Polystyrene micro- and nano-particle coexposure injures fetal thalamus by inducing ROS-mediated cell apoptosis.

The adverse effects of plastic on adult animal and human health have been receiving increasing attention. However, its potential toxicity to fetuses has not been fully elucidated. Herein, biodistribution of polystyrene (PS) particles was determined after the maternal mice were orally given PS micro- and/or nano-particles with and without surface modifications during gestational days 1 to 17. The results showed that PS microplastics (MPs) and nanoparticles (NPs) mainly emerged in the alimentary tract, brain, uterus, and placenta in maternal mice, and only the latter infiltrated into the fetal thalamus. PS NPs and carboxyl-modified NPs induced differentially expressed genes mainly enriched in oxidative phosphorylation and GABAergic synapse. Maternal administration of PS particles during gestation led to anxiety-like behavior of the progenies and their γ-aminobutyric acid (GABA) reduction in the prefrontal cortex and amygdala at Week 8. N-Acetylcysteine (NAC), an antioxidant, alleviated PS particles-induced oxidative injury in the fetal brain and rescued the anxiety-like behavior of the progenies. Additionally, PS nanoparticles caused excessive ROS and apoptosis in neuronal cell lines, which were prevented by glutathione supplementation. These results suggested that PS particles produced a negative effect on fetuses by inducing oxidative injury and suppressing GABA synthesis in their brain. The findings contribute to estimating the risk for PS particles to human and animal health.

Baicalin alleviates endometrial inflammatory injury through regulation of tight junction proteins.

Endometritis is the foremost reason for reduced reproductive performance, which impedes the establishment of pregnancy in ruminants. Baicalin is extensively acknowledged as a tocolytic drug. However, the preventive effect of baicalin on endometrial inflammatory injury remains unclear. The present study aimed to determine the potential benefits of baicalin on endometrial inflammatory injury in animal and cellular models. The results showed that baicalin alleviated the impairment of tight junctions (TJs) and inflammation in the endometrium induced by LPS treatment. Baicalin increased claudin 3 (CLDN3) and tight junction protein 1 (TJP1) levels in a dose-dependent manner in endometrial epithelial cells (EECs) accompanied by autophagy activation with or without LPS treatment. Immunofluorescence staining revealed that baicalin pretreatment prompted MAP1LC3B-positive structures to surround TJ proteins in the cytoplasm and decreased the abnormal aggregation of CLDN3 and TJP1 in the cytosol of EECs. Activation or blockage of autophagy using pharmacologic methods affected the redistribution of TJ proteins by baicalin pretreatment with LPS treatment. The role of autophagy in the modulation of TJ proteins was also confirmed by ATG7 and TFEB overexpression, as evidenced by accelerated redistribution of CLDN3 and TJP1 from the EEC cytosol to the membrane and a loss of membranous CLDN2 in EECs. These data demonstrate that baicalin influences the redistribution of TJ proteins to maintain the barrier function during LPS-induced endometrial inflammatory injury by regulating autophagy and provides a new therapeutic to potentially prevent embryo loss and endometritis.

The involvement of the primo vascular system in local enteritis and its modification by electroacupuncture.

Introduction: The primo vascular system (PVS), an intensive network structure, has been claimed to be representative of the acupuncture meridian. Here, we explored the role of the PVS in local enteritis and its modification by acupuncture. Methods: Chronic cecitis in rabbits was induced by 2,4,6-trinitro-benzene-sulfonic acid (TNBS). The PVS on the cecum was visualized with trypan blue staining, and collected with the help of microsurgical forceps under an optical stereomicroscope. Results: The increased primo vessels (PVs) and primo nodes (PNs) of the PVS on the surface of the cecum were induced by local inflammation, which was positively correlated with the inflammatory cells in the cecal mucosa. Tandem mass tag (TMT) based proteomic analysis revealed that 110 differentiated proteins of the PVS existed between TNBS-treated and control rabbits; 65 proteins were upregulated, while 45 proteins were downregulated. These proteins were mainly enriched in inflammation- and immunity-related processes, such as inflammatory cell proliferation, antigen presentation, and cell adhesion in the proliferated PVS (data are available via ProteomeXchange with the identifiers PXD034280). Importantly, TNBS-induced cecitis, the proliferated PVS and inflammation response-related proteins (CD40, CD45, HLA-DRA1, LAMP1, JAGN1 and FGL1) in the PVS were alleviated or reversed by repetitive electroacupuncture (EA) stimulations. Conclusion: These results suggest that the proliferated PVS and its active inclusions were related to the inflammatory process, which was modified by EA. Our study provides a new avenue for further exploration of the mechanism by which EA exerts anti-inflammatory effects.

The patterns of exercise-induced ß-endorphin expression in the central nervous system of rats.

Exercise at different intensities is able to induce different physical and psychological statuses of the subjects. The ß-endorphin (ß-EP) in central nervous system is thought to play an important role in physical exercise. However, its expression patterns and physiological effects in the central nuclei under different exercise states are not well understood. Five-week old male Sprague-Dawley rats were randomly divided into two groups of 21 each: Control and Exercise. Control rats were sedentary while Exercise rats were arranged to run on a treadmill (5-week adapting or moderate exercise and 2-week high-intensity exercise). Seven rats were taken from each group at day33, day42 and day49 for examination of blood biochemical parameters (lactate, Lac; blood urea nitrogen, BUN; glucose) and for detection of nuclei ß-EP level with immunohistochemistry. The results showed that Lac and BUN levels were significant increased after the high intensity exercise. The five-week exercise caused a significantly increased ß-EP in caudate putamen (CPu), amygdala, paraventricular thalamic nucleus (PVT), ventromedial hypothalamus nucleus (VMH) and gigantocellular reticular nucleus (Gi). The high intensity exercise induced an elevated ß-EP in CPu and nucleus of the solitary tract (Sol), but a decreased ß-EP in globus pallidus (GP). Compared with Control, exercise rats showed an elevated ß-EP in CPu, PVT, VMH, accumbens nucleus, Gi and Sol, and a decreased ß-EP in GP at day49. The ß-EP levels in acurate nucleus, periadueductal gray and parabrachial nucleus were not changed at day33, 42 and 49. In conclusion, ß-EP levels in different nuclei changed under the moderate and high intensity exercises, which may contribute to modifying exercise-produced psychological and physiological effects.