Baicalin ameliorates Mycoplasma gallisepticum-induced lung inflammation in chicken by inhibiting TLR6-mediated NF-κB signalling. Issue 2 (4th March 2021)

• Record Type: Journal Article
• Authors: Zou, M.; Yang, L.; Niu, L.; Zhao, Y.; Sun, Y.; Fu, Y.; Peng, X.
• Is Part Of: British poultry science. Volume 62:Issue 2(2021)
• Page Start: 199
• Page End: 210
• Publication Date: 2021-03-04
• Subjects: Baicalin -- Mycoplasma gallisepticum -- lung inflammation -- chicken -- gene expression; Poultry -- Periodicals; Poultry industry -- Periodicals; 636.500941
• DOI: 10.1080/00071668.2020.1847251
• Languages: English
• ISSNs: 0007-1668

Abstract

ABSTRACT: 1. Mycoplasma gallisepticum (MG) causes severe lung inflammation and cell damage by activating toll-like receptor (TLR) signalling, the nuclear factor-kappaB (NF- κ B) pathway and pro-inflammatory cytokine gene expression. Baicalin (BA) is a flavonoid extracted from Scutellaria baicalensis, which possesses anti-inflammatory and anti-bacterial properties. This study investigated the effect of BA in MG-induced lung inflammation and its potential mechanism in MG-infected chicken embryo lungs and DF-1 cells. 2. The histopathological examination result showed that BA treatment alleviated MG-induced lung pathological changes. In addition, CCK-8 and cell cycle assays showed that BA treatment inhibited MG-induced cell proliferation and cell cycle progression in DF-1 cells. 3. The ELISA and RT-qPCR results demonstrated that BA treatment decreased the expression of interleukin-1beta (IL-1 β ), IL-6, and tumour necrosis factor-alpha (TNF- α ) both in MG-infected chicken embryo lungs and DF-1 cells. 4. The results revealed that BA inhibited mRNA expression levels of toll-like receptor-6 (TLR6), myeloid differentiation primary response gene-88 (MyD88) and nuclear factor- κ B (NF- κ B), and the nuclear translocation of NF- κ B-p65 5. In conclusion, the results showed that BA has a protective effect against MG-induced lung inflammation in chicken by inhibiting the TLR6-mediated NF-κB signalling.