Experimental assessment of platelet-rich plasma efficacy for spermatogenesis correction in the rat: evaluation of two experimental models
Epifanova, MV1; Chaliy, ME2; Andreev-Andrievskiy, AA3; Artemenko, SA2; Mashkin, MA4; Manskikh, VN5; Popova, AS4
1: Research Institute for Uronephrology and Reproductive Health, Sechenov First Moscow State Medical University (Moscow, Russia); 2: Department of Urology, Sechenov First Moscow State Medical University (Moscow, Russia); 3: M.V. Lomonosov Moscow State university, biology faculty; MSU institute of mitoengineering, LLC (Moscow, Russia); 4: MSU institute of mitoengineering, LLC (Moscow, Russia); 5: M.V. Lomonosov Moscow State university, biology faculty (Moscow, Russia)
Objective: Approximately 25% of the couples cannot conceive within the first year, among these cases 30 to 40% are due to male fertility problems. Spermatogenesis deficiency is one of the major causes of male infertility. Use of platelet-rich plasma (PRP) can become a novel treatment for cases of azoospermia of several etiologies. In order to investigate the efficiency of PRP for azoospermia treatment we have initiated an animal study in a rat model. Among rat models of spermatogenesis insufficiency, surgical models based on transitory ischemia reached through spermatic cord ligation and pharmacological models, employing cytostatic drugs treatment are the most widely used. Here we report the first results of this study, namely experimental evaluation of two azoospermia models in the rat.
Material and Method: Azoospermia was induced in male Wistar rats weighing 250-300 g either surgically, via spermatic cord ligation for 12, 24 or 36 h (L12, L24 and L36 respectively, n=9 per group) or pharmacologically by cisplatin administration (1 mg/kg once daily for 5 consecutive days, CIS, n=9). Control rats (CON, n=9) received no treatment. Epidydimal sperm count, testes histopathology, male reproductive organ weights and hematological parameters were evaluated 7, 14 and 28 days after the disease induction (n=3 per time point).
Result: Testes and epididymal mass were decreased 7 and 14 days after cisplatin administration, while prostate weight was reduced in CIS and L24 animals indicative of lower level of bioavailable testosterone. Total serum testosterone did not differ over the groups. Epididymal sperm count was lower in L12, L24 and L36 rats 7 and 28 days after reperfusion and at 7 and 14 days in CIS animals. No sperm morphology or motility changes were observed. Testicular histological parameters in the ligated rats did not differ from CON animals, while the seminiferous tubules had a lower diameter and the total tubal area was lower in CIS animals at d7 and d14. In CIS rats, but not in the other groups, RBC, HCT and PLT were reduced compared to CON 7 and 14 days after the disease induction.
Conclusion: Temporal ligation of the testicular chord seems to be an unrepresentative model of azoospermia in the rat, as the decrease in sperm count is governed by vas deference obstruction rather than spermatogenesis inhibition. The cytostatic model induces reversible inhibition of spermatogenesis and will be used for evaluation of platelet-rich plasma efficiency for azoospermia treatment.
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