Combined Amelioration of Prebiotic Resveratrol and Probiotic Bifidobacteria on Obesity and Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) and obesity are becoming increasingly common globally and characteristic as gut microbiota disturbance. Supplement of probiotics is considered as a promising strategy for NAFLD and obesity treatment. However, this effect varied from each other in clinical trials. We proposed that combination with a prebiotic substrate may improve the effects of probiotics. Thus, in this study, we investigated the separated and combined effects of Bifidobacteria and resveratrol (RSV) against obesity and NAFLD. NAFLD was caused by high-fat diet (HFD) feeding for 8 weeks. HFD-treated mice were orally treated with B. longum (1 × 109 CFU/mouse/day), RSV (100 mg/kg/day), and both of them from the fifth week. HFD feeding caused obesity and NAFLD as indicated by significantly increased body and liver weights, liver steatosis, elevated serum transaminases and lipid profiles, increased inflammation and imbalanced redox status. Based on these physical and biochemical parameters, inflammatory and antioxidant markers, individual administration of B. longum and RSV alleviated obesity and NAFLD, while coadministration of both products further enhanced the efficacy. These data suggested that combined prebiotic RSV and probiotic B. longum would be a potential candidate or adjuvant for the treatment of obesity and NAFLD.

Melatonin reverses the decreases in hippocampal protein serine/threonine kinases observed in an animal model of autism.

Lower global cognitive function scores are a common symptom of autism spectrum disorders (ASDs). This study investigates the effects of melatonin on hippocampal serine/threonine kinase signaling in an experimental ASD model. We found that chronic melatonin (1.0 or 5.0 mg/kg/day, 28 days) treatment significantly rescued valproic acid (VPA, 600 mg/kg)-induced decreases in CaMKII (Thr286), NMDAR1 (Ser896), and PKA (Thr197) phosphorylation in the hippocampus without affecting total protein levels. Compared with control rats, the immunostaining of pyramidal neurons in the hippocampus revealed a decrease in immunolabeling intensity for phospho-CaMKII (Thr286) in the hippocampus of VPA-treated rats, which was ameliorated by chronic melatonin treatment. Consistent with the elevation of CaMKII/PKA/PKC phosphorylation observed in melatonin-treated rat, long-term potentiation (LTP) was enhanced after chronic melatonin (5.0 mg/kg) treatment, as reflected by extracellular field potential slopes that increased from 56 to 60 min (133.4 ± 3.9% of the baseline, P < 0.01 versus VPA-treated rats) following high-frequency stimulation (HFS) in hippocampal slices. Accordingly, melatonin treatment also significantly improved social behavioral deficits at postnatal day 50 in VPA-treated rats. Taken together, the increased phosphorylation of CaMKII/PKA/PKC signaling might contribute to the beneficial effects of melatonin on autism symptoms.