Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation

Table 3 Protective effect of astragaloside IV on lung disease

Disease categories	Study object/model	Effect induced by autophagy	Mechanism (targets or pathways)	Ref.
Lung injury	PM2.5-induced lung toxicity in rats	(-) PM2.5-induced lung toxicity; (+) autophagic flux	(+) AMPK/mTOR pathway	Wang et al[36]
Lung injury	PM2.5 in rats and rat alveolar macrophages	(-) Severe inflammation and oxidative stress, (+) autophagic flux mainly via autophagosome degradation	(-) The PI3K/Akt/mTOR pathway to (+) autophagy and (-) inflammation	Pei et al[37]
Lung injury	LPS in pulmonary epithelial cell	(-) Apoptosis in cell model, (-) autophagy initiation	(-) The oxidative stress and inflammatory response	Liu et al[34]
Lung adenocarcinoma	Bevacizumab in A549 cells	(-) Proliferation inhibition and apoptosis promotion (-) inhibiting autophagy pathway	Autophagy-related proteins (p62, LC3 II/LC3 I), p-AKT and p-Mtor	Li et al[57]
NSCLC	Cisplatin-resistant the NSCLC cell lines	(-) Chemoresistance to cisplatin in NSCLC cells via (-) inhibition of ER stress or autophagy	Autophagy-related proteins (Beclin1, LC3 II/I)	Lai et al[35]

AMPK: AMP-activated protein kinase; LPS: Lipopolysaccharide; LC: Lung cancer; NSCLC: Non-small cell lung cancer; ER: Endoplasmic reticulum