Icariin attenuates DNA damage in testicular germ cells of natural aging rats by activating Nrf2/HO-1 signaling pathway / 中草药

ABSTRACT

Objective: To study the protective effects of icariin on DNA damage of testicular germ cells in natural aging rats and explore the possible mechanism. Methods: In the study, the SD rats were separated into four groups at random, with eight rats in each group adult control group (2 months old), aging model group (16 months old), low and high doses of icariin-treated groups (2 mg/kg and 6 mg/kg, 16 months old). The adult control group and the aging model group were fed with normal diet for four months. Icariin-treated groups were given medicated feed for four months. After fasting for 12 h, all the rats were put to death. The testicular morphology was observed using HE staining. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in testicular tissue were detected by xanthine oxidase method and thiobarbituric acid method, respectively. The protein expression of Nrf2 and γ-H2AX were detected by immunofluorescence. The relative protein expression levels of Nrf2, HO-1, NQO1, γ-H2AX, p-p53, and p21 were detected by Western blotting. Results: HE staining results showed that icariin significantly improved the structure of testicular tissue of natural aging rats. Compared with the aging model group, icariin significantly increased the SOD activity and decreased the MDA content in testis. In addition, immunofluorescence results showed that icariin significantly decreased the expression of DNA damage response protein γ-H2AX and increased the protein expression of Nrf2 in testicular germ cells of aging rats.Moreover, Western blotting results showed that icariin significantly increased the relative protein expression levels of Nrf2, HO-1 and NQO1 in testis, when compared with aging model group. In parallel, the relative protein expression levels of γ-H2AX, p-p53, and p21 were significantly decreased. Conclusion: Icariin attenuates DNA damage in testicular germ cells of natural aging rats, which may be associated with the activation of Nrf2/HO-1 signaling pathway.