4.4 Article

Strontium fructose 1, 6-diphosphate alleviate cyclophosphamide-induced oligozoospermia by improving antioxidant and inhibiting testicular apoptosis via FAS/FASL pathway

Journal

ANDROLOGIA
Volume 47, Issue 9, Pages 995-1003

Publisher

WILEY
DOI: 10.1111/and.12369

Keywords

Cyclophosphamide; oligozoospermia; strontium fructose 1; 6-diphosphate

Categories

Funding

  1. National Natural Science Foundation of China [81373478]
  2. Doctoral Program of Higher Education of China (SRFDP) [20133221120010]
  3. Jiangsu Province Natural Science Fund for Colleges and Universities [13KJB350003]
  4. Program for Changjiang Scholars and Innovative Research Team in University [IRT1066]

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This study investigated the treatment effects of a new compound, strontium fructose 1, 6-diphosphate (FDP-Sr), in cyclophosphamide (CP)-induced oligozoospermia. FDP-Sr, with extra high-energy supply, could reverse male hypogonadism in the testis. Male Wistar rats were randomly divided into three groups: control group (vehicle treated), CP group and CP + FDP-Sr group. Both CP group and CP + FDP-Sr groups were orally administered CP (20mgkg(-1)) consecutively for the first 7days to establish CP-induced testicular toxic models. Subsequently, CP group was given orally distilled water per day, whereas CP + FDP-Sr group was received FDP-Sr (200mgkg(-1)) for 49days. Compared to the CP group, the FDP-Sr group showed significantly increased levels of serum testosterone, testis relative weights and epididymal sperm counts in rats. In addition, rats treated by FDP-Sr showed the recuperative activities of testicular marker enzymes and normalised levels of antioxidants in tissue. Testicular protection of FDP-Sr was further demonstrated by enhancing expression of P450scc, reducing ability of FAS/FASL and generating cytoprotection in the histopathological study. FDP-Sr appeared to possess an ability to attenuate CP-induced reproduction toxicity via the activation of antioxidants and steroidogenesis enzymes, and alleviate oligozoospermia via inhibition of testicular apoptosis by FAS/FASL pathway.

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