Metformin protects spermatological damages induced by cisplatin in rats
Metformin protects spermatological damages induced by cisplatin in rats
Marjan Firouzi,1,*Masoud Alasvand Zarasvand,2Sara Chavoshinezhad,3Erfan Daneshi,4Ehsan Motaghi,5
1. Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran 2. Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran 3. Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran 4. Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran 5. Neuroscience Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
Introduction: Cisplatin (CP), a commonly prescribed anticancer drug, causes serious organ toxicity, including damage to male reproductive systems. Because of its extensive use in cancer treatment, there is an immediate clinical need to find ways to reduce its harm to healthy tissue. The reproductive toxicity of CP is mediated by inflammation and oxidative cascades. Metformin (MET), a common antidiabetic medicine, improves reproduction and lifespan by targeting organs and tissues with antioxidant and anti-inflammatory properties. Recently, MET has been shown to be effective in several testicular dysfunction models. The aim of the current study was to determine if MET treatment protects rats against spermatological damage induced by CP.
Methods: 32 adult male Wistar rats, weighing between 280 and 320 grams, were subdivided into four groups, each with 8 animals. The control group received MET solvent IP for 20 days and three IP injections of physiological saline (PS) on days 8–10. Animals in the CP group were injected IP with MET solvent for 20 days and given three IP injections of 2 mg/kg CP on days 8–10. For 20 days, the MET 25+ CP group received IP MET (25 mg/kg) and three IP CP (2mg/kg) injections on days 8–10. The MET 40+ CP group received three IP injections of CP (2 mg/kg) on days 8 to 10, in addition to 20 days of IP treatment with MET (40 mg/kg). After 24 h from the last Met injection, animals were sacrificed and spermatological parameters as progressive motility, viability, and morphological abnormalities were assessed.
Results: CP group exhibited significantly decreased sperm motility and viability along with increased head, neck, and tail defects than control. The results showed that rats treated with MET dose 25 mg/kg only showed improvements in sperm viability; other sperm parameters did not change significantly when compared to the CP group. However, treatment with a 40 mg/kg dose of MET could prevent all spermatological damage caused by CP.
Conclusion: According to our study, CP causes spermatological impairment in adult rats, which can be dose-dependently alleviated with MET treatment. This implies that MET should be evaluated further as a targeted protective drug against testicular damage caused by chemotherapy agents.