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Mesenchymal stem cells suppress lung inflammation and airway remodeling in chronic asthma rat model via PI3K/Akt signaling pathway

机译:间质干细胞通过PI3K / Akt信号通路抑制慢性哮喘大鼠模型的肺部炎症和气道重塑

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摘要

Background: Mesenchymal stem cells (MSCs) came out to attract wide attention and had become one of the hotspots of most diseases’ research in decades. But at present, the mechanisms of how MSCs work on chronic asthma remain undefined. Our study aims at verifying whether MSCs play a role in preventing inflammation and airway remodeling via PI3K/AKT signaling pathway in the chronic asthma rats model. Methods: First, an ovalbumin (OVA)-induced asthma model was built. MSCs were administered to ovalbumin-induced asthma rats. The total cells in a bronchial alveolar lavage fluid (BALF) and inflammatory mediators in BALF and serum were measured. Histological examination of lung tissue was performed to estimate the pathological changes. Additionally, the expression of phosphorylated-Akt (p-Akt) in all groups was measured by western blot and immunohistochemistry (IHC). Results: Compared to normal control group, the degree of airway inflammation and airway remodeling was significantly increased in asthma group. On the contrary, they were obviously inhibited in MSCs transplantation group. Moreover, the expression of p-Akt was increased in lung tissues of asthmatic rats, and suppressed by MSCs transplantation. Conclusion: Our results demonstrated that MSCs transplantation could suppress lung inflammation and airway remodeling via PI3K/Akt signaling pathway in rat asthma model.
机译:背景:间充质干细胞(MSCs)引起了广泛的关注,并已成为数十年来大多数疾病研究的热点之一。但是目前,关于MSCs如何治疗慢性哮喘的机制尚不清楚。我们的研究旨在验证在慢性哮喘大鼠模型中,MSC是否通过PI3K / AKT信号通路在预防炎症和气道重塑中发挥作用。方法:首先,建立卵清蛋白(OVA)诱导的哮喘模型。将MSCs施用给卵白蛋白诱导的哮喘大鼠。测量支气管肺泡灌洗液(BALF)中的总细胞以及BALF和血清中的炎症介质。进行肺组织的组织学检查以估计病理变化。另外,通过蛋白质印迹和免疫组织化学(IHC)测量所有组中磷酸化Akt(p-Akt)的表达。结果:与正常对照组相比,哮喘组气道炎症和气道重塑程度明显增加。相反,它们在MSCs移植组中明显受到抑制。此外,p-Akt的表达在哮喘大鼠的肺组织中增加,并被MSCs移植抑制。结论:我们的结果表明,MSCs移植可以通过PI3K / Akt信号通路抑制大鼠哮喘模型中的肺部炎症和气道重塑。

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