Royal jelly protects from taxol-induced testicular damages via improvement of antioxidant status and up-regulation of E2f1
| Autor: | Hamed Janbaze-Acyabar, Hassan Malekinejad, Mona Khoramjouy, Fatemeh Delkhoshe-Kasmaie, Ali Rezaei-Golmisheh |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Male
Antioxidant food.ingredient Paclitaxel Urology medicine.medical_treatment Biology Antioxidants Nitric oxide Andrology chemistry.chemical_compound food Downregulation and upregulation Royal jelly Testis medicine E2F1 Animals RNA Messenger Rats Wistar Fatty Acids Malondialdehyde Sperm Antineoplastic Agents Phytogenic Spermatozoa Rats Up-Regulation Seminiferous tubule medicine.anatomical_structure Reproductive Medicine chemistry Immunology E2F1 Transcription Factor DNA Damage |
| Zdroj: | Systems biology in reproductive medicine. 60(2) |
| ISSN: | 1939-6376 |
| Popis: | This study was carried out to evaluate the protective effects of royal jelly (RJ) on taxol (TXL)-induced damage of the testis. Wistar rats were divided into control and test groups. The test group was divided into five subgroups; the first four groups along with TXL administration (7.5 mg/kg body weight (bw), weekly), received various doses of RJ (0, 50, 100, and 150 mg/kg bw). The last group received only RJ at 100 mg/kg. Royal jelly lowered the TXL-induced malondialdehyde and nitric oxide levels and enhanced the total thiol molecules in the testis. Remarkably RJ reduced the TXL-induced pathological injuries such as cellular shrinkage and seminiferous tubule depletion. Taxol-reduced sperm viability (27.5 ± 2.98 % vs. 85.0 ± 8.6% in the control group) was recovered by RJ administration as 80.5 ± 10.6% of the sperm were found alive in the group of animals which received 150 mg/kg RJ. The TXL-exposed and TXL plus RJ-administered animals showed a significant up-regulation of transcription factor E2f1 mRNA. Our data suggest that the TXL-induced histopathological and biochemical alterations could be protected by the administration of RJ. The RJ protective effects might be attributed to its antioxidant capacity and its capability in the regulation of E2f1 expression. |
| Databáze: | OpenAIRE |
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