1. Academic Validation
  2. Baicalin ameliorates cigarette smoke-induced airway inflammation in rats by modulating HDAC2/NF-κB/PAI-1 signalling

Baicalin ameliorates cigarette smoke-induced airway inflammation in rats by modulating HDAC2/NF-κB/PAI-1 signalling

  • Pulm Pharmacol Ther. 2021 Oct;70:102061. doi: 10.1016/j.pupt.2021.102061.
Hu Zhang 1 Baojun Liu 1 Shan Jiang 1 Jin-Feng Wu 2 Chun-Hui Qi 3 Nabijan Mohammadtursun 1 Qiuping Li 1 Lulu Li 1 Hongying Zhang 1 Jing Sun 4 Jing-Cheng Dong 5
Affiliations

Affiliations

  • 1 Huashan Hospital, Fudan University, Shanghai, China; Department of Integrative Medicine, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai, 200040, China.
  • 2 Huashan Hospital, Fudan University, Shanghai, China; Department of Dermatology, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai, 200040, China.
  • 3 Department of Respiratory Medicine, Qingpu District Traditional Chinese Medicine Hospital, Institute of Integrative Medicine, Fudan University, Shanghai, China.
  • 4 Huashan Hospital, Fudan University, Shanghai, China; Department of Integrative Medicine, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai, 200040, China. Electronic address: sjing0610@163.com.
  • 5 Huashan Hospital, Fudan University, Shanghai, China; Department of Integrative Medicine, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai, 200040, China. Electronic address: jcdong2004@126.com.
Abstract

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease distinguished by airway remodelling and progressive inflammation. PAI-1 is an important regulator of fibrosis. Recent studies have shown that PAI-1 seems to be involved in COPD progression. Elevated levels of PAI-1 have been found in the lungs of patients with acute inflammation. PAI-1 has been shown to regulate the levels of proinflammatory cytokines in the lungs, such as tumour necrosis factor (TNF)-α and interleukin (IL)-6, indicating that PAI-1 may play a fundamental role during inflammation. In the present study, we investigated the anti-inflammatory role of baicalin, the main active component of Scutellaria baicalensis, against cigarette smoke (extract) (CS/CSE)-induced airway inflammation in vivo and in vitro. For the in vivo study, SD rats were exposed to CS for 1 h/day, 6 days/week, for 24 weeks and treated with baicalin (40, 80 and 160 mg/kg) or budesonide (0.2 mg/kg). For this study, HBE cells were pretreated with baicalin (10, 20, 40 μM) or dexamethasone (10-7 M) and then exposed to CSE. We found that baicalin treatment could ameliorate CS-induced airway inflammatory infiltration in rats and decrease PAI-1 expression. The ELISA results showed that baicalin significantly inhibited the levels of TNF-α and IL-1β in CS/CSE-exposed rats and cells. Mechanistic studies showed that baicalin enhanced histone deacetylase 2 (HDAC2) protein expression and inhibited the expression of NF-κB and its downstream target PAI-1, and these effects were reversed by the HDAC2 Inhibitor CAY-10683. In conclusion, baicalin ameliorated CS-induced airway inflammation in rats, and these effects were partially attributed to the modulation of HDAC2/NF-κB/PAI-1 signalling.

Keywords

Baicalin; COPD; Cigarette smoke; Inflammation; PAI-1.

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