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A new pyranocoumarin as an analogue of calophyllolide, compound 6, is firstly prepared and reported to have potent anti-inflammatory activity on carrageenin-induced edema in rats.
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The aim of the present study is to investigate the effects of Vam3 which is one of the dihydroxystilbene compounds on expressions of ICAM-1 in the lungs of OVA-induced asthmatic mice and the mechanisms of anti-airway inflammation. Balb/c mice were challenged with OVA inhalation. Lung tissues were stained with Mayer's hematoxylin and eosin for histopathologic examination. The expression of ICAM-1 in the lungs of mice was analyzed by Western blotting and immunohistochemistry method. The NF-kappaB activities were detected by NF-kappaB-luc reporter genetic transient transfection method. The activities of MMP-9 induced by LPS, TNF-alpha and PMA in THP-1 cells were determined by gelatin zymography method. The results showed that Vam3 could inhibit the expression of ICAM-1 in the OVA-induced mouse model. In addition, Vam3 could significantly suppress the activities of NF-kappaB in A549 cells and MMP-9 in THP-1 cells induced by LPS, TNF-alpha and PMA. These results suggested that Vam3 could alleviate the asthmatic inflammation by decreasing ICAM-1 expression in asthmatic mice, down regulating NF-kappaB and MMP-9 activities. Compound Vam3 showed inhibitory effects on inflammatory signal pathways involved in asthma.
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Aim To study the effects of ginsenoside-Ro on cell proliferation and cytokine production in murine splenocytes. Methods The effect of ginsenoside-Ro on murine splenocytes proliferation was studied using [3 H] thymidine incorporation assay. Effects of ginsenoside-Ro on the production of cytokines interleukin-2 (IL-2), interferon-γ (IFN-γ) and interleukin-4 (IL-4) from murine splenocytes were detected by ELISA method. Effects of ginsenoside-Ro on mRNA level of Th1 cytokine IFN-γ and Th2cytokine IL-4 were evaluated by reverse transcription polymerase chain reaction (RT-PCR) analysis.Results Ginsenoside-Ro showed no mitogenic effect on unstimulated murine splenocytes. It enhanced the proliferation of Con A-induced murine splenocytes and the production of IL-2 at concentrations of 1 - 10decreased the production and expression of Th1 cytokine IFN-γ in Con A-induced murine splenocytes at regulating the production and expression of Th1/Th2 cytokines in murine splenocytes.
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AIM To study the protective effect of Gn-3 (a stilbene polymer isolated from Gnetum parvifolium) against liver injury induced by CCl4, N-acetyl-p-aminophenol (APAP) and Bacillus Calmette-Guerin (BCG) plus bacterial lipopolysaccharide (LPS) in mice. METHODS The experimental model of liver injury were induced by 0.1% CCl4 ip (10 mL*kg-1*d-1 for 3d), APAP ip (150 mg*kg-1) or BCG (5 mg) plus LPS (7.5 μg) in mice. The levels of ALT in serum, MDA and GSH in liver tissues were detected. The histopathologic changes were observed by light microscope. RESULTS Gn-3 was shown to markedly reduce the elevated serum ALT levels, liver tissue MDA and improve the histopathological changes in all the three experimental liver injury models. No effect of Gn-3 was observed on the liver GSH level in liver injury mice. CONCLUSION Gn-3 was found to inhibit the development of liver injury caused by CCl4, APAP, or BCG plus LPS. This means that Gn-3 has liver protective effects.
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AIM To investigate the effects of ginkgolide B on arachidonic acid (AA) metabolizing enzymes and the level of intracellular calcium in rat polymorphonuclear leukocytes. METHODS Intracellular free calcium was quantitated by Fura-2 fluoresence technique. Phospholipase A2 (PLA2) activity was determined by incorporating 3H-arachidonic acid in leukocytes. 5-Lipoxygenase (5-LO) activity was evaluated by RP-HPLC. RESULTS In comparison with control, ginkgolide B at final concentration of 0.1-10 μmol*L-1 inhibited A23187 induced AA release by 10.9%-22.2%; at final concentration of 0.1-50 μmol*L-1, ginkgolide B inhibited LTB4 and 5-HETE synthesis stimulated by PAF by 29.4%-88.8% and 26.2%-89.3% respectively. At the final concentration of 0.1-100 μmol*L-1, ginkgolide B decreased the rise of intracelluar calcium level induced by pletelet activating factor (PAF) and N-formyl-methionine-leucine-phenglalanine (fMLP) by 13.9%-51.4% and 2.2%-36.6%, respectively. CONCLUSION Ginkgolide B was found to significantly inhibit PLA2 and 5-LO activities, as well as the increase of the intracellular calcium induced by PAF.
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AIM To study the inhibitory effects of indomethacin and meloxicam on NF-κB from lipopolysaccharide (LPS) stimulated peritoneal macrophages of mice. METHODS NF-κB was measured with the method of electrophoretic mobility shift assay (EMSA). RESULTS After induction by LPS at the concentrations of 1 and 3 μg.mL-1, the NF-κB content of the mouse peritoneal macrophages increased markedly. Indomethacin and meloxicam, at the concentrations of 10-7-10-5 mol.L-1, decreased the activation of NF-κB at the concentrations of 1 and 3 μg.mL-1 in activated mouse peritoneal macrophages induced with LPS at the concentrations of 1 and 3 μg.mL-1. CONCLUSION The inhibitory effects of indomethacin and meloxicam on NF-κB activation may be one of their mechanisms of antiinflammatory actions.
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A protein designated as Flammulina Velutipes (FV) protein was isolated from the cultured mycelium of FV and purified to homogeneity by CM cellulose CM 52 and gel filtration chromatography. The molecular weight of FV protein were found to be 1.75?10~4u with pI 4.3. Amino acid analysis of FV protein indicated the presence of 14 kinds of amino acids, especially rich in Glu, Asp and Thr.Potent inhibitory effect of FV protein on thrombus formation, in the blood was observed in vitro when rats were given intravenously. The length of thrombus was shortened and the dry weight of the thrombus decreased significantly at the dose of 7.5?10~(-7) mol/kg. Thrombus formation was completely inhibited at the dose of 10~()-8 mol/kg. The IC_(50) was found to be 4.4?10~(-7) mol/kg. FV protein was shown to inhibit collegen induced aggregation of rat platelets both in vitro and in vivo. Its concentration for complete inhibition in vitro was 7.5?10~(-5) mol/L. The IC_(50) was found to be 4?10~(-5)mol/ L. However, FV protein dose of 1.25?10~(-5) mol/kg was required for 60% inhibition in vivo