Effect of Huaji Jianpi Decoction on the semen quality of high-fat diet-induced obese mice.

Background: At present, the incidence of obesity is increasing. Several studies have shown that obesity can reduce male fertility by affecting spermatogenesis and semen quality. Traditional Chinese medicine (TCM) has fewer side effects and stable efficacy in the treatment of related diseases. This study aimed to investigate the effect of Huaji Jianpi Decoction on the semen quality of high-fat diet-induced obese mice. Methods: The obese male mice model was constructed by using high-fat diet and the Huaji Jianpi Decoction was processed into an aqueous extract. Mice were allocated in the normal group (n=30) and five different treatment groups (n=50). Huaji Jianpi Decoction was applied in low-, medium- and high-dose [17.52 g/(kg·d), 35.04 g/(kg·d) and 70.07 g/(kg·d), respectively]. The body weight, body fat, testis wet weight, testis coefficient, and routine sperm parameters were detected and analyzed. Meanwhile, transmission electron microscope (TEM) was used to observe testis ultrastructure. reverse-transcription quantitative PCR (RT-qPCR) was used to measure the expression of tumour necrosis factor α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1). Results: Compared with normal mice (ND), the testis wet weight and testis coefficient of mice in the blank group were significantly decreased, while the number of mitochondria was observed to be decreased on testis ultrastructure examination, and apoptotic cells and germ cells in the spermatogenic tubules were shed. After Huaji Jianpi Decoction administration, the body fat and blood lipid levels of obese mice were decreased, the testis wet weight and testis coefficient were increased, and semen parameters were increased. Different doses of Huaji Jianpi Decoction could improve testicular weight, sperm density, sperm motility, forward motility, and total sperm motility. Huaji Jianpi Decoction could also downregulate TNF-α and MCP-1 expression and inhibit germ cell apoptosis to improve semen quality. Conclusions: Huaji Jianpi Decoction can improve the semen quality of high-fat diet-induced obese mice by reducing weight and lipid levels.

Prenatal exposure to air pollution and neurodevelopmental delay in children: A birth cohort study in Foshan, China.

BACKGROUND: Prenatal exposure to air pollution may have adverse effects on neurodevelopment in children, but epidemiological evidence remains inconclusive. OBJECTIVE: To investigate the associations between prenatal air pollution exposure and neurodevelopmental delay. METHODS: We conducted a birth cohort study based on pregnancy and birth registry in Foshan, China. Exposure to particulate matter of aerodynamic diameter < 1 µm, 2.5 µm, 10 µm (PM1, PM2.5, PM10), nitrogen dioxide (NO2) and sulfur dioxide (SO2) over pregnancy (trimester 1, 2, 3 and entire pregnancy) was estimated at each woman's residential address using spatial-temporal models. Neurodevelopmental assessment was performed by pediatricians using a five-domain scale and developmental quotient (DQ) was calculated as a global measure. Logistic regression models were used to investigate the associations between prenatal air pollution exposure and neurodevelopmental delay (DQ < 75) with adjustment for potential confounders. RESULTS: We included 15,778 child-mother pairs in this analysis, including 1013 children with neurodevelopmental delay. We observed positive associations between prenatal exposure to air pollution and higher risk of neurodevelopmental delay in children. The adjusted odds ratios (ORs) per 10 µg/m3 elevation in PM1, PM2.5, PM10, NO2 and SO2 in entire pregnancy were 1.12 [95% confidence interval (CI): 1.01, 1.25], 1.15 (95% CI: 1.03, 1.29), 1.12 (95% CI: 1.02, 1.24), 1.06 (95% CI: 0.94, 1.19) and 1.58 (95% CI: 1.11, 2.23), respectively. The associations were more robust for trimester 1 and trimester 2, especially trimester 1. CONCLUSIONS: Exposure to air pollution during pregnancy, especially early-to-mid pregnancy, was associated with increased risk of neurodevelopmental delay in young children, indicating its adverse neurodevelopmental effects in early-life stage.

Preliminary investigation of the effects of an FCF inhibitor interference with Septin in the early stage embryos in mice.

The objective of the present study was to investigate the effects of for chlorfenuron (FCF) interference with the septin protein on early stage embryos in mice. The 1­cell embryos were collected and divided into an FCF interference group and a control group. The FCF interference group was cultured in FCF media and the control group was cultured in dimethyl sulphoxide media at 37˚C with 5% CO2 until the desired phase was achieved. Septin2 protein expression was detected using immunofluorescence and western blot analysis. Blastocyst α­tubulin was stained by immunofluorescence to observe the alterations in spindles and microtubules. The rate of early embryo development into blastocysts was significantly reduced following FCF treatment (P<0.05). In the control group, septin2 was observed with a confocal microscope; septin2 was expressed in embryos at all stages and mainly in the blastomeres from the 2­cell stage onwards, with the expression concentrated in the nuclei of the blastomeres as identified by strong fluorescence. In the FCF interference group, septin2 was weakly expressed in the nuclei of blastomeres at the 2­ and 4­cell stages, and in the granulated blastomeres at the 4­ and 8­cell stages. Expression was barely observed in and following the morula. Granulation was observed starting from the 4­ and 8­cell stages. Compared with the control group, the FCF interference group exhibited irregular microtubules, abnormal spindle morphology and disordered chromosome arrangement in the blastocysts. The septin2 protein was expressed throughout the early stage embryo from the 2­cell stage to the blastocyst and localized in the nuclei of blastomeres. When the septin protein experienced interference by the FCF inhibitor, septin2 protein expression was reduced, which simultaneously resulted in abnormal embryonic development, uneven cytoplasmic division, various sizes and a reduced number of blastomeres, granulation in the blastomeres, disordered blastocyst microtubule distribution, spindle shape alterations and an abnormality of chromosome arrangement.

[Effects of obesity on global genome DNA methylation and gene imprinting in mouse spermatozoa].

OBJECTIVE: To investigate the influence of high fat diet-induced obesity (HFDIO) on the differentially methylated region (DMR) of the imprinted gene and global genome methylation of sperm DNA. METHODS: We performed bisulfite sequencing on the DMR of the imprinted gene and global genome methylation of sperm DNA in the mouse model of HFDIO. RESULTS: No statistically significant differences were found between the HFDIO model and normal control mice in MEG3-IG (93.73 vs 97.26%, P = 0.252), H19 (98.00 vs 97.83%, P = 0.920), IGF2 (97.34 vs 96.25%, P =0.166), IGF2R (1.43 vs 1.11%, P = 0.695), PEG3 (0.19 vs 0.38%, P = 0.537), MEST (0.23 vs 0.68%, P = 0.315), NNAT (0.31 vs 0.00%, P = 0.134), or SNRPN (1.88 vs 3.13%, P = 0.628). A total of 8 942 DMRs were detected across the sperm genome (P <0.05). Gene functional enrichment analysis indicated that the enriched terms with the largest numbers of genes were the metabolic process (n = 1 482), RNA synthesis (n = 779), and transcription (n = 767). CONCLUSIONS: The methylation level underwent no significant change in the DMRs of the imprinted genes from the mice with HFDIO, but the CG methylation of the genes involved in the metabolic process, RNA synthesis and transcription were significantly altered.