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Aim To explore the protective roles of lic-ochalcone A ( LA) on mice with cigarette smoke-medi-ated acute lung injury and the related mechanisms. Methods In vivo: Mice were exposed to cigarette smoke ( CS) to establish acute lung injury model. The bronchoalveolar lavage fluid ( BALF ) was conducted for cell counting. The mRNA and protein expression of keratinocyte-derived chemokine ( KC ) , tumor necrosis factor alpha ( TNF-α) , interleukin 1β ( IL-1β) and matrix metalloproteinases ( MMP)-9 in lungs were de-termined. The myeloperoxidase ( MPO ) , superoxide dismutase ( SOD ) activities and glutathione ( GSH ) levels in lungs were quantified. The paraffin sections of lungs were prepared and stained with HE. In vitro:Human lung epithelial cells (BEAS-2B) were exposed to cigarette smoke extract ( CSE ) , which induced cell injury. The releases of interleukin 8 (IL-8) and MMP-9 were assessed. The phosphorylation of mitogen-acti-vated protein kinases ( MAPKs, including ERK1/2, p38 and JNK ) and nuclear factor-κB ( NF-κB ) p65 protein were analyzed by Western blot. Results In vi-vo: The accumulation of inflammatory cells was lower in LA groups than that in model group. In comparison with normal control group, the mRNA and protein lev-els of KC, TNF-α, IL-1βand MMP-9 were significant-ly increased in model group. Following treatment with LA, the above indicators were significantly decreased as compared to model group. In the CS-exposed mice, the MPO activity in lungs was significantly increased, meanwhile the SOD activity and GSH level were signif-icantly decreased compared with the air-exposed ani-mals. CS-induced activity of MPO was significantly in-hibited, which were accompanied by increases in SOD and GSH levels by LA. In vitro: CSE-induced mRNA levels of IL-8 and MMP-9 were significantly inhibited by LA at 2 . 5 and 5 μmol · L-1 . The CSE-induced phosphorylation of ERK1/2 and nucleus NF-κB p65 protein expression were prevented by pretreatment with LA. Conclusions LA has protective effects on CS-ex-posed acute lung injury in mice by preventing CS-in-duced pulmonary inflammation, oxidative stress and protease rise. The exploration of the mechanisms sug-gests that LA exerts protective effects via suppressing ERK1/2/NF-κB pathways.
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Objective Ginger (Zingiber officinale) is widely used as a spice in cooking and as a medicinal herb in traditional herbal medicine. The present study was to investigate the analgesic and anti-inflammatory activities of ginger oil in experimental animal models. Methods The analgesic effect of the oils was evaluated by the acetic acid and hot-plate test models of pain in mice. The anti-inflammatory effect of the oil was investigated in rats, using rat paw edema induced by carrageenan, adjuvant arthritis, and vascular permeability induced by bradykinin, arachidonic acid, and histamine. Indomethacin (1 mg/kg), Aspirin (0.5 g/kg) and Dexamethasone (2.5 mg/kg) were used respectively as reference drugs for comparison. Results The ginger oil (0.25-1.0 g/kg) produced significant analgesic effect against chemically- and thermally-induced nociceptive pain stimuli in mice (P < 0.05, 0.01). And the ginger oil (0.25-1.0 g/kg) also significantly inhibited carrageenan-induced paw edema, adjuvant arthritis, and inflammatory mediators-induced vascular permeability in rats (P < 0.05, 0.001). Conclusion These findings confirm that the ginger oil can be used to treat pain and chronic inflammation such as rheumatic arthritis.
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<p><b>OBJECTIVE</b>To investigate the effect of cryptoporus polysaccharide(CP)on lipopolysaccharide(LPS)-induced production of monocyte chemoattractant protein-1(MCP-1)in human lung epithelial A549 cells.</p><p><b>METHODS</b>A549 cells were stimulated with LPS in the presence or absence of CP. The protein concentration and mRNA expression of MCP-1 were determined by enzyme-linked-immunosobent assay(ELISA)and semi-quantitative RT-PCR, respectively.</p><p><b>RESULT</b>The protein concentration of MCP-1 was significantly increased by LPS 1000 microg/L at 24 h. There were no effects on the growth and viability of A549 cells in the presence of CP 100 microg/L or dexamethasone 1 mumol/L. However, CP 100 microg/L or dexamethasone 1 micromol/L significantly inhibited the protein concentration and mRNA expression of MCP-1 induced by LPS.</p><p><b>CONCLUSION</b>CP can regulate MCP-1 production, which may be associated with its effects on lung inflammation.</p>
Subject(s)
Humans , Cell Line , Chemokine CCL2 , Genetics , Metabolism , Epithelial Cells , Cell Biology , Metabolism , Lipopolysaccharides , Pharmacology , Polyporaceae , Chemistry , Polysaccharides , Pharmacology , Pulmonary Alveoli , Cell Biology , RNA, Messenger , MetabolismABSTRACT
Aim To investigate the changes of phosphodiesterase4(PDE4,type 4 cAMP-specific PDE) activity,TNF-? and neutrophil recruitment in experimental rat lung injury(ALI).Methods ALI in the rat was induced by lipopolysacdharide(LPS).PDE4 activity was measured with HPLC,and the level of TNF-? was detected with ELISA,neutrophil infiltration in bronchoalveolar lavage fluid(BALF) and lung tissues was detected by cell count and morphological analysis.Result Lung tissue PDE4 activity significantly increased as early as 1 h,peaked 6 h,and then markedly lowered at 24 h after intratracheal administration of LPS,while there was a same time-course change of total white cell and neutrophil in the BALF(r=0.83,P
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Objective To study the mechanism of anti-inflammatory effects of licorice flavonoids(LF) isolated from the roots of Glycyrrhiza uralensis(licorice) on lipopolysaccharide(LPS)-induced lung inflammation in mice.Methods Mice were intratracheally instillated with either LPS(4 mg/kg) or saline.At 6 or 24 h after LPS intratracheal instillation,pathological examination and bronchoalveolar lavage were performed and the lung wet/dry weight ratio as an index of acute lung injury was assessed.Then,the numbers of total leukocytes,neutrophils and the activity of superoxide dismutase(SOD) and TNF-? protein in bronchoalveolar lavage fluid(BALF) were measured.LPS-induced myeloporoxidase(MPO) activity and expressions of TNF-? and IL-1? at the mRNA levels and TNF-? at the protein level in lung tissues were determined by RT-PCR and ELISA.Results LPS caused a severe lung inflammation,as indicated by the pathological findings and the lung wet/dry weight ratio.However,oral LF could attenuate these LPS-induced abnormalities.LF could decrease the numbers of total leukocyte cells and neutrophils,and increase the levels of SOD and TNF? BALF.In addition,LF significantly suppressed the MPO activity,TNF-? and IL-1? mRNA expression levels,and TNF-? protein level in the lung tissues.Conclusion Inhibition of inflammatory cytokines expressions and regulation of oxidation/antioxidation of LF may be its anti-inflammatory mechanism in LPS-induced lung inflammation in mice.
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Objective To study the time-course relationship of eotaxin mRNA and TNF-? mRNA expression in the lung tissue of sensitized mice after antigen challenge and the effects of Cryptoporus polysaccharide (CP) on these expression. Methods Eotaxin mRNA and TNF-? mRNA expression was determined by semi-quantitative RT-PCR. The function implications of eotaxin mRNA and TNF-? mRNA expression were examed by detecting the number of total leucocyte and eosinophils in bronchoalveolar lavage fluid (BALF). Results Peak level of TNF-? mRNA expression appeared at 8 h and eotaxin mRNA expression at 24 h in the lung tissue of sensitized mice after antigen challenge. Compared with the control group, total numbers of leukocyte and eosinophil in BALF increased in sensitized mice. CP 3, 10, and 30 mg/kg inhibited eotaxin mRNA and TNF-? mRNA expression, and inflammatory cells accumulation in airway of the sensitized mice in a dose-dependent manner. Conclusion The mechanism of inhibitory effects of CP on eotaxin mRNA and TNF-? mRNA expression may be related to the anti-allergic inflammation.
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Objective To establish a model of asthma mice with spleen-deficiency syndrome (asthma-SDS) and to investigate the effects of Cryptoporus volvatus ferment substance (CVFS) on the airway hyperresponsiveness and inflammation in model mice. Methods An asthma-SDS model of mice was established by ovalbumin (OVA)-sensitized plus over-eating and over-exerting. The changes of lung resistance (R_L), inflammatory cells in bronchoalveolar lavage fluid (BALF), lung tissue pathology, and spleen index were observed. Results Compared with the simple asthma model of mice, the airway hyperresponsiveness, eosinophils number in the BALF, lung tissue pathology, and spleen index in the asthma-SDS model of mice showed a significant difference (P
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Objective: To investigate the anti-inflammatory, bacteriostatic, diuretic, antispasmodic and immunoenhancement effect of Niao Gan Ning(NGN). Methods: The tests of inhibiting the leukocyte infiltration, in-vitro bacteriostasis, water loading with metabolism cage, isometric tension recording and the phagocytosis of abdominal macrophages(AM) were conducted. Results: NGN could obviously inhibit the wandering of leukocyte in abdominal cavity and decreased the number of WBC in mice, and exert bacteriostatic effect to various degrees. NGN also increase the urine volume in water load rats, inhibited contraction of bladder and ureter smooth muscle induced by Carbacol and histamine in rabbits and rats, and increased phagocytosis of the chicken red cells by AM. Conclusion: NGN has a strong anti-inflammatory, bacteriostatic, diuretic and antispasmodic effect.
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Aim Establish a novel mouse model of airway goblet cell hyperplasia and mucus hypersecretion.Method BALB/c mice were sensitized subcutaneously with ovalbumin(OVA) allergens in aluminium hydroxide at d 0,re-sensitized once intraperitoneally d 10 after first sensitization,and challenged with OVA aerosolly daliy from d 15 to d 21 after first sensitization.Inflammatory cell number in BALF,eosinophil infiltration in the lung tissue with HE stain and goblet cells in the bronchial mucous membrane with PAS stain were examined.Dexamethasone was employed to validate the model.Results Mice sensitized and challenged with OVA showed a significantly hyperplasia of goblet cells in the bronchial mucous membrane,increased mucus in the alveolar cavity,eosinophil infiltration in the lung tissue and increased number of inflammatory cells in BALF.Those pathological changes were inhibited by dexamethasone and mIL-2 plasmid.Conclusion This model helps to screen the new drugs for mucus hypersecretion and research on the pathological mechanism of airway mucus hypersecretion.
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a-Terpineol as an another antiasthmatic principle of essential oil of Artemisia argyi was studied. It had relaxant effect on isolated guinea pig tracheal smooth muscle preparations, the effective threshold concentrations being between 2. l-4.2x10-5 g/ml, and the EC50 being 0.71-1.15x10-4g/ml. It could protect guinea pigs from the acetylcholine and histamine-induced asthma when given orally or aer-osolly. The level of cAMP in the tracheal smooth muscle of guinea pigs was elevated in the presence of l0-4g/ml a- terpineol. The drug could block the development of desensitization to isoproterenol on isolated guinea pig tracheal smooth muscle preparations, and its relaxant effect did not be- influenced on the desensitized preparations also. In addition, a-terpineol had the Inhibitory effect of anaphylactic mediators release antagonistic effect of the mediators, antitussive and expectorant effect, and the inhibitory effect on isolated ed guinea pig atria. The toxiicological studies showed that it had good safety margin. ( + ) - a-Terpineol amd (-) a -terpineol had similarquality and potency of actions.