Abstract
Low-intensity extracorporeal shockwave therapy (Li-ESWT), as a microenergy therapy, has the effects of inhibiting oxidative stress, antiapoptosis, and tissue repair, which is increasingly applied to a variety of diseases. Our research aims to explore the protective effects of Li-ESWT in the aging rat model and its possible molecular mechanism through in vivo and in vitro experiments. In vitro, TM3 Leydig cells incubated with H2O2 were treated with Li-ESWT at 4 energy levels (0.01, 0.05, 0.1, and 0.2 mJ/mm2). In vivo, we employed an androgen-deficient rat model to simulate male aging and treated it with Li-ESWT at three different energy levels (0.01, 0.05, and 0.2 mJ/mm2). Li-ESWT increased the expression of vascular endothelial growth factor (VEGF) in TM3 cells, improved antioxidant capacity, and reduced apoptosis, with the effect being most significant at 0.05 mJ/mm2 energy level. In androgen-deficient rat model, LI-ESWT can improve sperm count, motility, and serum testosterone level, enhancing tissue antioxidant capacity and antiapoptotic ability, and the effect is most significant at 0.05 mJ/mm2 energy level. Therefore, Li-ESWT at an appropriate energy level can improve sperm count, motility, and serum testosterone levels in androgen-deficient rat models, reduce oxidative stress in the testis, and increase antioxidant capacity and antiapoptotic abilities. The mechanism of this condition might be related to the increased VEGF expression in Leydig cells by Li-ESWT.
Highlights
We found that Low-intensity extracorporeal shockwave therapy (Li-ESWT) showed a dramatic promotion effect on the expression of vascular endothelial growth factor (VEGF) in the cavernous body [14, 15], and VEGF can stimulate the release of testosterone in Leydig cells [16]
Western blot analysis was conducted to determine whether Li-ESWT could prevent oxidative stress damage of TM3 Leydig cells induced by H2O2
These results indicated that Li-ESWT could effectively prevent oxidative stress injury and reduce apoptosis of TM3 Leydig cells induced by H2O2, and the effect was most obvious at the energy level of 0.05 mJ/mm2
Summary
Aging is a complex phenomenon attributed to developmental, genetic defects, environmental, disease, and hereditary factors, which accumulate adverse changes that increase disease risk [1]. Testicular volume in elderly men is positively correlated with serum testosterone [4]. A comparative analysis [5] investigated the variation of testicular structure and function of 30 men age between 22-48 and 50-76 years, indicating that the average total number of Leydig cells in the oldest group. Oxidative Medicine and Cellular Longevity decreased by 44% and affected the production of testosterone. Age-related regulation of the Leydig cell population remains controversial, some evidence in the literature shows that change in the maintenance of the redox balance within the Leydig cells affects their function. Previous research revealed that the superoxide content in aging Leydig cells is remarkably higher than in young Leydig cells [8]. The evidence of elevated levels of reactive oxygen species has been reported to be detected in 3080% of infertile men’s semen, showing that oxidative stress plays a critical role in male infertility. Oxidative stress can negatively affect fertility through a variety of pathways, interference with spermatozoa capacitation, and peroxidative damage to sperm membranes, proteins, and DNA, which are deleterious to the sperm’s potential and decrease the chances of the fertilized egg developing into a healthy early embryo [9]
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