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郭朋璐,董 曼,严晓红,康 洁.雄激素对老年大鼠胃粘膜线粒体功能的影响及机制[J].中国比较医学杂志,2021,31(11):21~26,34.
雄激素对老年大鼠胃粘膜线粒体功能的影响及机制
Effect and mechanism of androgens on mitochondrial functions of gastric mucosa in aged rats
投稿时间:2020-11-17  
DOI:10. 3969 / j.issn.1671-7856. 2021. 11. 004
中文关键词:  雄激素  老年大鼠  胃粘膜  线粒体  睾丸切除
英文关键词:androgens  old rats  gastric mucosa  mitochondria  testicular resection
基金项目:
作者单位E-mail
郭朋璐 哈励逊国际和平医院,消化内科内镜室,河北 衡水 053000 fansuqin1988@ 163.com 
董 曼 哈励逊国际和平医院,消化内科内镜室,河北 衡水 053000  
严晓红 河北省以岭医院, 石家庄 050000  
康 洁 河北省以岭医院, 石家庄 050000  
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中文摘要:
       目的 探讨雄激素对睾丸切除(GDX)老年大鼠胃粘膜线粒体功能的影响及机制。 方法 36 只 SD 雄性大鼠随机分为 3 组:假手术组(Sham,n= 12)、模型组(GDX,n= 12)和补充雄激素的模型大鼠( n= 12)。 造模大鼠行 GDX,造模后雄激素组灌胃睾丸酮(13. 6 mg / (kg·d),溶于芝麻油中)。 假手术组和模型组大鼠使用芝麻油进行相同的治疗。治疗结束后收集胃组织标本,分别采用试剂盒检测胃粘膜线粒体中 Mn-SOD、GSH-Px、GSH、 GSSG、GSH/ GSSG 和 ROS 水平,罗丹明 123 荧光法检测线粒体膜电位,流式细胞仪检测细胞凋亡。体外试验以人永生胃粘膜细胞 GES-1 为研究对象,应用 H2O2 诱导细胞损伤,考察雄激素和 ALDH2 抑制剂 Disulfiram 对细胞活力和凋亡影响。 结果 与 Sham 组相比,GDX 组 ROS、GSSG 水平、胃粘膜细胞凋亡和裂解的 Caspase-3、细胞质 Cyt c 蛋白表达显著增加(P<0. 05),而 Mn-SOD、GSH-Px、GSH、GSH/ GSSG 水平、线粒体膜电位、ATP 水平和线粒体 Cyt c 蛋白、ALDH2 蛋白表达显著降低(P<0. 05)。在雄激素治疗后,GDX 老年大鼠上述变化显著逆转(P<0. 05)。 体外实验中,雄激素处理显著逆转了 H2O2 对 GES-1 细胞的损伤作用(P<0. 05);然而,当联合加入 Disulfiram 时,雄激素的治疗活性明显降低(P<0. 05)。 结论 雄激素缺乏导致老年大鼠胃粘膜细胞线粒体功能障碍和线粒体 ROS 积累增加,诱导胃黏膜细胞凋亡,这种损害作用至少部分与 ALDH2 的抗氧化功能抑制有关。
英文摘要:
       Objective To investigate the effect and mechanism of androgens on mitochondrial functions of gastric mucosa in aged gonadectomized male (GDX) rats. Methods 36 male SD rats were randomly divided into three groups: sham operation group (Sham, n= 12), model group (GDX, n= 12) and androgen-supplemented model rats ( n= 12). GDX rats were used for modeling. After modeling, the AG group was administered testosterone ( 13. 6 mg / ( kg·d), dissolved in sesame seed oil). Rats in sham operation and model groups were treated with sesame seed oil. After the treatment, gastric tissue samples were collected and the levels of Mn-SOD, GSH-Px, GSH, GSSG, GSH/ GSSG and ROS in gastric mucosa mitochondria were measured by kits, the mitochondrial membrane potential was measured by rhodamine 123 fluorescence, and apoptosis was analyzed by flow cytometry. In vitro, GES-1 cells were used as the research object. H2O2 was used to induce cellular injury. The effects of androgens and ALDH2 inhibitor disulfiram on cell viability and apoptosis were investigated. Results Compared with Sham group, ROS and GSSG levels, gastric mucosal cell apoptosis and cleaved Caspase-3 and cytoplasmic Cyt c protein expression were significantly increased in the GDX group (P<0. 05), while Mn-SOD, GSH-PX, GSH and GSH/ GSSG levels, the mitochondrial membrane potential, ATP level and mitochondrial Cyt c and ALDH2 protein expression were decreased significantly (P<0. 05). After androgen treatment, the above changes in GDX elderly rats were reversed significantly ( P< 0. 05). In vitro, androgen treatment significantly reversed damage induced by H2O2 in GES-1 cells (P<0. 05). However, when combined with Disulfiram, the therapeutic activity of androgen was reduced significantly ( P< 0. 05). Conclusions Androgen deficiency leads to mitochondrial dysfunction and increased mitochondrial ROS accumulation in gastric mucosal cells of elderly rats and induces gastric mucosal cell apoptosis, which is at least partly related to inhibition of the antioxidant function of ALDH2.
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