The present study demonstrated that hsa-miR-27b-3p, hsa-miR-151a-5p and hsa-miR-206 play an important role in the effects of l-carnitine treatment of the spermatozoa in asthenospermia patients.
In addition, RT-qPCR results revealed that the expression levels of 4 genes coding fructokinase (FRK), citrate synthase (CS), succinate dehydrogenase (SDH), and spermine synthase (SMS), which were related to energy metabolism, were decreased in the AS group.
The present study demonstrated that hsa-miR-27b-3p, hsa-miR-151a-5p and hsa-miR-206 play an important role in the effects of l-carnitine treatment of the spermatozoa in asthenospermia patients.
In addition, RT-qPCR results revealed that the expression levels of 4 genes coding fructokinase (FRK), citrate synthase (CS), succinate dehydrogenase (SDH), and spermine synthase (SMS), which were related to energy metabolism, were decreased in the AS group.
In addition, RT-qPCR results revealed that the expression levels of 4 genes coding fructokinase (FRK), citrate synthase (CS), succinate dehydrogenase (SDH), and spermine synthase (SMS), which were related to energy metabolism, were decreased in the AS group.
In addition, RT-qPCR results revealed that the expression levels of 4 genes coding fructokinase (FRK), citrate synthase (CS), succinate dehydrogenase (SDH), and spermine synthase (SMS), which were related to energy metabolism, were decreased in the AS group.
Expression of these markers were assessed by qRT-PCR, and analysis of data show that mean of hypoxia markers (P53, HIF-1α) and also TNF- α were significantly higher in infertile men with asthenozoospermia compared to fertile men (p < 0.05).
The meta-analysis showed significant improvement in semen parameters for selenium (200µg/day and 100µg/day) (standard mean difference [SMD] 0.64 for oligozoospermia, 1.39 for asthenozoospermia), L-carnitine (2 g/day) and acetyl-L-carnitine (LAC; 1 g/day) combined (SMD 0.57 for asthenozoospermia), and co-enzyme Q10 (200 and 300 mg/day) (SMD 0.95 for oligozoospermia, 1.48 for asthenozoospermia, 0.63 for teratozoospermia).
The pairs that were uncorrelated in the infertile populations and displayed the best biomarker potential were hsa-miR-942-5p/hsa-miR-1208 (asthenozoospermia), hsa-miR-296-5p/hsa-miR-328-3p (teratozoospermia), hsa-miR-139-5p/hsa-miR-1260a (oligozoospermia), and hsa-miR-34b-3p/hsa-miR-93-3p (UMI).
We report here for the first time that an abnormal AA metabolic network could reduce sperm motility via P38 MAPK activation through the LOX, cytochrome P450 and COX metabolic pathways, which might be an underlying pathomechanism of asthenozoospermia.
The SP humanin concentrations in patients with normospermia were significantly higher than those in patients with oligospermia (p < 0.001), asthenospermia (p = 0.002), and oligoasthenospermia (p < 0.001).
We report here for the first time that an abnormal AA metabolic network could reduce sperm motility via P38 MAPK activation through the LOX, cytochrome P450 and COX metabolic pathways, which might be an underlying pathomechanism of asthenozoospermia.
We report here for the first time that an abnormal AA metabolic network could reduce sperm motility via P38 MAPK activation through the LOX, cytochrome P450 and COX metabolic pathways, which might be an underlying pathomechanism of asthenozoospermia.
As F-actin is required for maintaining structural integrity and hyperactivated motility in sperm, our finding has significant implications in light of our previous reports of reduced GRP78 phosphorylation and the actin-based motility pathway being significantly altered in asthenozoospermia.
Subsequently, seven miRNAs were selected to validate by RT-PCR that showed MiR-888-3p significantly overexpressed in AZS cases (p = 0.014) in comparison with controls.
We aimed to study the effect of varicocelectomy on the serum and seminal leptin in patients with asthenozoospermia and the correlation between leptin levels, sperm parameters and varicocele grade.
We report here for the first time that an abnormal AA metabolic network could reduce sperm motility via P38 MAPK activation through the LOX, cytochrome P450 and COX metabolic pathways, which might be an underlying pathomechanism of asthenozoospermia.
We report here for the first time that an abnormal AA metabolic network could reduce sperm motility via P38 MAPK activation through the LOX, cytochrome P450 and COX metabolic pathways, which might be an underlying pathomechanism of asthenozoospermia.
We report here for the first time that an abnormal AA metabolic network could reduce sperm motility via P38 MAPK activation through the LOX, cytochrome P450 and COX metabolic pathways, which might be an underlying pathomechanism of asthenozoospermia.