Shengjing Capsule Improves Spermatogenesis through Upregulating Integrin α6/β1 in the NOA Rats. (22nd August 2019)

• Record Type: Journal Article
• Authors: Wang, Jiamin; Zhao, Shankun; Luo, Lianmin; Liu, Yangzhou; Li, Ermao; Zhu, Zhiguo; Zhao, Zhigang
• Other Names: Arena Arielle Cristina Guest Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2019(2019)
• Publication Date: 2019-08-22
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2019/8494567
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Objective . To evaluate the therapeutic effect of Shengjing capsules on nonobstructive azoospermia (NOA) in the rat model. Methods . Twenty-five male Sprague–Dawley rats were randomly divided into five groups as follows (n = 5 per group): normal group, NOA group, and three Shengjing capsule treatment groups (low-dose, medium-dose, and high-dose groups, respectively). HE staining and semen smear were performed to assess sperm quality. The expression levels of PI3K/AKT and integrinα 6 / β 1 were measured by qRT-PCR and western blot analyses. Results . In the NOA group, almost all of the seminiferous tubules were vacuolated with a thin layer of basal compartment containing some spermatogonial stem cells. The counts of sperms in the NOA group were strongly lower than those of the normal group (P = 0.0001 ). The expression of PI3K/AKT and integrinα 6 / β 1 was scarcely expressed in the NOA group. All indexes mentioned above were significantly different from those of the medium- and high-dose groups (P = 0.001, all). The sperm count of rats treated with Shengjing capsules was significantly higher than that of the NOA group (P = 0.0001 ). The rats of Shengjing capsule groups had more layers of spermatogonial stem cells and spermatocytes, and some had intracavitary sperms. Conclusions . Shengjing capsules may be a promising therapeutic medicine for NOA. The underlying mechanisms might involve activating SSCs by upregulating the integrinα 6 / β 1 expression via the PI3K/AKT pathway.