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芍药苷通过减轻氧化应激和自噬改善卵清蛋白诱导的哮喘小鼠气道炎症和免疫反应。

Paeoniflorin ameliorates airway inflammation and immune response in ovalbumin induced asthmatic mice: From oxidative stress to autophagy.

机构信息

School of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, China.

First Affiliated Hospital of Guizhou Universit of Traditional Chinese Medicine (TCM), Guiyang, China.

出版信息

Phytomedicine. 2022 Feb;96:153835. doi: 10.1016/j.phymed.2021.153835. Epub 2021 Oct 30.

DOI:10.1016/j.phymed.2021.153835
PMID:34799185
Abstract

BACKGROUND

Asthma characterized by airway remodeling is a multiple pulmonary disease, which is associated with various physiological processes including inflammation reaction, immune response, oxidative stress and autophagy.

PURPOSE

This study aimed to investigate whether these processes are modulated by the total glucosides of Paeonia lactiflora Pall (TGP), and its active compound paeoniflorin (PF) with anti-inflammatory and immune-regulatory effects could alleviate ovalbumin (OVA)-induced mouse asthma.

METHODS

In vivo, models of mouse asthma were established by intraperitoneally with a mixture of OVA and aluminum hydroxide, plus a single nasal injected with OVA to female C57BL/6 mice. The results were observed with PET imaging, TEM, RT-PCR, western blotting. In vitro, CD4 T cells were isolated and detected with flow cytometry.

RESULTS

TGP, either in its crude or processed form, and PF effectively ameliorated lung injury in mice induced by OVA, regulated immune/inflammatory response by inhibiting the release of pro-inflammatory cytokines, thereby decreasing Th2 cell proportion, inhibited oxidative stress by recovering mitochondrial membrane potential and regulating metabolic activity in dose-dependent manner. Moreover, PF could inhibit autophagy by regulating mitochondrial function. In addition, the therapeutic effects of TGP and PF on pulmonary injury in asthmatic mice were not affected by processing.

CONCLUSION

PF may be a valuable agent in ameliorating inflammation and immune response in asthmatic mice, and the possible mechanism involved in this response rang may from oxidative stress to autophagy.

摘要

背景

哮喘的特征是气道重塑,这是一种多系统疾病,与多种生理过程有关,包括炎症反应、免疫反应、氧化应激和自噬。

目的

本研究旨在探讨这些过程是否受白芍总苷(TGP)及其具有抗炎和免疫调节作用的活性化合物芍药苷(PF)的调节,以及它们是否能缓解卵白蛋白(OVA)诱导的小鼠哮喘。

方法

体内,通过腹腔注射 OVA 和氢氧化铝混合物,加上单次鼻腔注射 OVA,建立雌性 C57BL/6 小鼠哮喘模型。采用 PET 成像、TEM、RT-PCR、western blot 观察结果。体外,分离 CD4 T 细胞,用流式细胞术检测。

结果

白芍总苷(TGP)及其粗品和炮制品、芍药苷(PF)有效改善了 OVA 诱导的小鼠肺损伤,通过抑制促炎细胞因子的释放调节免疫/炎症反应,从而降低 Th2 细胞比例,通过恢复线粒体膜电位和调节代谢活性,以剂量依赖性方式抑制氧化应激。此外,PF 还可以通过调节线粒体功能抑制自噬。此外,TGP 和 PF 对哮喘小鼠肺损伤的治疗作用不受炮制的影响。

结论

PF 可能是一种有价值的药物,可改善哮喘小鼠的炎症和免疫反应,其作用机制可能涉及从氧化应激到自噬。

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