Cognitive impairment is a common finding in patients with chronic obstructive pulmonary disease (COPD), but little attention has been focused on therapeutic intervention for this complication. Chronic intermittent hypoxia hypercapnia (CIHH) exposure is considered to be responsible for the pathogenesis of COPD. Dl-3n-Butylphthalide (NBP), extracted from Apium graveolens Linn, has displayed a broad spectrum of neuroprotective properties. Our study aimed to investigate the potential of NBP on CIHH-induced cognitive deficits. The cognitive function of rats after CIHH exposure was evaluated by the Morris water maze, which showed that the NBP treated group performed better in the navigation test. NBP activated BDNF and phosphorylated CREB, the both are responsible for neuroprotection. Additionally, NBP decreased CIHH induced apoptosis. Moreover, NBP further induced the expression of HIF-1α, accompanied by the up-regulation of the autophagy proteins Bnip3, Beclin-1 and LC3-II. Finally, NBP also reversed the decreased expression of SIRT1 and PGC-1α, but the expression of Tfam, Cox II and mtDNA remained unchanged. These results suggested that the neuroprotective effects of NBP under CIHH condition possibly occurred through the inhibition of apoptosis, promotion of hypoxia-induced autophagy, and activation of the SIRT1/PGC-1α signalling pathway, while stimulation of mitochondrial biogenesis may not be a characteristic response.

Background: Prolyl hydroxylases (PHDs) are linked to inflammatory bowel diseases (IBD); however, the exact role of PHD3, a member of PHD family, in IBD is unknown. Results: Deletion of Phd3 in mice intestinal epithelial cells causes spontaneous colitis. Conclusion: PHD3 protects the intestinal epithelial barrier function. Significance: The results are helpful for the development of therapeutic strategies for IBD.

The probiotic properties of two selected lactobacilli strains were assessed. L. salivarius and L. plantarum displayed higher hydrophobicity (48% and 54%, resp.) and coaggregation ability with four pathogens (from 7.9% to 57.5%). L. salivarius and L. plantarum had good inhibitory effects on S. aureus (38.2% and 49.5%, resp.) attachment to Caco-2 cells. Live lactobacilli strains and their conditioned media effectively inhibited IL-8 production (<14.6 pg/mL) in TNF-α-induced Caco-2 cells. Antibiotic-treated and the sonicated lactobacilli also maintained inhibitory effects (IL-8 production from 5.0 to 36.3 pg/mL); however, the heat-treated lactobacilli lost their inhibitory effects (IL-8 production from 130.2 to 161.0 pg/mL). These results suggest that both the structural components and the soluble cellular content of lactobacilli have anti-inflammatory effects. We also found that pretreatment of Caco-2 cells with lactobacilli inhibited S. typhimurium-induced IL-8 production (<27.3 pg/mL). However, lactobacilli did not inhibit IL-8 production in Caco-2 cells pretreated with S. typhimurium. These results suggest that the tested lactobacilli strains are appropriate for preventing inflammatory diseases caused by enteric pathogens but not for therapy. In short, L. salivarius and L. plantarum are potential candidates for the development of microbial ecological agents and functional foods.