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肉桂醛亚微米乳剂通过抑制炎症、氧化应激和上皮-间充质转化改善博来霉素诱导的特发性肺纤维化。

Submicron emulsion of cinnamaldehyde ameliorates bleomycin-induced idiopathic pulmonary fibrosis via inhibition of inflammation, oxidative stress and epithelial-mesenchymal transition.

机构信息

Department of Natural Medicine, School of Pharmacy, The Fourth Military Medical University, 169 Changle West Road, Xi'an, 710032, China.

School of Pharmacy, Shaanxi University of Chinese Medicine, Century Road, Xianyang, 712000, China.

出版信息

Biomed Pharmacother. 2018 Jun;102:765-771. doi: 10.1016/j.biopha.2018.03.145. Epub 2018 Apr 5.

DOI:10.1016/j.biopha.2018.03.145
PMID:29604596
Abstract

AIMS

Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. The pathogenesis is associated with inflammation and oxidative stress and epithelial-mesenchymal transition (EMT). Cinnamaldehyde exhibits antiinflammatory and antioxidant properties, but its effect on IPF is unknown. The present study is to investigate the anti-fibrotic effect and action mechanism of cinnamaldehyde on IPF.

MATERIALS AND METHODS

IPF was induced by intratracheal bleomycin in mice. Submicron emulsion of cinnamaldehyde was given by intraperitoneal injection once everyday for 7 or 21 continuous days after bleomycin administration. Lung histological and injury indexes were analyzed. The protein expressions of inflammation and oxidative stress as well as EMT markers alpha-smooth muscle actin (α-SMA) and E-cadherin in mice and cultured A549 cells were measured.

RESULTS

Cinnamaldehyde attenuated the bleomycin-induced histological injury, reduced hydroxyproline level and improved pulmonary function by the inhibiting inflammatory cytokines and reactive oxygen species production as well as enhancing total superoxide dismutase activity in bleomycin-induced mice. Cinnamaldehyde also inhibited EMT in both bleomycin-induced mice and TGF-β1-stimulated A549 cells.

CONCLUSIONS

Cinnamaldehyde ameliorated bleomycin-induced IPF via inhibition of inflammation and oxidative stress and EMT.

摘要

目的

特发性肺纤维化(IPF)是特发性间质性肺炎中最常见和最严重的一种。其发病机制与炎症和氧化应激以及上皮-间充质转化(EMT)有关。肉桂醛具有抗炎和抗氧化特性,但它对 IPF 的影响尚不清楚。本研究旨在探讨肉桂醛对 IPF 的抗纤维化作用及其作用机制。

材料和方法

通过气管内注射博莱霉素在小鼠中诱导 IPF。在博莱霉素给药后,每天通过腹腔注射给予肉桂醛亚微米乳剂,连续 7 或 21 天。分析肺组织学和损伤指标。测量小鼠和培养的 A549 细胞中炎症和氧化应激以及 EMT 标志物α-平滑肌肌动蛋白(α-SMA)和 E-钙黏蛋白的蛋白表达。

结果

肉桂醛通过抑制博莱霉素诱导的小鼠中的炎症细胞因子和活性氧的产生以及增强总超氧化物歧化酶的活性,减轻了博莱霉素诱导的组织学损伤,降低了羟脯氨酸水平并改善了肺功能。肉桂醛还抑制了博莱霉素诱导的小鼠和 TGF-β1 刺激的 A549 细胞中的 EMT。

结论

肉桂醛通过抑制炎症和氧化应激以及 EMT 改善了博莱霉素诱导的 IPF。

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