Cryptotanshinone Attenuates Airway Remodeling by Inhibiting Crosstalk Between Tumor Necrosis Factor-Like Weak Inducer of Apoptosis and Transforming Growth Factor Beta 1 Signaling Pathways in Asthma

Chongyang Wang; Chongyang Wang; Mingyu Zheng; Mingyu Zheng; Yunho Choi; Jingzhi Jiang; Jingzhi Jiang; Li Li; Li Li; Junfeng Li; Junfeng Li; Chang Xu; Chang Xu; Zhemin Xian; Zhemin Xian; Yan Li; Yan Li; Hongmei Piao; Hongmei Piao; Liangchang Li; Liangchang Li; Guanghai Yan; Guanghai Yan

doi:10.3389/fphar.2019.01338

Frontiers in Pharmacology (Nov 2019)

Cryptotanshinone Attenuates Airway Remodeling by Inhibiting Crosstalk Between Tumor Necrosis Factor-Like Weak Inducer of Apoptosis and Transforming Growth Factor Beta 1 Signaling Pathways in Asthma

Chongyang Wang,
Chongyang Wang,
Mingyu Zheng,
Mingyu Zheng,
Yunho Choi,
Jingzhi Jiang,
Jingzhi Jiang,
Li Li,
Li Li,
Junfeng Li,
Junfeng Li,
Chang Xu,
Chang Xu,
Zhemin Xian,
Zhemin Xian,
Yan Li,
Yan Li,
Hongmei Piao,
Hongmei Piao,
Liangchang Li,
Liangchang Li,
Guanghai Yan,
Guanghai Yan

Affiliations

Chongyang Wang: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Chongyang Wang: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Mingyu Zheng: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Mingyu Zheng: College of Pharmacy, Yanbian University, Yanji, China
Yunho Choi: Department of Anatomy, Medical School, Institute for Medical Sciences, Chonbuk National University, Jeonju, South Korea
Jingzhi Jiang: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Jingzhi Jiang: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Li Li: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Li Li: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Junfeng Li: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Junfeng Li: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Chang Xu: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Chang Xu: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Zhemin Xian: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Zhemin Xian: Department of Respiratory Medicine, Affiliated Hospital of Yanbian University, Yanji, China
Yan Li: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Yan Li: Department of Respiratory Medicine, Affiliated Hospital of Yanbian University, Yanji, China
Hongmei Piao: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Hongmei Piao: Department of Respiratory Medicine, Affiliated Hospital of Yanbian University, Yanji, China
Liangchang Li: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Liangchang Li: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China
Guanghai Yan: Department of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China
Guanghai Yan: Jilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China

DOI: https://doi.org/10.3389/fphar.2019.01338
Journal volume & issue: Vol. 10

Abstract

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The study is to investigate the effect of cryptotanshinone (CTS) on airway remodeling and the possible mechanism. Male BALB/c mice were pretreated with CTS or dexamethasone 30 min before nebulized inhalation of ovalbumin (OVA). CTS significantly inhibited OVA-induced increases of eosinophils and neutrophils infiltration of bronchoalveolar lavage fluids (BALFs), reduced airway resistance in asthmatic mice, decreased the accumulation of inflammatory cells, the hyperplasia of goblet cells and the deposition of collagen in asthmatic mice lung tissue, as well as markedly attenuated the leakage of inflammatory cells and the level of OVA-specific immunoglobulin E in BALFs. CTS also inhibited the expressions of alpha-smooth muscle actin, tumor necrosis factor-like weak inducer of apoptosis (TWEAK), Fn14, transforming growth factor (TGF)-β1, Smad4, and phosphorylation of Smad2/3 and STAT3 (Tyr705). In comparison to TWEAK inhibitor or TWEAK small interfering RNA (siRNA), which were used to inhibit TWEAK/STAT3 signaling pathways, CTS caused a similar effect as them on airway remodeling. Additionally, CTS also played a similar role as the TGF-β1 inhibitor or TGF-β1 siRNA in TGF-β1/STAT3 signaling pathways in airway remodeling. The anti-inflammatory effects of CTS against OVA-induced airway remodeling may be through inhibiting STAT3, which further suppresses TWEAK and TGF-β1 signaling cross talk in asthma. CTS may be a promising therapeutic reagent for asthma treatment.

Published in Frontiers in Pharmacology

ISSN: 1663-9812 (Online)
Publisher: Frontiers Media S.A.
Country of publisher: Switzerland
LCC subjects: Medicine: Therapeutics. Pharmacology
Website: http://journal.frontiersin.org/journals/pharmacology

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