An enriched environment improves long-term functional outcomes in mice after intracerebral hemorrhage by mechanisms that involve the Nrf2/BDNF/glutaminase pathway.

Post-stroke depression exacerbates neurologic deficits and quality of life. Depression after ischemic stroke is known to some extent. However, depression after intracerebral hemorrhage (ICH) is relatively unknown. Increasing evidence shows that exposure to an enriched environment (EE) after cerebral ischemia/reperfusion injury has neuroprotective effects in animal models, but its impact after ICH is unknown. In this study, we investigated the effect of EE on long-term functional outcomes in mice subjected to collagenase-induced striatal ICH. Mice were subjected to ICH with the standard environment (SE) or ICH with EE for 6 h/day (8:00 am-2:00 pm). Depressive, anxiety-like behaviors and cognitive tests were evaluated on day 28 with the sucrose preference test, tail suspension test, forced swim test, light-dark transition experiment, morris water maze, and novel object recognition test. Exposure to EE improved neurologic function, attenuated depressive and anxiety-like behaviors, and promoted spatial learning and memory. These changes were associated with increased expression of transcription factor Nrf2 and brain-derived neurotrophic factor (BDNF) and inhibited glutaminase activity in the perihematomal tissue. However, EE did not change the above behavioral outcomes in Nrf2-/- mice on day 28. Furthermore, exposure to EE did not increase BDNF expression compared to exposure to SE in Nrf2-/- mice on day 28 after ICH. These findings indicate that EE improves long-term outcomes in sensorimotor, emotional, and cognitive behavior after ICH and that the underlying mechanism involves the Nrf2/BDNF/glutaminase pathway.

Bioinformatic prediction of the structure and characteristics of human sperm acrosome membrane-associated protein 1 (hSAMP32) and evaluation of its antifertility function in vivo.

Human sperm acrosome membrane-associated protein 1 (hSAMP32) plays an important role in the acrosome reaction, sperm-egg primary binding, secondary binding and fusion processes. However, its spatial structural and invivo antifertility function remain unknown. In this study, we first analysed the physical and chemical characteristics and antigenic epitopes of immunised mice using bioinformatics. Then, we constructed the prokaryotic expression vector pcDNA3.1-hSAMP32 to immunise BALB/c mice invivo. IgG antibodies in the serum were detected, and the litter size of female mice and the number of the hamster eggs penetrated were counted. hSAMP32 was found to contain six hydrophilic regions and a signal peptide beginning at amino acid position 29. The transmembrane region of hSAMP32 was located within amino acids 217-239 with α-helices and random coil structures. We predicted five antigenic epitopes. The molecular weight of hSAMP32 was 59 kDa. Moreover, the results of invivo studies revealed that 56 days after the first immunisation, the litter size was significantly smaller for female pcDNA-3.1(+)-hSAMP32-immunised (mean±s.d. 4.33±1.21) than control mice (9.50±0.55), indicating that the immunocontraception vaccine had an antifertility effect. This experiment presents a theoretical and experimental basis for in-depth study of the hSAMP32 mechanism within the sperm-egg fusing process and for the screening of antigenic epitopes with immunocontraceptive properties.

Establishment of rapid risk assessment model for cigarette smoke extract exposure in chronic obstructive pulmonary disease.

Rapid risk assessment models for different types of cigarette smoke extract (CSE) exposure are critical to understanding the etiology of chronic obstructive pulmonary disease. The present study investigated inflammation of cultured tracheal tissues with CSE exposure. Rat trachea rings were isolated, cultured, then exposed to various concentrations of CSE from 3R4 F reference cigarettes for 4 h. Tissue/cellular morphology, ultrastructure, viability and damage, inflammatory cell infiltration, and inflammatory protein levels were measured and compared to untreated controls. Human bronchial epithelial cells (BEAS-2B) exposed to 0 or 300 µg/mL CSE were cocultured with macrophages to assess extent of mobilization and phagocytosis. Endotracheal epithelium cilia densities were significantly reduced with increasing CSE concentrations, while mucous membranes became increasingly disordered; both eventually disappeared. Macrophages became larger as the CSE concentration increased, with microvilli and extended pseudopodium covering their surface, and many primary and secondary lysosomes present in the cytoplasm. Inflammatory cell infiltration also increased with increasing CSE dose, as did intracellular adhesion molecule-1(ICAM-1), interleukin-6(IL-6). The method described here may be useful to qualitatively characterized the effects of the compound under study. Then, we use BEAS-2B cell line system to strength the observation made in the cultured tissues. Probably, an approach to integrate results from both experiments will facilitate its application. These results demonstrate that cultured rat tracheal rings have a whole-tissue structure that undergoes inflammatory processes similar to in vivo tissues upon CSE exposure.