), Myeloid differentiation primary response gene 88 (MyD88), by mRNA expression in drug treated LPS-induced murine macrophage model. To explore the mechanism of anti-inflammatory activity, we evaluated expression of c-Jun N-terminal kinases (JNK), nuclear factor kappa-B cells (NF-kB), and NF-kB inhibitor alpha (IK-Ba). Furthermore, we determined the acute and sub-acute toxicity of D. regia extract in BALB/c mice. This study established a significant anti-inflammatory activity of D. regia extract and β-Elemene along with the inhibition of TNF-a, IL-1b, IL-6 and IL-12 expressions. Further, the expression of TLR4, NF-kBp65, MyD88, iNOS and COX-2 molecules were reduced in drug-treated groups, but not in the LPS-stimulated untreated or control groups, Thus, our results collectively indicated that the D. regia extract and β-Elemene can efficiently inhibit inflammation.

Topics: Acetic Acid; Animals; Anti-Inflammatory Agents; Capillary Permeability; Carrageenan; Cyclooxygenase 2; Cytokines; Disease Models, Animal; Edema; Fabaceae; Granuloma; Inflammation Mediators; Mice; Mice, Inbred BALB C; Plant Extracts; Rats; Rats, Wistar; Sesquiterpenes; Signal Transduction; Toll-Like Receptor 4

This paper explores the underlying mechanism through which β-elemene inhibits the growth of intraocular melanoma in a mouse model. C57BL/6J mice were administered a subretinal injection of B16F10 melanoma cells and divided into two groups: treatment and control. The treatment group was administered β-elemene through an intravitreal injection and the control group was injected with a blank emulsion. After 21 days of continuous treatment, tumor masses were removed and weighed. The mRNA expression levels of the urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), matrix metalloproteinase (MMP)-2, and MMP-9 were assayed by real-time PCR, and the protein expression levels of uPA, uPAR, MMP-2, and MMP-9 were assayed by immunocytochemistry and western blotting. Tumor size was inhibited by β-elemene in the treatment group, and the expressions of uPA, uPAR, MMP-2, and MMP-9 were all downregulated at both the mRNA and the protein level compared with the control group. In a mouse model of intraocular melanoma, β-elemene inhibits tumor growth by downregulating the expression of uPA, uPAR, MMP-2, and MMP-9.

Topics: Animals; Disease Models, Animal; Eye Neoplasms; Gene Expression Profiling; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Immunohistochemistry; Male; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Medicine, Chinese Traditional; Melanoma; Melanoma, Experimental; Mice; Mice, Inbred C57BL; Neoplasm Invasiveness; Neoplasm Metastasis; Neoplasm Transplantation; Receptors, Urokinase Plasminogen Activator; Sesquiterpenes; Urokinase-Type Plasminogen Activator

The present study aimed at investigating the possible effects of β-elemene on the progression of atherosclerosis in a rabbit model. The rabbit atherosclerosis model was established by the combination of balloon angioplasty-induced endothelial injury and an atherogenic diet fed to the rabbits. New Zealand White rabbits were randomly divided into four groups (8/group): the normal control group (fed with normal chow diet), and three experimental groups, placebo group, atorvastatin group, and β-elemene group (received the atherogenic diet). After two weeks on the diet, the three experimental groups underwent balloon injury at right common carotid artery and were treated with drugs or placebo for five weeks. Serum lipids were measured. Carotid artery lesions were isolated for histological and immunohistochemical analysis. In vitro, RAW264.7 macrophages were pretreated with β-elemene and ox-LDL for 24 h and the viability of macrophages was assayed using the MTT method. TNF-α and IL-6 were also determined. Compared with the control group, the thickness of the atherosclerosis lesion in the placebo group was significantly increased; The thickness the drug treatment groups were significantly decreased, compared with that of the placebo group. The infiltration of macrophage was markedly reduced in the β-elemene group compared with that of the placebo group. β-elemene treatment also reduced the levels of TC, TG, and LDL-C, compared with the placebo group. β-elemene decreased the TNF-α and IL-6 levels in vitro. In conclusion, our results demonstrated that β-elemene retarded the progression of atherosclerosis in vivo and in vitro, which may be related to the capacity of β-elemene to reduce the infiltration of macrophages and suppress inflammatory factors.

Topics: Animals; Atherosclerosis; Disease Models, Animal; Disease Progression; Humans; Interleukin-6; Macrophages; Male; Rabbits; Sesquiterpenes; Tumor Necrosis Factor-alpha

β-Elemene, a novel antitumor plant drug extracted from the traditional Chinese medicinal herb Zedoary, has been shown to be effective against a wide variety of tumors. Recent studies have indicated that β-elemene can inhibit the growth of lung cancer cells; however, the exact mechanism of β-element's action in lung cancer remains largely unknown. In the present study, the antitumor effect of β-elemene on human lung cancer cells and the mechanism involved has been investigated.. The inhibitory effects of β-elemene on cell growth were measured by Trypan Blue exclusion and MTT assay. Flow cytometric analysis was used to detect the cells' apoptotic rate. The expression of P53 mRNA and protein were measured by RT-PCR and Western blot analysis, respectively. Exosomes were isolated by differential centrifugation steps and analyzed by electron microscopy and western blotting. P53 knockdown cells were established through transfection with P53 siRNA. To investigate the effect of β-elemene on the tumor growth in vivo, a Xenograft nude mouse model was established by injecting the A549 cells into the back of a BABL/c nude mouse.. β-Elemene markedly inhibited growth and induced apoptosis in lung cancer cells. The levels of the anti-apoptotic genes Bcl-2 and Bcl-xl in A549 cells decreased, while expression of P53 and production of exosomes increased after β-elemene treatment. Further siRNA studies suggested that the effect of β-elemene on A549 cells is dependent on P53 expression. Exosomes derived from A549 cultured with a human lung cancer cell line exhibited decreased tumor cell proliferation. The in vivo study demonstrated that β-elemene inhibited tumor growth, and up-regulated the expression of P53 and the release of exosome.. Our results demonstrated β-elemene acts on lung cancer cells in a P53 dependent manner and exosomes are involved in the regulation of cell proliferation.

Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Line, Tumor; Cell Proliferation; Cell Survival; Disease Models, Animal; Exosomes; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Male; Sesquiterpenes; Tumor Burden; Tumor Suppressor Protein p53; Up-Regulation; Xenograft Model Antitumor Assays

β-Elemene, an active component of herb medicine Curcuma wenyujin, has been shown to antagonize glioblastoma cells by inducing apoptosis. However, how β-elemene induces apoptosis of these cells remains unclear. In this study, we report that β-elemene disrupted the formation of the Hsp90/Raf-1 complex, a key step in maintaining the conformation stability of Raf-1, and caused deactivation of Raf-1 and inhibition of the ERK pathway, thereby leading to apoptosis of glioblastoma cells. Specifically, treatment of glioblastoma cell lines with β-elemene attenuated phosphorylation of multiple members of the kinase families in the Ras/Raf/MEK/ERK cascade, including Raf-1 and ERK as well as downstream signaling targets such as Bcl-2. These results suggest that the Hsp90/Raf-1 complex could be a promising molecular target for new drug development for the treatment of glioblastoma.

Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Brain Neoplasms; Cell Line, Tumor; Disease Models, Animal; Dose-Response Relationship, Drug; Flow Cytometry; Gene Expression Regulation, Neoplastic; Glioblastoma; HSP90 Heat-Shock Proteins; Humans; Immunoprecipitation; Mice; Mice, Nude; Proto-Oncogene Proteins c-bcl-2; Proto-Oncogene Proteins c-raf; Sesquiterpenes; Signal Transduction; Time Factors; Xenograft Model Antitumor Assays

It is generally accepted that the oxidative stress and the proliferative activity of vascular smooth muscle cells (VSMCs) contribute to the pathogenesis of neointimal hyperplasia after vascular injury. Although β-elemene (β-1-methyl-1-vinyl-2, 4-diisopropenyl-cyclohexane) has been used as an antitumour drug, its therapeutic effect on vascular diseases has not yet been determined. In this study, we investigated whether β-elemene could inhibit oxidative damage of vascular endothelial cells, suppress VSMCs growth and prevent neointimal hyperplasia.. β-elemene can increase the survival rate of human umbilical vein endothelial cells in vitro. By measuring the malondialdehyde content, total antioxidant capacity, superoxide dismutase activity, catalase activity, glutathione peroxidase activity and nitric oxide levels, we assessed the protective effect of β-elemene in the vascular endothelium model against oxidant-induced injury. Μoreover, β-elemene inhibited cell proliferation and induced apoptosis in cultured VSMCs. In a flow culture system, β-elemene reduced the migration distance of VSMCs. By transwell migration assay, β-elemene was found to reduce the migration cell number of VSMCs, but not affect the HUVECs migration. In a rat carotid artery balloon injury model, administration of β-elemene significantly reduced the ratio of intimal area to medial area and neointima formation.. Our results indicate that β-elemene is effective in protecting the endothelial cells from injury induced by hydrogen peroxide in vitro, inhibiting smooth muscle cell proliferation/migration and inhibiting neointima formation in vivo after vascular injury.

Topics: Animals; Carotid Arteries; Cell Movement; Cell Proliferation; Cell Survival; Disease Models, Animal; Endothelial Cells; Humans; Hydrogen Peroxide; Hyperplasia; Male; Neointima; Oxidative Stress; Rats; Rats, Sprague-Dawley; Sesquiterpenes; Umbilical Veins

It has been demonstrated that β-elemene could protect against carbon tetrachloride (CCl(4))-induced liver fibrosis in our laboratory work, and the aim of this paper is to reveal the protective mechanisms of β-elemene. The hepatic fibrosis experimental model was induced by the hypodermical injection of CCl(4) in Wistar male rats. β-elemene was intraperitoneally administered into rats for 8 weeks (0.1 mL/100 g bodyweight per day), and plasma endotoxin content was assayed by biochemistry. The serum TNF-α level was detected using radioactive immunity. CD14 expression in rat livers was measured by immunohistochemistry and Western blot. The results showed that β-elemene can downregulate the levels of plasma endotoxins, serum TNF-α, and hepatic CD14 expression in rats with liver fibrosis. β-elemene plays an important role in downregulating the lipopolysaccharide signal transduction pathway, a significant pathway in hepatic fibrosis development.

Topics: Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; China; Curcuma; Disease Models, Animal; Down-Regulation; Endotoxins; Injections, Intraperitoneal; Lipopolysaccharide Receptors; Liver; Liver Cirrhosis; Male; Plant Preparations; Rats; Rats, Wistar; Sesquiterpenes; Tumor Necrosis Factor-alpha

The objective of this work was to investigate the antiulcerogenic and anti-inflammatory activities of the essential oil from Pterodon emarginatus seeds.. The following tests were used: ulcers induced by ethanol, indometacin and HCl/ethanol, and pleurisy induced by carrageenan in Swiss albino rats. The rats were treated by the oral route with essential oil of P. emarginatus seeds.. The essential oil at 100, 300 and 500 mg/kg exhibited significant protection against ulcers induced by ethanol, indometacin and HCl/ethanol (P < 0.001). The essential oil caused a marked reduction in the exudate volume and inhibited leucocyte and neutrophil influx (P < 0.05) in carrageenan-induced pleurisy. Moreover, the essential oil significantly decreased nitric oxide (NO) and interleukin-1 (IL-1) levels, without affecting tumour necrosis factor-alpha production.. The results demonstrated the marked antiulcerogenic and anti-inflammatory effects of the essential oil from P. emarginatus, which are, at least in part, a consequence of NO and IL-1 modulation. P. emarginatus or its constituents might represent new therapeutic options to treat gastric ulcers and inflammatory diseases.

Topics: Administration, Oral; Alkyl and Aryl Transferases; Animals; Anti-Inflammatory Agents; Anti-Ulcer Agents; Brazil; Carrageenan; Disease Models, Animal; Dose-Response Relationship, Drug; Ethanol; Fabaceae; Indomethacin; Interleukin-1alpha; Male; Medicine, Traditional; Mice; Monocyclic Sesquiterpenes; Nitric Oxide; Oils, Volatile; Omeprazole; Peptic Ulcer; Pleurisy; Polycyclic Sesquiterpenes; Ranitidine; Seeds; Sesquiterpenes; Tumor Necrosis Factor-alpha