儿茶素调节MAPK通路改善幼鼠变应性气道炎症的机制

Xiaohua Zhang
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引用次数: 1

摘要

目的探讨儿茶素调节丝裂原活化蛋白激酶(MAPK)通路改善幼鼠变应性气道炎症的机制。方法spf级BALB/c小鼠50只,随机分为模型组、正常组、阳性对照组、儿茶素低剂量组和儿茶素高剂量组。除正常组外,其余各组小鼠均制备过敏性哮喘模型。造模成功后,阳性对照组小鼠给予0.5 mg/kg地塞米松溶液、低剂量儿茶素和儿茶素。高剂量组分别灌胃1 mg/kg、2 mg/kg儿茶素溶液。模型组和正常组大鼠ig生理盐水,每日1次。观察小鼠支气管肺泡灌洗液(BALF)细胞、细胞总数、白细胞介素-13 (IL-13)、IL-5、IL-4水平,检测小鼠肺组织中p-p38MAPK、ERK、p-ERK、p38MAPK蛋白表达和p38MAPK、ERK mRNA表达。结果与正常组比较,模型组大鼠BALF中IL-13、IL-5、IL-4水平升高。与模型组比较,阳性对照组、儿茶素低剂量组和儿茶素高剂量组大鼠心肌梗死均较小。BALF中IL-13、IL-5、IL-4水平降低,差异均有统计学意义(P<0.05)。与正常组比较,模型组小鼠肺组织中p-p38MAPK、p-ERK的表达。蛋白表达增加。与模型组比较,阳性对照组、儿茶素低剂量组和儿茶素高剂量组大鼠肺组织中P - p38mapk、P - erk蛋白表达降低,差异均有统计学意义(P<0.05);与正常组比较,模型组大鼠肺组织中p38MAPK、ERK mRNA表达升高;与对照组、阳性对照组相比,儿茶素低剂量组和高剂量组小鼠肺组织中p38MAPK、ERK mRNA均降低,差异均有统计学意义(均P<0.05)。结论儿茶素可有效改善变应性哮喘小鼠气道炎症,其机制可能与抑制ERK/MAPK信号通路激活有关。关键词:过敏性哮喘;气道炎症;儿茶素
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Mechanism of catechin regulating MAPK pathway in improving allergic airway inflammation in young rats
Objective To explore the mechanism of catechin regulating mitogen-activated protein kinase (MAPK) pathway in improving allergic airway inflammation in young rats. Methods There were 50 SPF-class BALB/c mice randomly divided into model group, normal group, positive control group, low dose catechin group and high dose catechin group each group.In addition to the normal group, all other groups of mice prepared an allergic asthma model.After successful modeling, the positive control group mice were given a dose of 0.5 mg/kg of dexamethasone solution, a low dose of catechin and catechin.The high-dose group was intragastrically dosed with 1 mg/kg and 2 mg/kg catechin solution.The model group and the normal group were intragastrically administered with normal saline once daily.The cells, total cell count, interleukin-13 (IL-13), IL-5 and IL-4 levels in bronchoalveolar lavage fluid (BALF) of mice were observed, p-p38MAPK, ERK, p-ERK, p38MAPK protein expression and p38MAPK, ERK mRNA expression in lung tissue of mice were detected. Results Compared with the normal group, the levels of IL-13, IL-5 and IL-4 in BALF of the model group were increased.Compared with the model group, the positive control group, the low dose group of catechin and the high dose group of catechin were small.The levels of IL-13, IL-5 and IL-4 in BALF were decreased, and the difference was statistically significant (all P<0.05). Compared with normal group, p-p38MAPK and p-ERK in lung tissue of model group mice.The protein expression was increased.Compared with the model group, the expression of p-p38MAPK and p-ERK protein in the lung tissue of the positive control group, the low-dose catechin group and the high-dose catechin group were decreased, and the difference was statistically significant (all P<0.05); Compared with the normal group, the expression of p38MAPK and ERK mRNA in the lung tissue of the model group increased; Compared group, positive control group, the lung tissue catechins catechin low dose group and high dose group mice p38MAPK, ERK mRNA was decreased, there was significant difference (all P<0.05). Conclusions Catechin can effectively improve the airway inflammation in allergic asthma mice, and its mechanism may be related to the inhibition of ERK/MAPK signal pathway activation. Key words: Allergic asthma; Airway inflammation; Catechin
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