This study was conducted to explore the effects of maternal exposure to perfluorooctanoic acid (PFOA) on reproduction and development of male offspring mice. Pregnant mice were given 1, 2.5 or 5 mg/kg BW PFOA daily by gavage during gestation. The results showed that the survival number of offspring mice at weaning was significantly decreased. There were no differences in the testicular index of offspring mice between PFOA exposure groups and non-PFOA group. Maternal exposure to PFOA reduced the level of testosterone in the male offspring mice on PND 21 (p < 0.01) but increased in 1 mg/kg group and decreased in 2.5 and 5 mg/kg groups on PND 70 (p < 0.01). There were different degrees of damage to testis in a dose-dependent manner, and the number of Leydig cells markedly decreased (p < 0.01) in 2.5 and 5 mg/kg PFOA groups on PND 21 and PND 70. The expression of Dlk1-Dio3 imprinted gene cluster showed a decreasing trend, where Glt2, Rian and Dio3 gene expressions were significantly reduced (p < 0.05) on PND 21. Therefore, PFOA exposure during pregnancy reduces the number of survival offspring mice, damages testis, disrupts reproductive hormones and reduces the mRNA expressions of the Dlk1-Dio3 imprinted cluster in testis.
This study investigated the anti-inflammatory effects and possible underlying mechanisms of Salvia miltiorrhiza polysaccharides (SMP) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The cytotoxicity of SMP was detected by the MTT method. The morphological change of RAW264.7 was observed by Diff-Quik staining. Enzyme-linked immunosorbent assay was used to evaluate the production of cytokines in LPS-induced RAW264.7 cells. The nitric oxide (NO) kit assay detected the NO release from LPS-induced RAW264.7 cells. Real-time polymerase chain reaction was used to detect the transcriptions of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), inducible NO synthase (iNOS), and cyclooxygenase (COX)-2 in LPS-induced RAW264.7 cells. The protein expression of nuclear NF-κB was measured by Western blot. The results showed that the safe medication range of SMP was less than 3 mg/mL. Compared with the LPS model group, SMP (2, 1, and 0.5 mg/mL) improved the degree of cell deformation and reduced the amount of pseudopodia, and statistically reduced the secretions of cytokines in cells induced by LPS (P < 0.01) at different time points. SMP significantly inhibited the mRNA transcriptions of TNF-α, IL-6, iNOS, and COX-2 and the protein expressions of NF-κB, p-p65, and p-IκBa. In conclusion, this study preliminarily proved the protective effect of SMP on LPS-induced RAW264.7 macrophage. Its mechanism might be related to inhibition of NF-κB signal pathway and the gene expressions and secretion of cytokines.
The present study investigated the reproductive toxicity of bisphenol A (BPA) exposure to the mother on the offspring mice. BPA was given to pregnant mice at 50 mg/kg, 500 mg/kg, and 2500 mg/kg BW BPA daily by gavage during the whole gestation period. The offspring mice were sacrificed at 8 weeks of age. Results showed that exposure of BPA to the mother increased the mortality (P < 0.05). Maternal exposure of BPA reduced the levels of T (♂) and FSH (♀) (P < 0.01) and elevated E2 (♀) level in the adult offspring (P < 0.01). BPA exposure caused testicular damage as shown by less Leydig cells and ovarian injury as shown by more vacuoles and less corpus granules in the adult offspring mice. Immunohistochemistry revealed that maternal exposure of BPA increased Bax and decreased Bcl-2 at the protein levels in testicular and ovary tissues in the offspring mice. BPA significantly reduced the expression of StAR in male offspring (P < 0.05). Interestingly, the mRNA levels of Cyp11a were significantly decreased in 50 mg/kg groups and were increased in 500 mg/kg group in the males. Reduced Kitlg and elevated Amh at the mRNA levels were detected in the female offspring.
To investigate the regulatory mechanism of the follicular–luteal phase transition in Turpan black sheep (Ovis aries), the genome‐wide expression patterns of microRNAs (miRNAs) and genes were investigated in ovaries of six sheep (3 years and single lamb with 3 consecutive births) during follicular and luteal phases of the oestrous cycle. Bioinformatic analysis was used to screen potential miRNAs and genes related to Turpan black sheep ovarian function. RT‐qPCR was used to validate the sequencing results. In total, we identified 139 known and 71 novel miRNAs in the two phases with miRNA‐seq, and a total of 19 miRNAs were significantly differentially expressed, of which 7 were up‐regulated and 12 were down‐regulated in the follicular phase compared with luteal phase. A total of 150 genes were significantly differentially expressed, including 63 up‐regulated and 87 down‐regulated in the follicular phase compared with the luteal phase by RNA‐seq data analysis. Those DEGs were significantly enriched in 103 GO terms and several KEGG pathways, including metabolic pathway, ovarian steroidogenesis, steroid hormone biosynthesis and oestrogen signalling pathway. In addition, we created a miRNA–mRNA regulatory network to further elucidate the mechanism of follicular–luteal transition. Finally, we identified key miRNAs and genes including miR‐143, miR‐99a, miR‐150, miR‐27a, miR‐125b, STAR, STAT1, which might play crucial roles in reproductive hormone biosynthesis and follicular development. The miRNA–mRNA interactive network clearly illustrates molecular basis involving in follicular–luteal transition.
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