Salecan ameliorates LPS-induced acute lung injury through regulating Keap1-Nrf2/HO-1 pathway in mice.

Acute lung injury (ALI) is a severe clinical condition with high mortality, characterized by rapid onset and limited treatment options. The pathogenesis of ALI involves inflammation and oxidative stress. The polysaccharide salecan, a water-soluble ß-(1,3)-D-glucan, has been found to possess numerous pharmaceutical effects, including anti-inflammatory properties, inhibition of oxidative stress, and anti-fatigue effects. This study aims to investigate the protective effect and underlying mechanism of salecan against LPS-induced ALI in mice. Using an in vivo LPS-induced ALI mouse model and an in vitro RAW264.7 cell system, we investigated the role of salecan in ALI with various experimental approaches, including histological staining, quantitative real-time PCR, flow cytometry, western blot analysis, and other relevant assays. Pre-treatment with salecan effectively attenuated LPS-induced ALI in vivo, reducing the severity of pulmonary edema, inflammation, and oxidative stress. NMR-based metabolomic profiling analysis revealed that salecan attenuated LPS-induced metabolic imbalances associated with ALI. Furthermore, salecan downregulated Keap1 and upregulated Nrf2 and HO-1 protein levels, indicating its modulation of the Keap1-Nrf2/HO-1 signaling pathway as a potential mechanism underlying its protective effects against ALI. In vitro studies on RAW264.7 cells revealed that salecan exhibited binding affinity towards macrophages, thereby alleviating LPS-induced apoptosis and inflammation, which underpin its therapeutic potential against ALI. Our study suggests that salecan can alleviate LPS-induced ALI by modulating oxidative stress, inflammatory response, and apoptosis through the activation of the Keap1-Nrf2/HO-1 pathway. These findings provide novel insights into the potential therapeutic use of salecan for the treatment of ALI.

In vitro and in vivo anti-Listeria effect of Succinoglycan Riclin through regulating MAPK/IL-6 axis and metabolic profiling.

Infectious diseases such as Listeria monocytogenes infection pose a great threat to the health of human beings and the development of livestock and poultry farming. Currently the treatment of Listeria infection mainly relies on antibiotics, which may result in excessive antibiotic residues in livestock and poultry products, as well as causing an increase in the occurrence of zoonotic diseases. Here, we demonstrate that Succinoglycan Riclin promoted the clearance of Listeria in the in vitro and in vivo infection model. The expression and secretion of inflammatory cytokines including IL-6 and IL-1ß were significantly increased after Riclin treatment upon infection. The protective effect of Riclin was mainly through activating MAPK/IL-6 axis. HO-1/IL-1ß signaling pathway was less important in this process. Moreover, Riclin caused significant metabolic changes including pathways involved in glycolysis, protein synthesis and oxidative stress during Listeria infection. These results suggest a potential use of Succinoglycan Riclin as non-antibiotic preventive and therapeutic anti-microbial agent in livestock and poultry farming and human diseases.