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Hippocampal neurogenesis plays an important role in the onset and treatment of depressive disorders. Previous studies suggest that paeoniflorin could be used as an antidepressant for treating rats subjected to chronic unpredictable stress. In this study, the effects of paeoniflorin on neurogenesis in the hippocampus dentate gyrus and potential mechanism of action are further investigated in chronic unpredictable stress-induced rat. Results suggest that paeoniflorin markedly increased both sucrose consumption and the number of 5-bromo-2-deoxyuridine-positive cells in the dentate gyrus of chronic unpredictable stress-induced rats, and the ratio of co-expressed 5-bromo-2-deoxyuridine and glial fibrillary acidic protein-positive cells, but exerted no significant effect on the ratio of co-expressed 5-bromo-2-deoxyuridine and neuronal nuclei-positive cells. Compared with the vehicle group, a significant increase was detected in the number of brain-derived neurotrophic factor-positive cells and the expression of brain-derived neurotrophic factor mRNA in the hippocampus of the paeoniflorin-treated group. According to the results, paeoniflorin promoted neural stem cell proliferation, their differentiation into astrocytes, and neurogenesis in the hippocampal dentate gyrus of chronic unpredictable stress-induced rats. Apart from enhancing the protein expression and gene transcription of brain-derived neurotrophic factor, it also activated the expression of tropomyosin receptor kinase B (a high-affinity receptor of brain-derived neurotrophic factor). This suggests that paeoniflorin might promote neurogenesis in the hippocampus dentate gyrus of chronic unpredictable stress-induced rats and act as an antidepressant by regulating the brain-derived neurotrophic factor-tropomyosin receptor kinase B signaling pathway.

There was an error published in the online full-text and PDF versions of Journal of Experimental Biology (2020) 223, [jeb223560][1] ([doi:10.1242/jeb.223560][2]). The common name of the study organism was originally given as striped hamsters in the title of the article. The correct name appears in

Among the important aspects of climate change, exposure to high temperatures (heat waves) is rapidly emerging as an important issue, in particular for female mammals during lactation. High temperatures adversely impact ability to dissipate heat, which has negative effects on reproductive output. The cumulative effects on growth of F1 offspring after weaning and future reproductive performance of offspring remain uncertain. In this study, the F1 mice that weaned from mothers lactating at 21°C and 32.5°C were housed at 21°C from day 19 till 56 of age; during which food intake and body mass were measured. The F1 adult females that had been weaned at the two temperatures were bred and then both exposed to 32.5°C during lactation. Energy intake, milk output and litter size and mass were determined. The F1 adults weaned at 32.5°C consumed less food and had lower body mass than their counterparts weaned at 21°C. Several visceral organs or reproductive tissues were significantly lower in mass in F1 weaned at 32.5°C than at 21°C. The exposure to 32.5°C significantly decreased energy intake, milk output and litter mass in F1 adult females during lactation. The F1 adult females weaned at 32.5°C produced less milk and raised lighter pups than those previously weaned at 21°C. The data suggest that transient exposure to hot temperature during lactation has long-lasting impacts on the offspring, including stunted growth and decreases in future reproductive performance when adult. This indicates that the offspring of females previously experiencing hot temperatures have a significant fitness disadvantage.

Food restriction (FR) is the most commonly used intervention to prevent the overweight. However, the lost weight is usually followed by “compensatory growth” when FR ends, resulting in overweight. The present study was aimed to examining the behavior patterns and hormones mechanisms underpinning the over-weight. Energy budget and body fat content, and several endocrine markers related to leptin signals were examined in the striped hamsters under 20% FR refed by either low-fat diet (LF group) or high-fat diet (HF group). Body mass and fat content significantly regained when FR ended, and the hamsters in HF group showed 49.1% more body fat than in LF group (P

Background: Hyperosmotic solutions have been used successfully in different shock resuscitations with cardioprotection. This study was to examine the effects of hyperosmotic sodium chloride on isolated heart function and heart responses to ischemia/reperfusion in normotensive and hypertensive rats. The roles of hyperosmolarity-induced antioxidants including hyperosmolarity-relevant heat shock proteins as well as vasodilating endothelial nitric oxide synthase (eNOS) and vasoactive catecholamines were investigated.Methods: Hearts of normal rats and stroke-prone spontaneously hypertensive rats were isolated and perfused for 30 min with control Krebs-Henseleit buffer (osmolarity 300 mOsm/L) or hyperosmotic buffer of different sodium chloride concentrations (320, 350 and 400 mOsm/L) before subjected to 40-min global ischemia followed by 10-min hyperosmotic reperfusion and 30-min normal buffer reperfusion. Heart function, creatine phosphokinase leakage and myocardial antioxidants were examined. Myocardial antioxidants after hyperosmotic perfusion with different osmolytes were assayed with Western blotting.Results: Pre-ischemic hyperosmotic sodium chloride perfusion enhanced heart contractility and diastole function and reduced coronary vascular resistance in both normal and hypertensive hearts. Post-ischemic recoveries of heart function were improved in hyperosmotic perfused hearts, associated with lower creatine phosphokinase leakage, higher coronary flow, reduced coronary resistance and lower norepinephrine overflow. At the end of reperfusion, the myocardial activities of total superoxide dismutase and catalase, glutathione content as well as osmosis-relevant heat shock protein 32 and 90 were increased in hyperosmotic hearts. In addition to sodium chloride, in vitro hyperosmotic mannitol, glucose and raffinose also increased protein expressions of antioxidants including superoxide dismutase, catalase, heat shock protein 32 and 90 and vasodilating eNOS.Conclusion: Hyperosmotic perfusion enhanced heart function and preconditioned normal and hypertensive hearts against ischemia/reperfusion injury. The hyperosmolarity-induced up-regulations in myocardial antioxidants including heat shock proteins and eNOS may play an important role in the hyperosmolarity-induced cardioprotection.