摘要
Background The mechanism of mucosal damage induced by ischemia-reperfusion （IR） after hemorrhagic shock is complex; mast cells （MC） degranulation is associated with the mucosal damage. Astragalus membranaceus can protect intestinal mucosa against intestinal oxidative damage after hemorrhagic shock, and some antioxidant agents could prevent MC against degranulation. This study aimed to observe the effects of astragalus membranaceus injection on the activity of intestinal mucosal mast cells （IMMC） after hemorrhage shock-reperfusion in rats Methods Thirty-two Wistar rats were randomly divided into the normal group, model group, low dosage group, （treated with Astragalus membranacaus injection, 10 g crude medication/kg） and high dosage group （treated with Astragalus membranacaus injection, 20 g crude medication/kg）. The rat model of hemorrhagic shock-reperfusion was induced by hemorrhage for 60 minutes followed by 90 minutes of reperfusion. The animals were administrated with 3 ml of the test drug solution before reperfusion. At the end of study, intestinal pathology, ultrastructure of IMMC, and expression of tryptase were assayed. The levels of malondisldehyde （MDA）, TNF-α, histamine, and superoxide dismutase （SOD） activity in intestine were detected, and the number of IMMC was counted. Results The Chiu＇s score of the rats in the model group was higher than in other groups （P〈0.01）. The Chiu＇s score in the high dosage group was higher than that in the low dosage group （P〈0.05）. Hemorrhage-reperfusion induced IMMC degranulation： Astragalus membranaceus injection attenuated this degranulation. Expression of tryptase and the number of IMMC in the model group increased compared with the other groups （P〈0.01） and was significantly reduced by the treatments of Astragalus membranaceus injection at both doses. There was no significant difference between the two treatment groups （P〉0.05）. MDA content and concentration of TNF-α in the model group were higher than tha
Background The mechanism of mucosal damage induced by ischemia-reperfusion （IR） after hemorrhagic shock is complex; mast cells （MC） degranulation is associated with the mucosal damage. Astragalus membranaceus can protect intestinal mucosa against intestinal oxidative damage after hemorrhagic shock, and some antioxidant agents could prevent MC against degranulation. This study aimed to observe the effects of astragalus membranaceus injection on the activity of intestinal mucosal mast cells （IMMC） after hemorrhage shock-reperfusion in rats Methods Thirty-two Wistar rats were randomly divided into the normal group, model group, low dosage group, （treated with Astragalus membranacaus injection, 10 g crude medication/kg） and high dosage group （treated with Astragalus membranacaus injection, 20 g crude medication/kg）. The rat model of hemorrhagic shock-reperfusion was induced by hemorrhage for 60 minutes followed by 90 minutes of reperfusion. The animals were administrated with 3 ml of the test drug solution before reperfusion. At the end of study, intestinal pathology, ultrastructure of IMMC, and expression of tryptase were assayed. The levels of malondisldehyde （MDA）, TNF-α, histamine, and superoxide dismutase （SOD） activity in intestine were detected, and the number of IMMC was counted. Results The Chiu＇s score of the rats in the model group was higher than in other groups （P〈0.01）. The Chiu＇s score in the high dosage group was higher than that in the low dosage group （P〈0.05）. Hemorrhage-reperfusion induced IMMC degranulation： Astragalus membranaceus injection attenuated this degranulation. Expression of tryptase and the number of IMMC in the model group increased compared with the other groups （P〈0.01） and was significantly reduced by the treatments of Astragalus membranaceus injection at both doses. There was no significant difference between the two treatment groups （P〉0.05）. MDA content and concentration of TNF-α in the model group were higher than tha
基金
This study was supported by the Chinese Traditional Medicine Foundation of Guangdong Province, China (No. 1040051).
