The aim of this study was to observe sperm aneuploidy, DNA integrity, seminal alpha-glucosidase (NAG) and acrosin activity (AA) under testicular heat stress (SH). Spermatozoa were obtained from 30 healthy adult volunteers subjected to scrotal warming at 43°C for 30-40 min on two successive days per week for 3 months between February 2012 and September 2016. Aniline blue (AB), acridine orange (AO) staining, TUNEL assay and FISH analysis to evaluate sperm function, sperm DNA integrity and chromosomal abnormalities were carried on before, during and after SH. Sperm AA and NAG was measured by microplate reader. The mean parameters of sperm parameters, AA and NAG were significantly decreased. In contrast, the mean percentage of sperm DNA fragmentation and the proportion of aneuploidy of chromosomes 13, 18, 21, X and Y were significantly increased for spermatozoa collected during SH versus before SH (p < .01-.001). After stopping scrotal heating for 3 months, most parameters were completely restored to pre-SH levels. Sperm parameters, sperm DNA integrity, chromosomes, AA and NAG are affected by scrotal exposure to constant SH temperatures several degrees over normal physiological temperature, and after treatment, these parameters were reversibly restored to the level before SH in adult men.

At present, male contraceptive methods are only vasectomy and condoms, so it is necessary to research on male contraceptive techniques. The aim of this study is to observe the effects of scrotal heating (SH) on semen parameters, seminal l-carnitine (LC), epidermal growth factor (EGF), macrophage migration inhibitory factor (MIF), reproductive hormones and sperm chromosome numbers of adult healthy men, and to provide the experimental data for male contraception. The scrotums of 30 healthy male volunteers were exposed to the condition of 40 to 43°C SH belt warming 40 minutes each day for successive 2 days per week. The course of SH was continuous for 3 months. Computer-assisted semen analysis and hypo-osmotic swelling test, sperm DNA integrity, l-carnitine, MIF and EGF, and sperm fluorescence in situ hybridization were performed before, during, and after SH. The serum level of follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) were measured by chemiluminescent immunoassay. The mean parameters of sperm concentration, vitality, and normal morphological sperm were significantly decreased in groups with sperms being collected during 1, 2, and 3 months of SH when compared with those in groups of pre-SH (P < 0.01). Statistically significant differences of sperm DNA fragmentation, normal sperm membrane functionality, levels of LC and MIF in semen, and LH, FSH, and T in serum were observed between the groups of before SH and after SH 3 months and the groups of during SH 1, 2, and 3 months (P < 0.001). The total rate of chromosome number for 13, 18, 21, X, and Y in the 3 months of SH was 13.7-fold greater (13.72%/1.69%) than before SH (P < 0.001). The constant SH can impact the semen quality, sperm DNA integrity, sperm chromosome, LC and MIF, and LH, FSH, and T in serum. Transient SH may be a new method for male contraception.

Chorioamnionitis (CAM), as a common intrauterine infectious disease, is the leading cause of premature birth, stillbirth, neonatal infection and sepsis. The formyl peptide receptor 2 (FPR2) is a member of GPCRs widely distributed in a variety of tissues and is associated with many inflammatory diseases. With the discovery of FPR2 in human placenta, the possibility of exploring the function of FPR2 in obstetrics is evolving. The Resolvin D1 (RvD1) plays an important role in the resolution of inflammation by combining with FPR2. In this study, we evaluated the role of FPR2 and RvD1 in CAM, not only in the human placenta but also in mouse models. The expression of FPR2 increased in the placenta of CAM patients and the downstream PPARγ/NF‐κB signalling changed accordingly. Moreover, Fpr2−/− mice were highly susceptible to LPS, displaying a worse CAM symptom, compared with WT mice. By establishing a model of trophoblast inflammation in vitro, it was confirmed that RvD1 rescued the effect of LPS on inflammation by combining with FPR2 and its downstream PPARγ/NF‐κB pathway. Otherwise, RvD1 improved the preterm labour in a mouse model of CAM induced by LPS. Altogether, these findings show that RvD1 alleviated the inflammation of trophoblast in vivo and in vitro through FPR2/PPARγ/NF‐κB pathway, suggesting RvD1/FPR2 might be a novel therapeutic strategy to alleviate CAM.

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