[ Objective ] This study was conducted to investigate Echinacea polysaccharide （EPS） on expression of tumor necrosis factor （TNF） under injury of intestinal epithelial cells （IEC-6） by lipopolysaccharide （LPS）...[ Objective ] This study was conducted to investigate Echinacea polysaccharide （EPS） on expression of tumor necrosis factor （TNF） under injury of intestinal epithelial cells （IEC-6） by lipopolysaccharide （LPS）, so as to discuss the action mechanism of EPS to injured cells. [Method] Total DNA was extracted with TRIzon reagent, TNF-α mRNA was amplified, and the amplification products were subjected to agarose gel electrophoresis and imaging. [Result] 50 μg/ml EPS could partially inhibited the production of IL-α mRNA by IEC-6 under the stimulation of LPS, while the inhibition of 2（10 and 500 μg/ml EPS on the level of IL-1α mRNA gradually increased with the concentration increasing; and IEC-6 cells pretreated with 50,100,200 and 500 μg/ml EPS for 24 h and then stimulated by 10 μml IPS for 1 and 4 h were analyzed by RT-PCR method, and it was found that the expression of IL-α mRNA induced by LPS could be effectively inhibited by EPS, and the inhibition rate at 4 h was higher than that at 1 h. [ Conclusion] EPS could play its role of protecting intestinal mucosa by inhibiting the secretion of IL-1α mRNA by cells under the stimulation of LPS, and such inhibition effects of EPS had concentration dependency and time dependency.展开更多
Interleukin1β (IL 1β) is a proinflammatory cytokine and plays an important role in the pathogenesis of cerebral ischemia. The expression of IL 1β and its receptor antagonist (IL 1Ra) after cerebral ischemia is not ...Interleukin1β (IL 1β) is a proinflammatory cytokine and plays an important role in the pathogenesis of cerebral ischemia. The expression of IL 1β and its receptor antagonist (IL 1Ra) after cerebral ischemia is not well defined so far. The aim of present study was to explore the effect of electroacupuncture (EA) on the expression of IL 1β and IL 1Ra in rats after middle cerebral artery occlusion (MCAo) and reperfusion. Using in situ hybridization and RT PCR techniques, it was found that in the MCAo group the expression of IL 1β mRNA was markedly increased at 2 hr, 6 hr and 12 hr after reperfusion in the ischemic cerebral cortex compared with normal group. The IL 1Ra mRNA expression was rapidly induced by MCAo, and also increased significantly at 12 hr, reaching a peak level at 24 hr of reperfusion in ischemic cortex. In ischemic striatum the IL 1Ra mRNA was increased only at 12 hr after ischemia/reperfusion and decreased significantly at 24 hr after ischemia/reperfusion. In EA + MCAo group the expression of IL 1β mRNA in ischemic cortex was significantly decreased at 2 hr, 6 hr and 12 hr; but the expression of IL 1Ra mRNA was increased significantly compared with MCAo group 24 hr after reperfusion in the cerebral cortex and stratium. Our results indicated that EA stimulation of "Shuigou" (GV 26) and "Baihui" (GV 20) acupoints could downregulate the IL 1β mRNA expression and upregulate the IL 1Ra mRNA expression in cerebral ischemic rats, which might be the neuroprotective effect of EA on cerebral ischemia, and one of the mechanisms of EA anti-ischemia.展开更多
基金Supported by Natural Science Foundation of China(31472230)Natural Science Foundation of Hebei Province(C2014407068)Fund from Science and Technology Department of Hebei Province(NO.14966610D)
文摘[ Objective ] This study was conducted to investigate Echinacea polysaccharide （EPS） on expression of tumor necrosis factor （TNF） under injury of intestinal epithelial cells （IEC-6） by lipopolysaccharide （LPS）, so as to discuss the action mechanism of EPS to injured cells. [Method] Total DNA was extracted with TRIzon reagent, TNF-α mRNA was amplified, and the amplification products were subjected to agarose gel electrophoresis and imaging. [Result] 50 μg/ml EPS could partially inhibited the production of IL-α mRNA by IEC-6 under the stimulation of LPS, while the inhibition of 2（10 and 500 μg/ml EPS on the level of IL-1α mRNA gradually increased with the concentration increasing; and IEC-6 cells pretreated with 50,100,200 and 500 μg/ml EPS for 24 h and then stimulated by 10 μml IPS for 1 and 4 h were analyzed by RT-PCR method, and it was found that the expression of IL-α mRNA induced by LPS could be effectively inhibited by EPS, and the inhibition rate at 4 h was higher than that at 1 h. [ Conclusion] EPS could play its role of protecting intestinal mucosa by inhibiting the secretion of IL-1α mRNA by cells under the stimulation of LPS, and such inhibition effects of EPS had concentration dependency and time dependency.
文摘Interleukin1β (IL 1β) is a proinflammatory cytokine and plays an important role in the pathogenesis of cerebral ischemia. The expression of IL 1β and its receptor antagonist (IL 1Ra) after cerebral ischemia is not well defined so far. The aim of present study was to explore the effect of electroacupuncture (EA) on the expression of IL 1β and IL 1Ra in rats after middle cerebral artery occlusion (MCAo) and reperfusion. Using in situ hybridization and RT PCR techniques, it was found that in the MCAo group the expression of IL 1β mRNA was markedly increased at 2 hr, 6 hr and 12 hr after reperfusion in the ischemic cerebral cortex compared with normal group. The IL 1Ra mRNA expression was rapidly induced by MCAo, and also increased significantly at 12 hr, reaching a peak level at 24 hr of reperfusion in ischemic cortex. In ischemic striatum the IL 1Ra mRNA was increased only at 12 hr after ischemia/reperfusion and decreased significantly at 24 hr after ischemia/reperfusion. In EA + MCAo group the expression of IL 1β mRNA in ischemic cortex was significantly decreased at 2 hr, 6 hr and 12 hr; but the expression of IL 1Ra mRNA was increased significantly compared with MCAo group 24 hr after reperfusion in the cerebral cortex and stratium. Our results indicated that EA stimulation of "Shuigou" (GV 26) and "Baihui" (GV 20) acupoints could downregulate the IL 1β mRNA expression and upregulate the IL 1Ra mRNA expression in cerebral ischemic rats, which might be the neuroprotective effect of EA on cerebral ischemia, and one of the mechanisms of EA anti-ischemia.
