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| Protective Effect of Baicalin on Oxidative Damage of Testes in Heat Stressed Mice (Mus musculus) |
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Abstract Abstract Reproductive function is most easily damaged by heat stress in all physiological functions. Heat stress causes the oxidative stress in tissues and damages spermatogenesis, which can affect the reproduction efficiency of animals. The main purposes of this study were to investigate the effect of baicalin on testicular injury in mice (Mus musculus) and to further investigate the antioxidant mechanism of baicalin. The mice were divided into four groups as following, normal temperature control group (Group C), baicalin group (Group C+B), heat stress group (Group H) and heat stress plus baicalin group (Group H+B). Mice in Group C and Group H were given saline via intraperitoneal injection, and mice in Group C+B and Group H+B were injected intraperitoneally with baicalin (50 mg/kg) for 7 days. Then, group H and Group H+B were treated with heat stress (41 ℃) for 2 hours on day 8. The mice in treatment groups and control groups were killed immediately after heat stress, and the testes and epididymis were removed and weighed. Testicular and epididymal organ coefficients were calculated, pathological injuries were detected in testis tissue sections, and the levels of malondialdehyde (MDA) in the testis tissue were examined. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were detected by using corresponding kits in testicular tissue. The cell apoptosis of testicular tissue was detected by terminal deoxynucleotidyl transferase assay (TdT-mediated dUTP, nick-end labeling, TUNEL). The expression of Fas/FasL protein in testis tissue was detected by Western blot. The results showed that the intercelluar space enlargement, seminiferous tube wall thinning, cell degeneration, vacuoles in cytoplasm, spermatognic cell apoptosis and shedding appeared in mice testicular tissues under heat stress. In addition, testicular and epididymal organ coefficients could be significantly reduced by heat stress (P＜0.05), while baicalin could alleviate this change induced by heat stress(P＜0.05). Moreover, compared with the heat stress group at 41 ℃, the contents of MDA in the heat stress with baicalin group significantly decreased, and the activities of SOD, CAT and GSH-Px increased significantly(P＜0.05). There was no significant difference between baicalin group and heat stress with baicalin group. Furthermore, the apoptotic rate of testis in heat treated group increased significantly compared with the control group (P＜0.01), while the apoptosis rate of testicular cells in heat stress plus baicalin group was significantly lower (P＜0.05) when compared with heat stress group. Besides, comparing with the control group, heat stress could significantly increase the expression of Fas (P＜0.05) and FasL (P＜0.01) protein in testes, but baicalin could significantly reduce the expression of Fas/FasL protein in the testis of mice induced by heat stress (P＜0.05). Overall, baicalin could reduce the apoptosis caused by oxidative damage in the testis of mice exposed to heat stress, and the mechanism of baicalin might be related to the increase of antioxidant enzyme activity and the inhibition of Fas/FasL protein expression to inhibit apoptosis. This study provides a theoretical basis for finding ways to alleviate the heat stress in animals.
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Received: 06 April 2017
Published: 06 August 2017
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