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原花青素对雄性小鼠生殖功能损伤作用及机制

Effect and mechanism of proanthocyanidins on reproductive function injury in male mice
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摘要 目的探讨原花青素对雄性小鼠生殖功能损伤的作用及其相关机制。方法将24只雄性健康C57/BL6J小鼠随机分入3组,每组各8只。对照组:小鼠灌胃或腹腔注射0.9%生理盐水。模型组:小鼠经0.9%生理盐水灌胃1 h后腹腔注射雷公藤甲素120μg/kg。干预组:原花青素250 mg/kg灌胃处理1 h后腹腔注射雷公藤甲素120μg/kg。连续处理28 d。比较3组小鼠的精子参数、体质量、睾丸脏器指数、血清生殖激素水平、氧化应激水平及核因子E2相关因子2(Nrf2)-Kelch样ECH关联蛋白1(Keap1)蛋白表达水平。结果模型组小鼠精子数量和活力低于对照组,干预组小鼠精子数量和活力高于模型组,差异有统计学意义(P<0.05)。3组小鼠体质量比较,差异无统计学意义(P>0.05)。模型组小鼠睾丸脏器指数低于对照组,干预组小鼠睾丸脏器指数高于模型组,差异有统计学意义(P<0.05)。模型组小鼠血清睾酮和雌二醇水平高于对照组,卵泡刺激素和黄体生成素水平低于对照组,差异有统计学意义(P<0.05);干预组小鼠血清睾酮和雌二醇水平低于模型组,卵泡刺激素和黄体生成素水平高于模型组,差异有统计学意义(P<0.05)。模型组小鼠丙二醛水平高于对照组,超氧化物歧化酶和谷胱甘肽过氧化物酶水平低于对照组,差异有统计学意义(P<0.05);干预组小鼠丙二醛水平低于模型组,超氧化物歧化酶和谷胱甘肽过氧化物酶水平高于模型组,差异有统计学意义(P<0.05)。模型组Nrf2蛋白和Keap1蛋白表达水平低于对照组,干预组Nrf2蛋白和Keap1蛋白表达水平高于模型组,差异有统计学意义(P<0.05)。结论原花青素能够改善雄性小鼠生殖功能损伤,其机制与调节Nrf2-Keap1抗氧化系统有关。 Objective To investigate the effects of proanthocyanidins on reproductive function injury in male mice and its related mechanisms.Methods A total of 24 healthy male C57/BL6J mice were randomly divided into 3 groups with 8 mice in each group.Control group:mice were intragastric or intraperitoneally injected with 0.9%normal saline.Model group:120μg/kg of triptolide was intraperitoneally injected into mice after 0.9%normal saline administration for 1 hour.Intervention group:120μg/kg triptolide was injected intraperitoneally after gavage of proanthocyanidin 250 mg/kg for 1 hour.The treatment was continued for 28 days.The sperm parameters,body mass,testicular organ index,serum reproductive hormone level,oxidative stress level and nuclear factor E2 related factor 2(Nrf2)-recombinant Kelch like ECH associated protein 1(Keap1)protein expression level of the 3 groups were compared.Results The sperm count and motility of mice in the model group were lower than those in the control group,and the sperm count and motility of mice in the intervention group were higher than those in the model group,with statistical significance(P<0.05).There was no significant difference in body weight among the three groups(P>0.05).The testicular organ index in the model group was lower than that in the control group,and the testicular organ index in the intervention group was higher than that in the model group,with statistical significance(P<0.05).The levels of serum testosterone and estradiol in model group were higher than those in control group,while the levels of follicle-stimulating hormone and luteinizing hormone in model group were lower than those in control group,with statistical significance(P<0.05).The levels of serum testosterone and estradiol in the intervention group were lower than those in the model group,and the levels of follicle-stimulating hormone and luteinizing hormone were higher than those in the model group,with statistical significance(P<0.05).The level of malondialdehyde in model group was higher than that in control group,but the level of superoxide dismutase and glutathione peroxidase in model group was lower than that in control group,the difference was statistically significant(P<0.05).The level of malondialdehyde in the intervention group was lower than that in the model group,and the levels of superoxide dismutase and glutathione peroxidase were higher than those in the model group,with statistical significance(P<0.05).The expression levels of Nrf2 protein and Keap1 protein in the model group were lower than those in the control group,and the expression levels of Nrf2 protein and Keap1 protein in the intervention group were higher than those in the model group,with statistical significance(P<0.05).Conclusion Proanthocyanidins can improve the reproductive function of male mice,and the mechanism is related to the regulation of Nrf2-Keap1 antioxidant system.
作者 赵莹莹 陈莉莎 闫丽 王恺悦 于月新 ZHAO Ying-ying;CHEN Li-sha;YAN Li;WANG Kai-yue;YU Yue-xin(Department of Reproductive Medicine,General Hospital of Northern Theater Command,Shenyang 110016,China)
出处 《临床军医杂志》 2023年第12期1244-1248,共5页 Clinical Journal of Medical Officers
基金 辽宁省科学技术计划(2020JH2/10300118)。
关键词 原花青素 生殖功能 氧化应激 信号通路 Anthocyanins Reproductive function Oxidative stress Signaling pathway
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