Polygonatum sibiricum polysaccharides prevent LPS‑induced acute lung injury by inhibiting inflammation via the TLR4/Myd88/NF‑κB pathway
Tian‐Yin Liu, Lili Zhao, S. R. Wayne Chen, Benchao Hou, Jian Huang, Xiu Hong, Qing Lian, Fang Yu, Zhe Tao
Abstract
Inflammation plays an important role in cases of acute lung injury (ALI), and the Toll‑like receptor 4/nuclear factor‑κB (TLR4/NF‑κB) pathway, which can be regulated by Polygonatum sibiricum polysaccharides (PSPs), is closely related to the dynamics of lipopolysaccharide (LPS)‑induced inflammation. Thus, we sought to evaluate whether or not PSPs prevent LPS‑induced ALI by way of inhibiting inflammation via the TLR4/NF‑κB pathway in rats. We established an ALI rat model by tracheal instillation of LPS, and by pre‑injection of PSPs into rats to examine PSPs in the ALI rat model. We found that PSPs attenuated LPS‑induced lung pathological changes in ALI rats, decreased LPS‑induced myeloperoxidase (MOP) activity, and elevated malondialdehyde (MDA) levels in lung tissue. However, PSPs also decreased the LPS‑induced increase in the neutrophil ratio, and decreased inflammatory factor levels in bronchoalveolar lavage fluid (BALF). Moreover, PSPs decreased LPS‑induced increases in inflammatory factors measured by mRNA expression, and altered the levels of expression of TLR4, medullary differentiation protein 88 (Myd88), p‑IKB‑α/IKB‑α and p‑p65/p65 proteins in lung tissue. In vitro, PSPs also reduced apoptosis induced by LPS in BEAS‑2B cells by suppressing inflammation through its effect of inhibiting the TLR4/NF‑κB pathway. In conclusion, our results suggest that PSPs may be a potential drug for effective treatment of LPS‑induced ALI, due to the ability to inhibit inflammation through effects exerted on the TLR4/Myd88/NF‑κB pathway.