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-1β, 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.

Fatigue induced by prolonged exercise not only leads to the decrease of exercise capacity, but also might be the cause of many diseases. In consideration of the side effects of pharmacological drugs, dietary supplements seem to be a better choice to ameliorate exercise-induced fatigue. The present study aimed to investigate the anti-fatigue effect of Salecan, a novel water-soluble β-glucan, during exercise and explore the underlying mechanisms. Male Institute of Cancer Research (ICR) mice were divided into five groups, including the Rest group and the other four Swim-groups treated with Salecan at 0, 25, 50, and 100 mg/kg/day for four weeks. Salecan treatment markedly increased the exhaustive swimming time of mice in the forced swimming test. Exercise fatigue and injury-related biochemical biomarkers including lactate, blood urea nitrogen (BUN), creatinine kinase (CK), alanine transaminase (ALT), and aspartate transaminase (AST) were ameliorated by Salecan. Salecan reversed the decreased serum glucose levels and glycogen contents caused by exercise. In addition, Salecan improved oxidative stress induced by exercise through regulating Nrf2/HO–1/Trx signaling pathway. Thus, the beneficial effects of Salecan against fatigue may be due to its positive effects on energy metabolism and antioxidation defence. Our results suggest that Salecan could be a novel potential candidate for anti-fatigue dietary supplements.

Exercise has been found to play important roles in regulating inflammation, although the mechanisms are unclear. The present systematic review and meta-analysis aimed to investigate whether regular exercise could regulate inflammation through inflammasome activation signalling in older adults. Five databases were searched, and 19 randomised controlled trials (RCTs) studying effects of regular exercise on inflammasome activation-related inflammatory cytokines interleukin (IL)-1β and IL-18 and other key molecules involved in inflammasome activation signalling such as NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1 in older adults aged 50 years or older were included. The results showed that regular exercise could significantly decrease the levels of IL-1β and IL-18, important end-products of inflammasome activation in older adults. Subgroup analyses showed that aerobic exercise is the most effective training modality, and low-to-moderate intensity and mixed intensity are better compared with high intensity to decrease IL-1β and IL-18. The effect of regular exercise on key molecules involved in inflammasome activation signalling including NLRP3, ASC and caspase-1 is understudied and needs to be further investigated. These findings demonstrate that regular exercise could effectively decrease inflammasome activation-related inflammatory cytokine levels in older adults.