Andrographolide attenuates Mycoplasma gallisepticum-induced inflammation and apoptosis by the JAK/PI3K/AKT signal pathway in the chicken lungs and primary alveolar type II epithelial cells

Abstract

Mycoplasma gallisepticum (MG) is the primary etiologic agent of chronic respiratory disease (CRD) in chickens. Respiratory tract inflammation and apoptosis are the main features of CRD. Andrographolide (Andro), a natural small molecule compound, is known for its excellent anti-pathogenic and anti-inflammatory properties. Hence, this study was to evaluate the anti-inflammation and anti-apoptosis effects of Andro as well as the underlying mechanism in the chicken lungs and primary alveolar type II epithelial cells (AEC II). Results showed Andro had no side effects on AEC II viability at concentrations below 200 μg/ml. Compared with the model group, terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL), western blot (WB), quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assays (ELISA) results showed Andro treatment significantly reduced apoptosis in the chicken lungs and AEC II, and down-regulated the expression levels of the protein of MG adhesin 1.2 (pMGA1.2), IL-1β, TNF-α, IL-6, Bax, Caspase 9 and Caspase 3, and up-regulated the expression levels of Bcl-2 and Bcl-xL in the chicken lungs, serum and AEC II (P ≤ 0.05). Moreover, Andro inhibited the MG-induced JAK/PI3K/AKT signal pathway activation in the chicken lungs and AEC II. Inhibiting of the JAK/PI3K/AKT signal pathway significantly alleviated MG-induced inflammation and apoptosis in the AEC II. Andro may exert an anti-inflammatory and anti-apoptotic effect by inhibiting the JAK/PI3K/AKT signal pathway in the chicken lungs and AEC II. In conclusion, Andro could act as a potential agent against MG infection by inhibiting the JAK/PI3K/AKT signal pathway and pMGA1.2 expression in the chickens.