No abstract

Serine alleviates inflammatory responses and is beneficial for gut health; however, whether it exerts any effects on ulcerative colitis or regulates intestinal microbiota remains unknown. We investigated the effects of serine supplementation on colonic morphology, inflammation, and microbiota composition in dextran sulfate sodium (DSS)-induced colitis model in mice. Acute colitis was induced through the oral intake of 3.5% DSS in water for 7 days. Mice with acute colitis were divided into two groups; The DSS and Ser-treated groups were rectally administrated with PBS or 1% (w/v) serine (40 mg/kg body weight) for 7 days. The results showed that serine decreased the disease activity index, as well as myeloperoxidase, eosinophil peroxidase, and proinflammatory cytokine concentrations in colonic tissue, while serine improved colonic morphology and inhibited cell apoptosis in colitis mice. In addition, 16S rRNA phylogenetic sequencing revealed a shift in bacterial community composition, and changes in microbiota functional profiles following serine supplementation, although no significant difference in α-diversity analysis was observed. The effects of serine supplementation helped on the recovery of major perturbations to macrobiotic functions, such as amino acids metabolism; tissue replication and repair; and cell growth and death. Serine might have great potential for the renewal of colonic tissue in DSS-induced colitis.

Propofol and ketamine may provide certain degree of neuroprotection, but the underlying mechanism remains unclear to date. The cAMP response element-binding protein (CREB) was proposed that its phosphorylation at Ser133 (P-CREB) constituted a convergence point involved in neuroprotection. The purpose of this study was to determine whether different dosages of propofol and ketamine could provide neuroprotection against permanent middle cerebral artery occlusion (MCAO)-induced ischemic injuries and the involvement of P-CREB. Eighty adult male BALB/c mice that underwent 6 h MCAO were randomly divided into eight groups: Sham-operation; MCAO + saline; MCAO + 25, 50, 100 mg/kg propofol; and MCAO + 25, 50, 100 mg/kg ketamine (intraperitoneal injection 30 min following MCAO). We found that 50, 100 (not 25) mg/kg propofol, and 25 (not 50 and 100) mg/kg ketamine could significantly reduce the infarct volume, edema ratio and neurological deficit (n = 10 per group) as well as inhibit the decrease of P-CREB level in peri-infarct region when compared with that of MCAO + saline group (n = 6 per group). In addition, the results of double-labeled immunofluorescent staining showed that P-CREB co-localized with neuron-specific marker, NeuN, in the peri-infarct region of 50 mg/kg propofol and 25 mg/kg ketamine treated 6 h MCAO mice (n = 4 per group). These results suggested that inhibition of neuron-specific P-CREB dephosphorylation in the peri-infarct region is involved in high dose propofol and low dose ketamine-induced neuroprotection of 6 h MCAO mice.