Hydrogen-rich saline attenuates spinal cord hemisection-induced testicular injury in rats
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Li Ge1, Li-Hua Wei1, Chang-Qing Du1, Guo-Hua Song2, Ya-Zhuo Xue3, Hao-Shen Shi4, Ming Yang4, Xin-Xin Yin4, Run-Ting Li4, Xue-er Wang5, Zhen Wang5 and Wen-Gang Song6
1Department of Histology and Embryology, Taishan Medical University, Tai-an City, PR China
2Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Institute of Atherosclerosis, Taishan Medical University, Tai-an City, PR China
3Department of Basic Nursing Teaching, Taishan Medical University, Tai-an City, PR China
4Department of Clinical Medicine, Taishan Medical University, Tai-an City, PR China
5Department of Physiology, Shandong University School of Medicine, Jinan, Shandong, PR China
6Department of Medical Immunology, Taishan Medical University, Tai-an City, PR China
Wen-Gang Song, email: [email protected]
Zhen Wang, email: [email protected]
Keywords: hydrogen-rich saline, hemisectioned spinal cord injury, rat, testis, spermatogenic cell
Received: July 20, 2016 Accepted: January 27, 2017 Published: March 03, 2017
To study how hydrogen-rich saline (HS) promotes the recovery of testicular biological function in a hemi-sectioned spinal cord injury (hSCI) rat model, a right hemisection was performed at the T11–T12 of the spinal cord in Wistar rats. Animals were divided into four groups: normal group; vehicle group: sham-operated rats administered saline; hSCI group: subjected to hSCI and administered saline; HRST group: subjected to hSCI and administered HS. Hind limb neurological function, testis index, testicular morphology, mean seminiferous tubular diameter (MSTD) and seminiferous epithelial thickness (MSET), the expression of heme oxygenase-1 (HO-1), mitofusin-2 (MFN-2), and high-mobility group box 1 (HMGB-1), cell ultrastructure, and apoptosis of spermatogenic cells were studied. The results indicated that hSCI significantly decreased the hind limb neurological function, testis index, MSTD, and MSET, and induced severe testicular morphological injury. The MFN-2 level was decreased, and HO-1 and HMGB-1 were overexpressed in testicular tissues. In addition, hSCI accelerated the apoptosis of spermatogenic cells and the ultrastructural damage of cells in the hypophysis and testis. After HS administration, all these parameters were considerably improved, and the characteristics of hSCI testes were similar to those of normal control testes. Taken together, HS administration can promote the recovery of testicular biological function by anti-oxidative, anti-inflammatory, and anti-apoptotic action. More importantly, HS can inhibit the hSCI-induced ultrastructural changes in gonadotrophs, ameliorate the abnormal regulation of the hypothalamic-pituitary-testis axis, and thereby promote the recovery of testicular injury. HS administration also inhibited the hSCI-induced ultrastructural changes in testicular spermatogenic cells, Sertoli cells and interstitial cells.
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