Gan Xiao-liang, Hei Zi-qing, Huang He-qing, Chen Li-xin, Li Shang-rong, Cai Jun
Department of Anesthesiology, Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China.
Chin Med J (Engl). 2006 Nov 20;119(22):1892-8.
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.
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-alpha, histamine, and superoxide dismutase (SOD) activity in intestine were detected, and the number of IMMC was counted.
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-alpha in the model group were higher than that in the other three groups (P < 0.05), and the concentration of TNF-alpha in the low dosage group was higher than that in the high dosage group (P < 0.05). SOD activity and the concentration of histamine in the model group were lower than the other three groups (P < 0.05). There was a negative correlation between the Chiu's score and the concentration of histamine and a positive correlation between the Chiu's score and the concentration of TNF-alpha and between the SOD activity and the concentration of histamine in the four groups (P < 0.05).
Astragalus membranaceus injection may reduce the damage to small intestine mucosa by inhibiting the activated IMMC after hemorrhagic shock.
失血性休克后缺血再灌注（IR）诱导的黏膜损伤机制复杂；肥大细胞（MC）脱颗粒与黏膜损伤相关。黄芪可保护失血性休克后的肠黏膜免受肠道氧化损伤，且一些抗氧化剂可防止MC脱颗粒。本研究旨在观察黄芪注射液对大鼠失血性休克再灌注后肠黏膜肥大细胞（IMMC）活性的影响。
32只Wistar大鼠随机分为正常组、模型组、低剂量组（用黄芪注射液治疗，10 g生药/kg）和高剂量组（用黄芪注射液治疗，20 g生药/kg）。通过出血60分钟后再灌注90分钟诱导大鼠失血性休克再灌注模型。在再灌注前给动物注射3 ml受试药物溶液。在研究结束时，检测肠道病理学、IMMC超微结构和类胰蛋白酶表达。检测肠道中丙二醛（MDA）、肿瘤坏死因子-α（TNF-α）、组胺水平及超氧化物歧化酶（SOD）活性，并计数IMMC数量。
模型组大鼠的Chiu评分高于其他组（P<0.01）。高剂量组的Chiu评分高于低剂量组（P<0.05）。出血再灌注诱导IMMC脱颗粒：黄芪注射液减轻了这种脱颗粒。与其他组相比，模型组类胰蛋白酶表达和IMMC数量增加（P<0.01），且两种剂量的黄芪注射液治疗均使其显著降低。两个治疗组之间无显著差异（P>0.05）。模型组MDA含量和TNF-α浓度高于其他三组（P<0.05），低剂量组TNF-α浓度高于高剂量组（P<0.05）。模型组SOD活性和组胺浓度低于其他三组（P<0.05）。四组中Chiu评分与组胺浓度呈负相关，Chiu评分与TNF-α浓度呈正相关，SOD活性与组胺浓度呈正相关（P<0.05）。
黄芪注射液可能通过抑制失血性休克后活化的IMMC来减轻小肠黏膜损伤。
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