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.

The associations between endocrine disrupting chemicals and markers of inflammation and immune responses: A systematic review and meta-analysis.

Exposure to endocrine disrupting chemicals (EDCs) may lead to dysregulated inflammatory responses, however, the detailed relationship between different EDCs and inflammation remains unclear. A systematic review and meta-analysis was conducted to evaluate the associations between four types of EDCs (bisphenol A (BPA), phthalates (PAEs), organochlorine pesticides (OCPs), and polychlorinated biphenyls (PCBs)) and markers of inflammation and immune responses in humans. Three databases were searched, and 36 studies with a total of 22055 participants were included. The associations between EDCs and 26 inflammation-related acute phase proteins and cytokines were analyzed. The results demonstrated that exposure to BPA was positively associated with circulating levels of C-reactive protein (CRP) and interleukin (IL)-6. Exposure to PAEs was associated with elevated levels of CRP, IL-6 and IL-10. Subgroup analysis found that three PAE metabolites mono-benzyl phthalate (MBzP), mono-isobutyl phthalate (MiBP), and mono-n-butyl phthalate (MnBP) were directly associated with a higher level of CRP, and two other PAE metabolites mono-carboxyisononyl phthalate (MCNP) and mono-3-carboxypropyl phthalate (MCPP) were positively associated with IL-6. The positive associations between PAEs and CRP, IL-6 and IL-10 were significant in the high-molecular-weight phthalate (HMWP) exposure group, not the low-molecular-weight phthalate (LMWP) exposure group. Exposure to OCPs was positively associated with CRP, IL-1ß, IL-2, and IL-10. No significant association was found between PCBs and inflammatory markers. These findings demonstrate that exposure to EDCs is closely linked to dysregulated inflammatory responses. More studies should be conducted in the future to get a comprehensive view of the associations between different EDCs and inflammation, and investigations on the underlying mechanisms are needed.

Effects of yeast ß-glucans for the prevention and treatment of upper respiratory tract infection in healthy subjects: a systematic review and meta-analysis.

PURPOSE: Yeast ß-glucans are known for their immune-modulating effects; however, their effects on human upper respiratory tract infections (URTIs) remain unclear. The aim of the present study was to use a systematic review and meta-analysis approach to investigate the effects of yeast ß-glucans for the prevention and treatment of URTIs in healthy subjects. METHODS: Databases including Pubmed, Web of Science, EMBASE and the Cochrane Library were searched and 13 RCTs investigating the effects of yeast ß-glucans on the incidence, duration, and severity of URTIs in healthy subjects were included. RESULTS: The results showed that compared to the placebo group, yeast ß-glucan could significantly reduce the incidence of URTIs (OR = 0.345, 95% CI = 0.192 to 0.620, p < 0.001), decrease the average number of URTI episodes (SMD = - 0.315, 95% CI = - 0.500 to - 0.130, p < 0.05), and decrease the duration of URTIs (SMD = - 0.312, 95% CI = - 0.561 to - 0.064, p < 0.001). Improved severity of symptoms was found in yeast ß-glucan group compared to the placebo group in the majority of included studies. In addition, yeast ß-glucan was well tolerated and safe in general. CONCLUSION: These findings suggest a positive effect of yeast ß-glucans on human URTIs. However, due to the high heterogeneity and small number of included studies, more high-quality research and clinical trials are warranted.