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Chinese Journal of Radiological Medicine and Protection ; (12): 328-334, 2022.
Artigo em Chinês | WPRIM | ID: wpr-932606

RESUMO

Objective:To investigate the effect of thoracic X-ray irradiation on the spermatogenesis of adult male mice.Methods:A total of 24 healthy adult male C57BL/6 mice (6-8 weeks old) were randomly divided into radiation group (Radiation) and sham-radiation group (Sham), 12 mice in each group. The area of thoracic irradiation was 1.5 cm× 2 cm, and the dose rate was 3.04 Gy/min, 8 Gy/d for 3 consecutive days, 24 Gy in total. At 7 d and 21 d after thoracic irradiation, the bilateral testes and epididymal tails were stripped and the testicular index was calculated. The morphology of testis was examined by haematoxylin-eosin (HE) staining, then the diameter of seminiferous tubules and the thickness of seminiferous epithelium were measured. The sperms were collected from the bilateral epididymal tails for sperm counting. The level of apoptosis in testis and levels of apoptosis-related proteins were detected by TUNEL and Western blot, respectively.Results:Compared with Sham group, the morphology of testis and epididymis was seriously damaged, the diameter of seminiferous tubules significantly decreased at 21 d after irradiation ( t = 8.93, P < 0.05), and the seminiferous epithelium significantly decreased at 7 d and 21 d after irradiation ( t = 4.24, 12.77, P < 0.05). In addition, the number of sperms significantly decreased ( t = 4.30, 2.98, P < 0.05). The number of TUNEL positive cells in the seminiferous epithelium significantly increased at 7 d and 21 d after irradiation ( t = -2.73, -3.74, P < 0.05). Meanwhile, the level of cleaved Caspase-3 protein significantly increased at 7 d and 21 d after irradiation ( t = -2.96, -2.46, P < 0.05). The concentrations of SCF and GDNF did not change at 7 d after irradiation, but were significantly increased at 21 d after irradiation ( t = -10.46, -5.42, P < 0.05). Conclusions:The thoracic X-ray irradiation could lead to spermatogenesis disorder in male adult mice, and the induction of spermatogenic cell apoptosis and the secretory dysfunction of sertoli cells may be involved.

2.
Chinese Journal of Endocrine Surgery ; (6): 110-114, 2017.
Artigo em Chinês | WPRIM | ID: wpr-608275

RESUMO

Objective To explore the effect of carbon nanoparticles-epirubicin suspension on proliferation and apoptosis in human breast cancer MCF-7 cells.Methods MCF-7 cells were cultured with different concentrations of CNP-EPI in vitro.CCK-8 assay was used for determinate inhibition effect of CNP-EPI on the proliferation of MCF-7 cells at different concentration and different time.According to the determination of IC90,5 μg/ml CNP-EPI was selected,and cell morphology and cell apoptosis rates were observed after 24 h.Results The inhibition effect of the CNP-EPI was stronger significantly in CNP-EPI group than in normal control group within 24 h,48 h,72 h when the concentration was from 1 μg/ml to 200 μg/ml (P<0.01).The inhibition of CNP-EPI on the proliferation of MCF-7 cells was gradually strengthened in a dose-dependent relation within the same time,and the inhibition effect is reduced in the same concentration of drugs with the time extension,but it still has a strong inhibitory effect in 72 h,and the inhibition effect of different concentration of CNP was not obvious on MCF-7 cells.Obvious changes of cell morphology were observed under inverted microscope such as:a lot of dead cells,cell adherent growth poor,cell morphology became round and karyopycnosis etc,in 5 μg/ml CNP-EPI group after 24 h.However,no obvious abnormity of cell norphology was observed in normal control group and corresponding CNP group.Late apoptosis rate was (14.57±2.41) %,the mortality rate could reach (78.63±-20.55)% in 5 μg/ml CNP-EPI group after 24 h.The mortality rate and apoptosis rate of cells was higher significantly in CNP-EPI group than in CNP group and normal control group (P<0.05).Conclusion CNP-EPI can obviously inhibit the proliferation or kill human breast cancer MCF-7cells,and the inhibition effect of CNP-EPI on proliferation of breast cancer cells might be the result of delayed releasing of EPI.

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