Background: Aurora B is one of the spindle assembly checkpoint proteins. It plays a crucial role in the regulation of mammalian female mitosis and meiosis. In this study, we examined the mechanism of small ubiquitin-related modifier modification (SUMOylation) of Aurora B on the chromosome arrangement of mice oocytes. Methods: Oocytes were randomly divided into three groups: Control group, AuroraB_K207R group, and the small ubiquitin-related modifier (SUMO) inhibitor group. The number of oocytes that developed at 2.5, 8, and 14 h were counted. Metaphase II (MII) oocytes in each group were selected for observing the arrangement of chromosomes and spindles. Meanwhile, MII oocytes in the control and AuroraB_K207R groups were collected for use in the Smart-seq2 protocol. Results: Messenger ribonucleic acid (mRNA) was obtained from the AuroraB_K207R group via the transcription of a linearized pMD 18T-T7-AuroraB_K207R plasmid. The proportion of metaphase I (MI) oocytes after 8 h in the SUMO inhibitor group was significantly lower than in the AuroraB_K207R and control groups (p < 0.05). The MII oocytes in the AuroraB_K207R and SUMO inhibitor groups decreased significantly compared with the control group after 14 h (p < 0.05). Furthermore, the rate of abnormal chromosome arrangement in the AuroraB_K207R and SUMO inhibitor groups increased significantly compared with the control group (p < 0.05). Using Smart-seq2, a total of 3288 differentially expressed genes were identified; 2874 of these genes involving Aurora B were upregulated and 414 genes were downregulated in the AuroraB_K207R group. Conclusions: Small ubiquitin-related modifier modifications may directly affect the regulatory function of Aurora B on chromosome arrangement in mice oocyte meiosis, leading to oocyte maturation disorder. Therefore, the SUMOylation of Aurora B plays an important role in chromosome arrangement in mice oocyte meiosis.

Objective The present study aims to evaluate the effect of monosodium glutamate on testicular spermatogenesis in mice from the perspective of the hypothalamic-pituitary-testicular axis and whether this destructive effect is alleviated with time. Methods Neonatal mice were randomly divided into a monosodium glutamate (MSG) group and a control group, just below the interscapular region after birth with 10 µL MSG to deliver 4 mg/g (body mass), or with equivalent volumes of 0.9% saline. Samples which involved blood, brains and testicles of mice were collected and measured at puberty at 60 days and adulthood at 90 days. Results The results show that the fluorescence intensity of GnRH nerve fibers, the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) hormones in the reproductive system, the number of spermatocytes and spermatozoa in testicular sections, the body length, body weight, testicular weight, and testicular index in the 60-day-old mice in monosodium glutamate group (MSG60 group) and the MSG90 group were lower than those in the 60-day-old mice in normal control group (NC60 group) (p < 0.05), but the number of apoptotic cells in the testicular section was higher than in the NC60 group (p < 0.05). When the 90-day-old mice in monosodium glutamate group (MSG90 group) was compared with the MSG60 group, except for body weight and testicular weight increase (p < 0.05), there is no significant difference in the other parameters mentioned above (p > 0.05). Conclusion Monosodium glutamate can cause reproductive toxicity to male mice by damaging GnRH neurons, and this reproductive toxicity cannot be relieved spontaneously over time. These findings are supported by observed histological changes.

The aim of the present study was to determine whether arcuate nucleus (ARC) lesions affect the ghrelin level in the plasma and the stomach in monosodium glutamate (MSG)‑treated mice. The aim of the present study was to investigate whether the ARC was destroyed in mice treated neonatally with MSG, and whether the ARC lesions affect the ghrelin level in the plasma and lipid mobilization in MSG‑treated mice. The results revealed that MSG led to a marked reduction in ARC cresyl violet staining, tyrosine hydroxylase-immunoreactive (IR) neurons and neuropeptide Y‑IR fibers, compared with saline controls. MSG‑treated mice exhibited significantly increased body mass compared with saline controls, and MSG treatment did not prevent food deprivation‑induced decrease in white adipose tissue mass compared with controls. Plasma ghrelin levels were significantly increased in MSG‑treated mice that were fasted for 48 h, compared with the levels prior to fasting and re‑feeding, and the preprandial peak of plasma ghrelin persisted in MSG‑treated mice. In summary, the ARC was not found to be essential for food deprivation‑induced lipid mobilization and preprandial peak in MSG‑treated mice. However, this finding does not mean that ARC neurons do not contribute to food sensing and lipid mobilization under normal conditions, as compensatory mechanisms may have emerged after the ablation of ARC neurons.