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  • Title: [Effects of honokiol on particulate matter 2.5-induced lung injury in asthmatic mice and its mechanisms].
    Author: Xu J, Lu X, Han F.
    Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2018 Jul 28; 43(7):718-724. PubMed ID: 30124206.
    Abstract:
    To explore the therapeutic effect of honokiol on particulate matter 2.5 (PM2.5)-induced lung injury in asthmatic mice and the possible mechanisms.
 Methods: A total of 32 BALB/C mice were randomly divided into four groups: a normal saline group, a model group, a PM2.5 group and a honokiol group (n=8 in each group). The asthma mouse model was established by ovalbumin treatment. The mice were treated with physiological saline, ovalbumin, PM2.5 and honokiol, respectively. Lung tissues and serum were collected. The pathological changes of lung tissues were evaluated. The levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were measured and the expressions of Toll like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), retinoid-related orphan receptor gamma-t (RORγt) and forkhead box protein 3 (Foxp3) in lung tissues were detected.
 Results: 1) The lung tissues of mice in the asthma group showed obvious pathological changes and inflammatory state, suggesting that the asthma model was established successfully. PM2.5 could aggravate the pathological condition of inflammatory injury in lung tissues in asthmatic mice. 2) Compared to the PM2.5 group, the pathological symptoms in the lung tissues were alleviated in the honokiol group and the percentage of inflammatory cells in BALF and the levels of inflammatory cytokines in BALF and serum were significantly reduced (all P<0.05). 3) Compared to the PM2.5 group, the expressions of TLR4, NF-κB (p-p65) and RORγt in lung tissues were significantly decreased, while the expression of Foxp3 was increased; the ratio of RORγt/Foxp3 was also decreased in the honokiol group (all P<0.05).
 Conclusion: Honokiol can resist lung injury induced by PM2.5 in asthmatic mice. These effects are through inhibiting TLR4-NF-κB pathway-mediated inflammatory response or regulating the balance of Th17/Treg cells. 目的：探究和厚朴酚对颗粒物2.5(particulate matter 2.5，PM2.5)诱导的哮喘小鼠肺损伤的治疗作用及其可能的作用机制。方法：32只BALB/C小鼠随机分为生理盐水组、模型组、PM2.5组和厚朴酚组，每组8只。使用卵清蛋白诱导哮喘小鼠模型，分别采用生理盐水、卵清蛋白、PM2.5和和厚朴酚处理，收集各组小鼠肺组织和血清，检测小鼠肺组织的病理损伤状态、支气管肺泡灌洗液(bronchoalveolar lavage fluid，BALF)和血清中炎性因子的表达水平，以及肺组织中Toll样受体4(Toll like receptor 4，TLR4)、核因子κB(nuclear factor kappa B，NF-κB)、维甲酸相关核孤儿受体γt(retinoid-related orphan receptor gamma-t，RORγt)和叉头状转录蛋白3(forkhead box protein 3，Foxp3)的蛋白表达水平。结果：1)模型组小鼠肺组织出现明显病理损伤和炎性状态，提示哮喘模型构建成功。PM2.5能够加重哮喘小鼠的肺组织病理损伤和炎性状态；2)与PM2.5组比较，和厚朴酚组小鼠肺组织的病理损伤状态得到缓解，BALF中炎性细胞减少，炎性因子水平降低(均P<0.05)。3)与PM2.5组比较，和厚朴酚组小鼠肺组织中TLR4，NF-κB(p-p65)和RORγt的表达减少，Foxp3表达水平增加，且RORγt/Foxp3比值减少(均P<0.05)。结论：和厚朴酚能够抵抗PM2.5诱导哮喘小鼠的肺损伤，这一方面可能是通过抑制TLR4-NF-κB信号通路介导的炎症反应，另一方面可能是通过影响T辅助细胞17/调节性T细胞平衡的方式来实现的。.
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