No abstract

Diabetes mellitus (DM) disturbs normal functions from the level of cells to the level of organs. In this study, the authors explore the detrimental effects of type 1 diabetes on meiotic regulation depending on the duration of DM. In non-diabetes-prone BioBreeding (BBdr) control rats, most of the large follicles had germinal vesicle (GV)-intact oocytes. Conversely, a decrease of intact GV that was dependent on the duration of diabetic symptoms was observed; only 54% of the large follicles of diabetes-prone BB (BBdp) rats had GV-intact oocytes at 6 weeks after diabetes induction. Furthermore, some of the secondary follicles in BBdp rats also had germinal vesicle breakdown (GVB) oocytes. The nuclear status of the euglycemia BBdp rat was similar to those of the BBdr rat. In BBdp rats, the rate of meiotic progression to the metaphase II stage was significantly lower; however, the rate of segregated oocytes was significantly increased compared with controls during induction of in vitro maturation. The rate of segregated oocytes was not affected by the presence of the cumulus after chronic symptoms. These results indicate that chronic DM has a detrimental effect on meiotic regulation during folliculogenesis and results in a reduced number of competent oocytes. In addition, these data suggest that the follicle cells can resume supporting the meiotic regulation under euglycemia through insulin administration, independent of the duration of DM.

Coal fly dust (CFD)-induced asthma model is used as an ambient particulate matter model of serious pulmonary damage. We aimed to evaluate the effects of a combination of ginseng and Salvia plebeia R. Br extract (KGC-03-PS; KG3P) and its individual components (hispidulin, nepetin and rosmarinic acid) in a CFD-induced mouse model of airway inflammation (asthma). We also evaluated signal transduction by KG3P and its individual components in the alveolar macrophage cell line, MH-S cells. In vitro, KG3P and its individual components inhibited nitric oxide production and expression of pro-inflammatory mediators and cytokines (iNOS, COX-2, IL-1β, IL-6 and TNF-α) through the NF-κB and MAPK pathways in coal fly ash (CFA)-induced inflammation in MH-S cells. Moreover, in the CFD-induced asthma model in mice, KG3P and its predominant individual component, nepetin, inhibited Asymmetric Dimethyl arginine (ADMA) and Symmetric Dimethyl arginine (SDMA) in serum, and decreased the histopathologic score in the lungs. A significant reduction in the neutrophils and immune cells in BALF and lung tissue was demonstrated, with significant reduction in the expression of the pro-inflammatory cytokines. Finally, IRAK-1 localization was also potently inhibited by KG3P and nepetin. Thus, KG3P extract can be considered as a potent candidate for amelioration of airway inflammation.

The production, use, and waste of plastics increased worldwide, which resulted in environmental pollution and a growing public health problem. In particular, microplastics have the potential to accumulate in humans and mammals through the food chain. However, the toxicity of microplastics is not well understood. In this study, we investigated the toxicity of 10–50 μm polyethylene microplastics following single- and 28-day repeated oral administration (three different doses of microplastics of 500, 1000, and 2000 mg/kg/day) in ICR mice. For the investigation, we administered the microplastics orally for single- and 28-day repeated. Then, the histological and clinical pathology evaluations of the rodents were performed to evaluation of the toxicity test, and Raman spectroscopy was used to directly confirm the presence of polyethylene microplastics. In the single oral dose toxicity experiments, there were no changes in body weight and necropsy of the microplastics-treated group compared with that of controls. However, a histopathological evaluation revealed that inflammation from foreign bodies was evident in the lung tissue from the 28-day repeated oral dose toxicity group. Moreover, polyethylene microplastics were detected in the lung, stomach, duodenum, ileum, and serum by Raman spectroscopy. Our results corroborated the findings of lung inflammation after repeated oral administration of polyethylene microplastics. This study provides evidence of microplastic-induced toxicity following repeated exposure to mice.