Abstract
Background Deficient spermatozoon motility is one of the main causes of male infertility. However, there are still no accurate and effective treatments in a clinical setting for male asthenospermia. Exploring the genes and mechanism of asthenospermia has become one of the hot topics in reproductive medicine. Our aim is to study the effect of SLRIP on human spermatozoon motility and oxidative stress. Methods Sperm samples were collected including a normospermia group (60 cases) and an asthenospermia group (50 cases). SLIRP protein expression in spermatozoa was examined by western blotting, and relative mRNA expression of SLIRP in spermatozoa was quantified by reverse transcription polymerase chain reaction. Levels of reactive oxygen species (ROS), adenosine triphosphate (ATP) content, and the activity of manganese superoxide dismutase (MnSOD) in spermatozoa were also measured. Results The mRNA level and protein expression of SLIRP in the asthenospermia group were significantly reduced compared with those in the normospermia group. The ROS active oxygen level in the asthenospermia group significantly increased; however, the ATP content decreased significantly as well as the activity of MnSOD. Conclusion SLIRP regulates human male fertility, and SLIRP and sperm progressive motility are positively correlated. The expression of SLIRP is declined, oxidative damage is increased, and energy metabolism is decreased in spermatozoa of asthenospermia patients compared to normospermia participants.
Highlights
About 10%-15% of couples of reproductive age have fertility disorders worldwide, and according to incomplete statistics, about 40% of infertility is related to male factors
The semen concentration was within the normal range, but 52:91 ± 25:26 ∗ 106/mL in the asthenospermia group appeared to be much lower than that in the normospermia group
There is no obvious difference in the proportion of normal morphology sperm: 3.28% in the normospermia group and 1.99% in the asthenospermia group
Summary
About 10%-15% of couples of reproductive age have fertility disorders worldwide, and according to incomplete statistics, about 40% of infertility is related to male factors. Sperm motility deficiency is one of the main causes of male infertility. Researchers [6] made model mice with SLIRP gene knockout to see if they could survive, but their fertility was weakened and their sperm motility was deficient. The loss or weakening of SLIRP destroys part of the structure of mitochondria, affects mitochondrial energy metabolism, and increases sperm or cell oxidative stress damage. The mRNA level and protein expression of SLIRP in the asthenospermia group were significantly reduced compared with those in the normospermia group. SLIRP regulates human male fertility, and SLIRP and sperm progressive motility are positively correlated. The expression of SLIRP is declined, oxidative damage is increased, and energy metabolism is decreased in spermatozoa of asthenospermia patients compared to normospermia participants
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