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ObjectiveTo investigate the expression of glial cell line-derived neurotrophic factor （GDNF） and androgen receptor （AR） in testicular peritubular cells （TPCs） of cryptorchidism mouse models and explore the theoretical significance of cryptorchidism-induced spermatogenesis dysfunction. MethodsA total of 30 five-week-old male ICR rats were divided randomly by using random number table method into 6 groups. Cryptorchidism was surgically induced in 3 randomly selected groups and the other 3 groups underwent sham surgery as the control groups. On days 4， 7 and 14 after surgery， we harvested the mice testes of the 3 groups and their corresponding control groups， then measured the testicular volumes， analyzed the testicular histopathology and detected the mRNA and protein expression levels of AR and GDNF in TPCs by immunofluorescence， real-time PCR and Western blot. ResultsIn normal control groups， on days 4， 7 and 14 after surgery， the testicular volumes were （125.58±19.22） mm3，（123.45±20.12） mm3， （140.09±13.62） mm3 ， respectively. Clear layers of spermatogenic cells were well arranged and abundant sperm cells were found. Peritubular cells were morphologically homogeneous， with slim-spindle appearance and normal cell thickness. The mRNA expression levels of AR were 1.00±0.05， 1.06±0.07 and 1.19±0.13； GDNF mRNA 1.00±0.04， 1.09±0.05， and 1.10±0.07. The protein expression levels of AR were 1.01±0.01， 0.79±0.02 and 1.01±0.04； GDNF protein （18.68±0.43） pg/mL， （14.39±0.36） pg/mL and （16.88±0.37） pg/mL. In cryptorchidism groups， on days 4， 7 and 14 after surgery， the testicular volumes were （115.64±3.91） mm3， （69.51±14.97） mm3 and （44.86±5.56） mm3， respectively. Spermatogenic cells were disorganized， seminiferous tubules were disrupted， peritubular cells shrank， bent and fractured. The mRNA expression levels of AR were 0.76±0.06， 0.53±0.04， and 0.29±0.02； GDNF mRNA 0.72±0.05， 0.42±0.02 and 0.30±0.03. The protein expression levels of AR were 0.54±0.02， 0.98±0.04 and 0.31±0.01； GDNF protein （8.50±0.34） pg/mL， （17.44±0.32） pg/mL and （6.83±0.34） pg/mL. Statistically significant differences （P < 0.05） were found in 7-day and 14-day testicular volumes between control and cryptorchidism groups but not in the 4-day testicular volume （P > 0.05）. Testicular volumes， AR and GDNF mRNA and protein expression in control groups had no statistically significant difference （P > 0.05）， while those in cryptorchidism groups showed a trend of gradual decline in the amount and the differences between groups were statistically significant （P < 0.05）. ConclusionsIn surgery-induced cryptorchidism mice， after the induction， the expression of AR and GDNF in TPCs showed a gradual decrease over time. AR and GDNF play a major role in mediating the TPCs damage in cryptorchidism. This study provides a theoretical basis for mechanism researches of cryptorchidism-induced spermatogenesis dysfunction.
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BACKGROUND: Total hip arthroplasy is an effective method to treat hip disease caused by ankylosing spondylitis. Long-term fol ow-up studies have shown that there have been hip function problems after total hip arthroplasy, and it stil lacks of perfect rehabilitation programs. OBJECTIVE: To systematical y review the influential factors for dysfunction after total hip arthroplasy in ankylosing spondylitis patients. METHODS: The first and second authors retrieved PubMed and Sciencedirect Databases, CNKI, and Wanfang digital database for relevant articles published from January 1970 to July 2015. The key words were “arthroplasty, replacement, hip, spondylitis, ankylosing, function”. Final y, relevant articles were included. RESULTS AND CONCLUSION: A total of 40 articles were summarized, including 8 Chinese articles and 32 English articles. After total hip arthroplasy, hip function problems were mainly associated with patient’s factors, disease, surgery, prosthesis, postoperative recovery and postoperative complications. Avoiding above relevant factors can improve joint function after total hip arthroplasy for ankylosing spondylitis patients, and improve patient’s quality of life.