ABSTRACT
<p><b>OBJECTIVE</b>To study the anti-inflammatory mechanisms of total glycosides of Acanthopanax Giraldii (TGA).</p><p><b>METHODS</b>The changes of prostaglandin E(2)(PGE(2)), tumor necrosis factor (TNF-alpha), nitric oxide (NO), and expressions of COX-1 mRNA and COX-2 mRNA in BALB/c mouse macrophages were observed by the radioimmunoassay, ELISA and nitric acid reduction and RT-PCR in the presence or absence of TGA.</p><p><b>RESULTS</b>(1) TGA could significantly decrease the production of PGE(2)and NO in mouse peritoneal macrophages. The inhibitory rate to LPS-induced PGE(2)production was 87% (TGA 100 mg/L, P<0.05, vs. LPS) and 62% (TGA 20 mg/L, P<0.05, vs. LPS), respectively. The inhibitory rate of NO production in mouse peritoneal macrophages was 49% (TGA 100 mg/L, P<0.05, vs. LPS) and 21% (TGA 20 mg/L, P<0.05 vs. LPS), respectively. TGA could not inhibit LPS-induced TNF-alpha production in mouse peritoneal macrophages. (2) TGA also inhibited the expression of COX-1 and COX-2 mRNA in RAW264.7 cells. The inhibitory rate of TGA to COX-1 mRNA was 22% (TGA 100 mg/L, P<0.05, vs. blank). The inhibitory rate of TGA to COX-2 mRNA was 55% (TGA 20 mg/L, P<0.05, vs. LPS) and 100% (TGA 100 mg/L, P<0.01 vs. LPS), respectively.</p><p><b>CONCLUSION</b>The anti-inflammatory mechanisms of TGA for inhibiting the production of NO and PGE(2)are through inhibiting COX-2 mRNA expression without TNF-alpha changes.</p>
Subject(s)
Animals , Female , Mice , Anti-Inflammatory Agents , Pharmacology , Cell Line , Cyclooxygenase 1 , Genetics , Cyclooxygenase 2 , Genetics , Dinoprostone , Metabolism , Drugs, Chinese Herbal , Pharmacology , Eleutherococcus , Gene Expression Regulation, Enzymologic , Glycosides , Pharmacology , Lipopolysaccharides , Pharmacology , Macrophages, Peritoneal , Cell Biology , Metabolism , Mice, Inbred BALB C , Nitric Oxide , Metabolism , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of slenderstyle acanthopanax root-bark on cyclooxygenase in vivo and in vitro.</p><p><b>METHOD</b>Contents of 6-keto-PGF1alpha in bovine aorta endothelial cells, PGE2 in mouse abdominal macrophages, and 6-keto-PGF1alpha in rat stomach tissue were determined. The ulcer index in rat gastric mucosa was measured.</p><p><b>RESULT</b>COX-1 and COX-2 were inhibited by slenderstyle acanthopanax root-bark, and the inhibitive rate of COX-2 was higher than that of COX-1 at the same concentration. Necrotic injuries in health gastric mucosa were not produced, but the injuries previously induced by the ethanol worsened.</p><p><b>CONCLUSION</b>One of the antirheumatic mechanisms of slender-root-bark might probably be mediating through inhibition of cyclooxygenase. style acanthopanax</p>
Subject(s)
Animals , Cattle , Female , Male , Mice , Rats , 6-Ketoprostaglandin F1 alpha , Metabolism , Aorta , Cyclooxygenase 1 , Metabolism , Cyclooxygenase 2 , Metabolism , Dinoprostone , Metabolism , Drugs, Chinese Herbal , Pharmacology , Eleutherococcus , Chemistry , Endothelial Cells , Gastric Mucosa , Macrophages, Peritoneal , Plant Roots , Chemistry , Plants, Medicinal , Chemistry , Rats, Sprague-DawleyABSTRACT
Aim The expression of NF-?B activation and the effect of antioxidant (N- acetylcysteine, NAC) on NF-?B activity in human airway epithelial cell was assessed. Methods Using the TNF-?,the airway epithelial cell strains of normal subject(16HBE) and tumor patient (H292) was activated and using Western-Blot and ELISA the expression of NF-?B and IL-8 were detected. Results It was found that the activity of NF-?B could be stimulated by the TNF-? and increase with the amount of TNF-? with the peak occurring at 2 to 4 hours after stimulation and then decreasing at six hours. At the same time, the level of IL-8 was elevated, but decreased with inhibition of NF-?B activity by NAC, that means the action of NAC has a dose-dependent effect. Conclusion NAC not only blocks the signal transmission activated by NF-?B, but also anticipates the transcription modulation of expression of many cell factors and inflammatory mediums. It suggests that NAC may play a role in the anti-inflammatory treatment of respiratory diseases.