| Background:Cadmium is widely used as a modern industry materials, agriculture and other industris,at the same time the improper discharge of cadmium and its compounds also caused great harm to the survival for humans and animals, in the livestock industry, livestock used to ingest cadmium from cadmium-polluted food and water, and it is extremely easy to cause reproductive function damaged and then lead to great economic losses.Sulforaphane is extracted from cruciferous and it is effective on antioxidant components,it is also can produce protective effect activation through Nrf2/ARE pathway.Objective:This study was aim to investigate protective effect of vitro sulforaphane in cadmium-induced mouse’s spermatogenic cells and its mechanism.Methods:Measured relative survival rate of spermatogenic cells which was induced by different concentrations of cadmium and sulforaphane by MTT; detect apoptosis rate by AO/ EB staining and flow cytometry methods; detect SOD, LDH activity and MDA content bycolor assay; measured mRNA levels of Nrf2, HO-1, NQO1, γ-GCS by RT-PCR. Measured protein expression level of Nrf2, HO-1, NQO1, γ-GCS byWestern blot.Results:1. Cdcan damage spermatogenic cells, low concentrations of sulforaphane has no effect on spermatogenic cells, sulforaphane has protective effect on cadmium-induced spermato genic cells and showed a dose effect relationship.2. compared with the Cd group, sulforaphane could decrease apoptosis rate of cad-mium induced spermatogenic cells (P<0.05, P<0.01); compared with the Cd group that sulforaphane can improve the activity of SOD and LDH (P<0.05, P<0.01), and significantly reduce the content of MDA (P<0.01).3. compared with the Cd group, sulforaphane can significantly up-regulated mRNA and protein expression of Nrf2 andits downstream target genes HO-1, NQO1,γ-GCS(P<0.01).Conclusion:sulforaphanehas a protective effect on mouse’soxidative damaged spermatogenic cells which caused bycadmium, and its activation maybe achieved through of Nrf2/ARE path-way. |
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