Chen Chang-Bo, Ma Jing, Jia Jian, Li Ying-Qi, Liu A-Qing, Dong Hai-Jun
PLA Medical Center of Traditional Chinese Medicine / Department of Traditional Chinese Medicine, Xijing Hospital of the Air Force Military Medical University, Xi'an, Shannxi 710032, China.
Department of Surgery, Shaanxi Provincial Hospital of Traditional Chinese Medicine, Xi'an, Shaanxi 710003, China.
Zhonghua Nan Ke Xue. 2019 Mar;25(3):248-256.
To compare the differentially expressed proteins in mice with kidney-yang deficiency and those with kidney-yin deficiency induced by hydrocortisone, and explore the similar and different material bases of male infertility caused by the two types of kidney deficiency.
Thirty Kunming mice were equally randomized into a normal control, a kidney-yang deficiency and a kidney-yin deficiency group. The animals of the normal control group were injected intraperitoneally with normal saline at 0.2 ml qd for 7 days, while those of the latter two groups with hydrocortisone at 25 mg/kg/d for 10 days and 50 mg/kg/d for 7 days, respectively, for establishment of kidney-yang deficiency and kidney-yin deficiency models. Then the pathological changes in the testicular tissue of the mice were observed by HE staining and the differentially expressed proteins were compared among different groups using isobaric tags for relative and absolute quantitation (iTRAQ) and the bioinformatics method.
Sod1 was found to be a reproduction-related node protein differentially expressed in the testis tissues of the two types of kidney-deficiency mice, more highly expressed in the kidney-yin than in the kidney-yang deficiency group (P < 0.05). Five reproduction-associated node proteins were co-expressed in the testes of the two groups of kidney-deficiency mice, with significantly up-regulated expression of Rps28 and down-regulated expressions of Rpl11, Rplp2, Svs2 and Svs3a (P < 0.01).
Sod1 may be one of the key material bases for the differentiation of male infertility caused by kidney-yang deficiency from that induced by kidney-yin deficiency, while Rps28, Rpl11, Rplp2, Svs2 and Svs3a may be the common material bases of male infertility caused by the two types of kidney deficiency.
比较氢化可的松诱导的肾阳虚和肾阴虚小鼠睾丸组织差异表达蛋白，探讨两种肾虚型男性不育症的异同物质基础。
30只昆明小鼠随机均分为正常对照组、肾阳虚组和肾阴虚组。正常对照组小鼠腹腔注射0.2 ml生理盐水，每日1次，连续7天；后两组分别以25 mg/kg/d注射氢化可的松10天、50 mg/kg/d注射7天，建立肾阳虚和肾阴虚模型。通过HE染色观察小鼠睾丸组织病理变化，采用相对与绝对定量同位素标记（iTRAQ）及生物信息学方法比较不同组间差异表达蛋白。
Sod1是两种肾虚型小鼠睾丸组织中差异表达的生殖相关节点蛋白，在肾阴虚组中的表达高于肾阳虚组（P<0.05）。两组肾虚型小鼠睾丸中共同表达5种生殖相关节点蛋白，其中Rps28表达显著上调，Rpl11、Rplp2、Svs2和Svs3a表达下调（P<0.01）。
Sod1可能是肾阳虚和肾阴虚所致男性不育症差异的关键物质基础之一，而Rps28、Rpl11、Rplp2、Svs2和Svs3a可能是两种肾虚型男性不育症的共同物质基础。
