ORIGINAL ARTICLE
Year : 2016  |  Volume : 18  |  Issue : 5  |  Page : 803-808

The calcium-sensing receptor participates in testicular damage in streptozotocin-induced diabetic rats


1 Department of Emergency Surgery, The Daqing Oilfield General Hospital, Daqing, China
2 Department of General Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, China
3 Department of Emergency Surgery, The Fourth Hospital of Jilin University, Changchun, China
4 Department of Pharmacology, Daqing Campus of Harbin Medical University, Daqing, China
5 Department of Urologic Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, China
6 The Hepatosplenic Surgery Center, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China
7 School of Nursing, Daqing Campus of Harbin Medical University, Daqing, China

Correspondence Address:
Lin-Lin Zhang
School of Nursing, Daqing Campus of Harbin Medical University, Daqing
China
Tie-Hui Zhang
Department of Urologic Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1008-682X.160885

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Male infertility caused by testicular damage is one of the complications of diabetes mellitus. The calcium-sensing receptor (CaSR) is expressed in testicular tissues and plays a pivotal role in calcium homeostasis by activating cellular signaling pathways, but its role in testicular damage induced by diabetes remains unclear. A diabetic model was established by a single intraperitoneal injection of streptozotocin (STZ, 40 mg kg−1 ) in Wistar rats. Animals then received GdCl 3 (an agonist of CaSR, 8.67 mg kg−1 ), NPS-2390 (an antagonist of CaSR, 0.20 g kg−1 ), or a combination of both 2 months after STZ injection. Diabetic rats had significantly lower testes weights and serum levels of testosterone compared to healthy rats, indicating testicular damage and dysfunction in STZ-induced diabetic rats. Compared with healthy controls, the testicular tissues of diabetic rats overexpressed the CaSR protein and had higher levels of malondialdehyde (MDA), lower superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity, and higher numbers of apoptotic germ cells. The testicular tissues from diabetic rats also expressed lower levels of Bcl-2 and higher levels of Bax and cleaved caspase-3 in addition to higher phosphorylation rates of c-Jun NH 2 -terminal protein kinase (JNK), p38, and extracellular signaling-regulated kinase (ERK) 1/2. The above parameters could be further increased or aggravated by the administration of GdCl 3 , but could be attenuated by injection of NPS-2390. In conclusion, the present results indicate that CaSR activation participates in diabetes-induced testicular damage, implying CaSR may be a potential target for protective strategies against diabetes-induced testicular damage and could help to prevent infertility in diabetic men.


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