Objective To establish allergic airway inflammation model in late-phase airway reaction of Sprague-Dawley (SD) rats. Methods Thirty-six SD rats were randomly divided into three groups-, control group (Group Ⅰ) ,singl...Objective To establish allergic airway inflammation model in late-phase airway reaction of Sprague-Dawley (SD) rats. Methods Thirty-six SD rats were randomly divided into three groups-, control group (Group Ⅰ) ,single challenge group (Group Ⅱ ),consecutive challenge group (Group Ⅲ). The rats in Group Ⅱ and Group Ⅲ were sensitized twice by injection of ovalbumin (OA) together with aluminum hydroxide and Bordetella pertussis as adjuvants, followed by challenge with aerosolized OA for 20 min once in Group Ⅱ or one time on each day for one week in, Group Ⅲ. The rats in Group Ⅰ received 0. 9% saline by injection and inhalation. Results Compared with group Ⅰ , there were positive symptoms observed in the group Ⅱ and group Ⅲ; the amount of total leucocytes and eosinophil percentage in brochoalveolar lavage fluid (BALF) significantly increased (P<0.05 or P<0. 01 respectively) in Group Ⅱ or Ⅲ ; histopathologic changes of lung showed acute allergic inflammation changes in Group Ⅱ: Disrupted epithelium damaged subepithelial structure and eosinophil infiltration in the airway wall. As for the Group Ⅲ, there were allergen- induced characteristic features of chronic allergic airways inflammation: hypertrophy and hyperplasia of bronchial smooth muscle, goblet cell hyperplasia, basement membrane thickening, eosinophil in filtration, edema. Conclusion The model of allergic airway inflammation in late-phase response of SD rats was successfully established by OA sensitization (twice) and consecutive challenge.展开更多
目的探讨三黄连合剂通过NOD样受体蛋白3(NOD-like receptor protein domain associated protein 3,NLRP3)/凋亡相关颗粒样蛋白(apoptosis-associated speck-like protein containing a CARD,ASC)/半胱氨酸天冬氨酸蛋白酶1(cysteine aspa...目的探讨三黄连合剂通过NOD样受体蛋白3(NOD-like receptor protein domain associated protein 3,NLRP3)/凋亡相关颗粒样蛋白(apoptosis-associated speck-like protein containing a CARD,ASC)/半胱氨酸天冬氨酸蛋白酶1(cysteine aspartic acid specific protease-1,Caspase-1)通路对哮喘患儿气道炎症的作用及机制。方法选取2021年1月—2023年10月就诊的90例哮喘患儿,采用数字表法随机分为观察组与对照组,各45例。观察2组哮喘患儿不良反应、1 s用力呼气容积(forced expiratory volume in the first second,FEV_(1)%)、最大呼气流量(peak expiratory flow,PEF)、用力肺活量(forced vital capacity,FVC)、白细胞介素-1β(interleukin-1β,IL-1β)及TNF-α(tumor necrosis factor-α,TNF-α)表达水平差异。结果观察组不良反应发生率为6.66%,对照组为11.11%,差异无统计学意义(P>0.05)。观察组总有效率为95.56%,高于对照组的80.00%(P<0.05)。治疗后FEV_(1)%、PEF、FVC、哮喘控制测试表(asthma control test,ACT)评分高于对照组(P<0.05)。治疗后观察组血清IL-1β、IL-6、IL-8、IL-17、IL-18水平低于对照组(P<0.05)。治疗后观察组患儿血清NLRP3、ASC、Caspase-1、IL-1β蛋白表达水平低于对照组(P<0.05)。结论三黄连合剂治疗能减轻哮喘患儿气道炎症反应,降低炎症因子水平,改善肺功能,减轻病情,提高疗效,其可能通过NLRP3/ASC/Caspase-1通路发挥作用。展开更多
基金Supported by the Natural Science Foundation of Jiangsu Province(BK2001160)
文摘Objective To establish allergic airway inflammation model in late-phase airway reaction of Sprague-Dawley (SD) rats. Methods Thirty-six SD rats were randomly divided into three groups-, control group (Group Ⅰ) ,single challenge group (Group Ⅱ ),consecutive challenge group (Group Ⅲ). The rats in Group Ⅱ and Group Ⅲ were sensitized twice by injection of ovalbumin (OA) together with aluminum hydroxide and Bordetella pertussis as adjuvants, followed by challenge with aerosolized OA for 20 min once in Group Ⅱ or one time on each day for one week in, Group Ⅲ. The rats in Group Ⅰ received 0. 9% saline by injection and inhalation. Results Compared with group Ⅰ , there were positive symptoms observed in the group Ⅱ and group Ⅲ; the amount of total leucocytes and eosinophil percentage in brochoalveolar lavage fluid (BALF) significantly increased (P<0.05 or P<0. 01 respectively) in Group Ⅱ or Ⅲ ; histopathologic changes of lung showed acute allergic inflammation changes in Group Ⅱ: Disrupted epithelium damaged subepithelial structure and eosinophil infiltration in the airway wall. As for the Group Ⅲ, there were allergen- induced characteristic features of chronic allergic airways inflammation: hypertrophy and hyperplasia of bronchial smooth muscle, goblet cell hyperplasia, basement membrane thickening, eosinophil in filtration, edema. Conclusion The model of allergic airway inflammation in late-phase response of SD rats was successfully established by OA sensitization (twice) and consecutive challenge.
文摘目的探讨三黄连合剂通过NOD样受体蛋白3(NOD-like receptor protein domain associated protein 3,NLRP3)/凋亡相关颗粒样蛋白(apoptosis-associated speck-like protein containing a CARD,ASC)/半胱氨酸天冬氨酸蛋白酶1(cysteine aspartic acid specific protease-1,Caspase-1)通路对哮喘患儿气道炎症的作用及机制。方法选取2021年1月—2023年10月就诊的90例哮喘患儿,采用数字表法随机分为观察组与对照组,各45例。观察2组哮喘患儿不良反应、1 s用力呼气容积(forced expiratory volume in the first second,FEV_(1)%)、最大呼气流量(peak expiratory flow,PEF)、用力肺活量(forced vital capacity,FVC)、白细胞介素-1β(interleukin-1β,IL-1β)及TNF-α(tumor necrosis factor-α,TNF-α)表达水平差异。结果观察组不良反应发生率为6.66%,对照组为11.11%,差异无统计学意义(P>0.05)。观察组总有效率为95.56%,高于对照组的80.00%(P<0.05)。治疗后FEV_(1)%、PEF、FVC、哮喘控制测试表(asthma control test,ACT)评分高于对照组(P<0.05)。治疗后观察组血清IL-1β、IL-6、IL-8、IL-17、IL-18水平低于对照组(P<0.05)。治疗后观察组患儿血清NLRP3、ASC、Caspase-1、IL-1β蛋白表达水平低于对照组(P<0.05)。结论三黄连合剂治疗能减轻哮喘患儿气道炎症反应,降低炎症因子水平,改善肺功能,减轻病情,提高疗效,其可能通过NLRP3/ASC/Caspase-1通路发挥作用。
