title: Alterations in gene expression and steroidogenesis in the testes of transient cerebral ischemia in male rats.
abstract: BACKGROUND
  Serum testosterone levels have been found lower in acute ischemic stroke male patients. However, the exact mechanism remains unclear. In the present study, we measured serum testosterone levels, steroidogenesis- related genes and Leydig cells number in experimental transient cerebral ischemia male rats to elucidate the mechanism.
  
  
  METHODS
  The middle cerebral arteries of adult male Sprague-Dawley rats were sutured for 120 minutes and then sacrificed after 24 hours. Blood was collected for measurement of serum testosterone, follicular stimulating hormone and estradiol levels, and testes were collected for measurement of steroidogenesis-related gene mRNA levels and number of Leydig cells.
  
  
  RESULTS
  Serum testosterone levels in rats after cerebral ischemia were significantly lower (0.53 ± 0.16) ng/ml, n = 7, mean ± SE) compared with control ((2.33 ± 0.60) ng/ml, n = 7), while serum estradiol and follicular stimulating hormone levels did not change. The mRNA levels for luteinizing hormone receptor (Lhcgr), scavenger receptor class B member 1 (Scarb1), steroidogenic acute regulatory protein (StAR), cholesterol side chain cleavage enzyme (Cyp11a1), 3β-hydroxysteroid dehydrogenase 1 (HSD3β1), 17α-hydroxylase/20-lyase (Cyp17a1) and membrane receptor c-kit (kit) were significantly downregulated by cerebral ischemia, while luteinizing hormone, Kit ligand (KitL), 17β-hydrosteroid dehydrogenase 3 (HSD17β3) and 5α-reductase (Srd5a1) were not affected. We also observed that, relative to control, the Leydig cell number did not change.
  
  
  CONCLUSIONS
  These results indicate that transient cerebral ischemia in the brain results in lower expression levels of steroidogenesis-related genes and thus lower serum testosterone level. Transient cerebral ischemia did not lower the number of Leydig cells.
authors.affiliation: Heilongjiang Key Laboratory of Anti-fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157001, China.
authors.forename: Bing-Hai
authors.initials: BH
authors.lastname: Zhao
authors.forename: Yan-Qin
authors.initials: YQ
authors.lastname: Guo
authors.forename: Hong-Zhi
authors.initials: HZ
authors.lastname: Li
authors.forename: Jie-Ting
authors.initials: JT
authors.lastname: Liu
authors.forename: Dan
authors.initials: D
authors.lastname: Wu
authors.forename: Xiao-Huan
authors.initials: XH
authors.lastname: Yuan
authors.forename: Rong-Wen
authors.initials: RW
authors.lastname: Li
authors.forename: Li-Xin
authors.initials: LX
authors.lastname: Guan
mesh_terms: D000818:Animals; D004797:Enzyme-Linked Immunosorbent Assay; D004958:Estradiol / Q000097:blood; D005640:Follicle Stimulating Hormone / Q000097:blood; D002546:Ischemic Attack, Transient / Q000097:blood* / Q000378:metabolism*; D007985:Leydig Cells / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D013737:Testis / Q000378:metabolism*; D013739:Testosterone / Q000097:blood
chemical_list: D013739:Testosterone; D004958:Estradiol; D005640:Follicle Stimulating Hormone