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[生精宝对少精子症小鼠模型精子发生的促进作用及其作用机制]

[Facilitation of Shengjingbao to spermatogenesis in oligospermia mouse models and its action mechanisms].

作者信息

Yang Li, Shen Ji-hong, Li Jin-kun, Xu Xiao-lin

机构信息

Department of Urology, the First Affiliated Hospital of Kunming Medical College, Kunming, Yunnan 650032, China.

出版信息

Zhonghua Nan Ke Xue. 2007 Sep;13(9):853-7.

Abstract

OBJECTIVE

To investigate the effects of Shengjingbao on spermatogenesis in the mouse model of oligospermia and its action mechanisms.

METHODS

Sixty male mice were randomly divided into 4 groups, Shengjingbao (Group 1), Vitamin E (Group 2), blank model control (Group 3) and normal blank control (Group 4). The first three groups were treated by celiac injection of cyclophosphamide for 5 successive days to make models, followed by intragastric administration of Shengjingbao and Vitamin E to Group I and 2, respectively, for 36 days. And then all the mice were sacrificed. The serum testosterone (T) level was determined by radioimmunology, and a suspension was made from the testis and epididymis of one side for sperm analysis, while the testis of the other side was sliced up and stained by HE method and TUNEL technique to detect the count of Leydig cells, the layers of spermatogenic epithelia and the apoptosis of spermatogenic cells.

RESULTS

Compared with Group 3, the serum T level, the layers of spermatogenic epithelia and the count of Leydig cells were obviously improved and even exceeded those in Group 2. The positive expression rate of spermatogenic cell apoptosis in Group 1 was evidently lower than Group 2 and 3. The above differences were statistically significant (P < 0.01 or P < 0.05), but no significant difference was noted between Group 1 and 4.

CONCLUSION

Shengjingbao can significantly increase the count of Leydig cells, elevate the T level that influences the layers of spermatogenic epithelia, and thus enhance spermatogenesis. The action mechanisms of Shengjingbao may lie in its capacity of inhibiting the apoptosis of spermatogenic cells, increasing the layers of spermatogenic epithelia and facilitating spermatogenesis. T may play a role in inhibiting the apoptosis of spermatogenic cells.

摘要

目的

探讨生精宝对少精子症小鼠模型精子发生的影响及其作用机制。

方法

将60只雄性小鼠随机分为4组,即生精宝组(第1组)、维生素E组(第2组)、空白模型对照组(第3组)和正常空白对照组(第4组)。前三组连续5天腹腔注射环磷酰胺造模,然后第1组和第2组分别灌胃给予生精宝和维生素E,共36天。之后处死所有小鼠。采用放射免疫法测定血清睾酮(T)水平,取一侧睾丸和附睾制成悬液进行精子分析,另一侧睾丸切片,采用苏木精-伊红(HE)染色法和末端脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)技术检测睾丸间质细胞计数、生精上皮层数及生精细胞凋亡情况。

结果

与第3组相比,第1组血清T水平、生精上皮层数及睾丸间质细胞计数明显改善,甚至超过第2组。第1组生精细胞凋亡阳性表达率明显低于第2组和第3组。上述差异具有统计学意义(P<0.01或P<0.05),但第1组与第4组之间无明显差异。

结论

生精宝可显著增加睾丸间质细胞计数,提高影响生精上皮层数的T水平,从而增强精子发生。生精宝的作用机制可能在于其抑制生精细胞凋亡、增加生精上皮层数及促进精子发生的能力。T可能在抑制生精细胞凋亡中发挥作用。

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