ABSTRACT
OBJECTIVE: To investigate the effect of a modified Wuzi Yanzong Pill (, WZYZP) on the male rats' testis after microwave radiation, as well as its potential mechanism. METHODS: Forty-five male rats were randomly assigned to three groups: the control group, the radiation group, and the WZYZP group. The rats in the radiation group and WZYZP group were exposed to microwave radiation for 15 min once, while the rats in the control group were not exposed to any radiation. The rats in the WZYZP group were given a modified of WZYZP by gavage daily for 7 days. Apoptosis in the testis was evaluated using terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay. Histopathological alterations of the testis were observed by haematoxylin-eosin (HE) staining. Tat-interactive protein, 60kD (Tip60) and p53 expressions were determined by Western blotting. RESULTS: The apoptosis index (AI) in the radiation group was higher than that of the WZYZP group and control group on day 1 (D1), day 7 (D7) day 14 (D14) after radiation (P<0.05). The seminiferous tubules were of normal morphology in the control group. In the radiation group, the partial seminiferous tubules were collapsed, basement membranes of the seminiferous epithelia became detached. WZYZP could restore the morphological changes. There was no expression of Tip60 among the three groups on D7 and D14. The expression of p53 was higher in the radiation group than in the control group (P<0.05). WZYZP could down-regulate the rising p53 induced by radiation on D7 and D14 (P<0.05). CONCLUSION: A modified WZYZP may affect germ cells, and its protective effects may partly result from its ability to intervene in Tip60 mediated apoptosis.
Subject(s)
Apoptosis , Drugs, Chinese Herbal/pharmacology , Microwaves , Testis/metabolism , Testis/pathology , Trans-Activators/metabolism , Animals , Apoptosis/drug effects , Male , Rats, Wistar , Testis/drug effects , Testis/radiation effects , Tumor Suppressor Protein p53/metabolismABSTRACT
Male infertility is a complicated disease with causes generally split into 2 broad categories: genetic factors and environmental factors. The present study was designed to investigate the association between the methylation patterns of H19 and SNRPN imprinting control region (ICR) and male infertility and to assess the gene-environment interactions between environmental factors and methylation patterns. A total of 205 DNA samples from 48 oligozoospermia (OZ), 52 asthenozoospermia (AZ), 55 teratozoospermia (TZ) patients, and 50 normozoospermia (NZ) men were analyzed. The mean methylation level of H19-ICR in OZ (80.40% ± 12.74%) and AZ patients (81.17% ± 13.18%) was significantly lower than methylation in men with NZ (88.51% ± 10.54%, P<.001, P<.001, respectively). The mean methylation level of SNRPN-ICR in AZ patients (7.74% ± 5.71%) and TZ patients (9.33% ± 5.48%) was significantly higher than in NZ men (6.32% ± 3.54%, P<.001, P<.001, respectively). Among environmental factors, smoking was correlated with OZ (odds ratio [OR] = 5.12, 95% CI: 2.05-12.83), AZ (OR = 5.65, 95% CI: 2.13-14.99), and TZ (OR = 5.54, 95% CI: 2.21-13.89). Gene-environment interaction analysis revealed that hypomethylation of H19-ICR in OZ patients and hypermethylation of SNRPN-ICR in AZ and TZ patients were significantly associated with an increased the risk of infertility in men who were smokers (OR = 15.30, 95% CI: 1.13-207.97; OR = 13.20, 95% CI: 1.21-143.57; OR = 10.59, 95% CI: 1.04-107.39, respectively). This study demonstrated that hypomethylation of H19-ICR and hypermethylation of SNRPN-ICR are associated with male infertility, and the risk is potentiated by smoking.
