Acute lung injury (ALI) is a common clinical disease with high morbidity in both humans and animals.
Ginsenoside Rg3, a type of
traditional Chinese medicine extracted from ginseng, is widely used to cure many
inflammation-related diseases. However, the specific molecular mechanism of the effects of
ginsenoside Rg3 on
inflammation has rarely been reported. Thus, we established a mouse model of
lipopolysaccharide (LPS)-induced ALI to investigate the immune protective effects of
ginsenoside Rg3 and explore its molecular mechanism. In wild type (WT) mice, we found that
ginsenoside Rg3 treatment significantly mitigated pathological damages and reduced
myeloperoxidase (MPO) activity as well as the production of pro-inflammatory
cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and
interleukin-6 (IL-6); furthermore, the production of anti-inflammatory mediators
interleukin-10 (IL-10) and
transforming growth factor-β (TGF-β), polarization of M2 macrophages and expression levels of the phosphorylation of
phosphatidylinositol 3-hydroxy
kinase (PI3K),
protein kinase B (PKB, also known as AKT),
mammalian target of rapamycin (mTOR) and Mer
receptor tyrosine kinase (
MerTK) were promoted. However, there were no significant differences with regards to the pathological damage, MPO levels, inflammatory
cytokine levels, and
protein expression levels of the phosphorylation of PI3K, AKT and mTOR between the LPS treatment group and
ginsenoside Rg3 group in
MerTK-/- mice. Taken together, the present study demonstrated that
ginsenoside Rg3 could attenuate LPS-induced ALI by decreasing the levels of pro-inflammatory mediators and increasing the production of anti-inflammatory
cytokines. These processes were mediated through
MerTK-dependent activation of its downstream the PI3K/AKT/mTOR pathway. These findings identified a new site of the specific anti-inflammatory mechanism of
ginsenoside Rg3.