Erectile dysfunction (ED) is an agonizing complication of diabetes mellitus (DM) and it is challenging to treat ED in DM patients. Platelet-rich plasma (PRP) is a unique therapeutic strategy comprising intrinsic growth factors. An attempt was made to explore the potentiality of the PRP treatment in DM-induced ED rats in various groups (control, DM-non-ED, DM-ED, and DM-ED treated with PRP). Streptozotocin (STZ) was used to induce DM in rats. The blood glucose levels of the DM rats were maintained at >300 mg/dl. In the 18-week experiment, survival rate, body weight, intracavernous pressure (ICP) variations, and arterial blood pressure were analyzed. The tissue restoration results were validated by histological, immunofluorescence, and transmission electron microscopic analysis. PRP treatment of DM-ED rats significantly increased all parameters of erectile function compared to pre-treatment of PRP and DM-ED treated with vehicle. The histological results revealed that PRP treatment substantially enhanced the regeneration of myelinated nerves and decreased the atrophy of corporal smooth muscle. Notably, the PRP treatment immensely enhanced the survival rate in post-surgery DM-ED rats. These results indicated certain benefits of PRP treatment in delaying damage and preventing post-surgery complications in DM patients. Hence, PRP treatment is a novel multifactorial strategy for DM-ED patients.

Age‐induced erectile dysfunction (ED) is a convoluted medical condition, and restoring erectile function (EF) under geriatric conditions is highly complicated. Platelet‐rich plasma (PRP) treatment is an inexpensive cell‐based therapeutic strategy. We have aimed to restore EF in aged‐ED rats with PRP as a therapeutic tool. Male rats were grouped into aged and young according to age. The young rats were considered as normal control (NC) and treated with saline. Aged were further divided into 2 groups and treated with intracavernous (IC) PRP and saline. Treatment was scheduled at the 9th and 10th week for NC and 41th and 42th week for aged‐ED rats, with EF analysis scheduled on the 12th week for NC and 44th week for aged‐ED rats, respectively. Erectile response, immunofluorescence staining, and electron microscopic analyses were performed. IC PRP treatment effectively reduced prostate hyperplasia (PH). EF response indicated a significant increase in crucial EF parameters in PRP‐treated aged‐ED rats. Histological evidence denoted a rigid and restored development of tunica adventitia of the dorsal artery, decreased vacuolation of the dorsal penile nerve, and structural expansion of the epineurium. Masson's trichrome and immunostaining results affirmed an elevated expression of α‐smooth muscle actin (α‐SMA) in the corpus cavernosum (CC). Ultrastructure findings revealed that PRP effectively rejuvenated degenerating nerves, preserved endothelium and adherent junctions of corporal smooth muscle, and restored the axonal scaffolds by upregulating neurofilament‐H (NF‐H) expression. Finally, PRP enhanced neural stability by enhancing the axonal remyelination processes in aged‐ED rats. Hence, PRP treatment was proven to restore EF in aged‐ED rats, which was considered a safe, novel, cost‐effective, and hassle‐free strategy for EF restoration in geriatric patients.

Traumatic brain injuries (TBIs) are a serious public health issue worldwide with increased mortality as well as severe disabilities and injuries caused by falls and road accidents. Unfortunately, there is no approved therapy for TBIs, and bladder dysfunction is a striking symptom. Accordingly, we attempted to analyze bladder dysfunction and voiding efficiency in rats with a TBI at different time-course intervals. Time-dependent analyses were scheduled from the next day until four weeks after a TBI. Experimental animals were grouped and analyzed under the above conditions. Cystometric measurements were used for this analysis and were further elaborated as external urethral sphincter electromyographic (EUS-EMG) activity and cystometrogram (CMG) measurements. Moreover, magnetic resonance imaging (MRI) studies were conducted to investigate secondary injury progression in TBI rats, and results were compared to normal control (NC) rats. Results of EUS-EMG revealed that the burst period, active period, and silent period in TBI rats were drastically reduced compared to NC rats, but they increased later and reached a stagnant phase. Likewise, in CMG measurements, bladder function, the voided volume, and voiding efficiency decreased immediately after the TBI, and other parameters like the volume threshold, inter-contraction interval, and residual volume drastically increased. Later, those levels changed, and all observed results were compared to NC rats. MRI results revealed the prevalence of cerebral edema and the progression of secondary injury. All of the above-stated results of the experiments were extensively substantiated. Thus, these innovative findings of our study model will surely pave the way for new therapeutic interventions for TBI treatment and prominently highlight their applications in the field of neuroscience in the future.

Background: Erectile dysfunction (ED) significantly affects both psychological and physiological well-being, with limited effective treatments available for nerve injury-induced ED. Stem cell therapy, particularly using human amniotic fluid stem cells (hAFSCs), shows promise due to the secretome (hAFSC-S), which is rich in growth factors and chemoattractants. This study investigated the paracrine effects of hAFSC-S on erectile function recovery in a rat model of bilateral cavernous nerve crush (BCNC) injury. Materials and methods: Thirty rats were divided into the sham and BCNC groups. The BCNC group received 200 µL of hAFSC-S via intracavernous injection. Western blotting was used to evaluate endothelial markers, while both Western blotting and enzyme-linked immunosorbent assay were used to characterize the secretome. Four weeks post-treatment, intracavernous pressure (ICP) was measured to assess erectile function. Histological analysis, immunofluorescence staining, and electron microscopy were conducted to examine penile tissue and nerve integrity. Results: The hAFSC-S-treated group demonstrated significantly higher ICP (91.77 ± 5.21 cmH ₂ O) compared to the untreated BCNC group (66.60 ± 3.64 cmH ₂ O). Histology revealed improved muscle integrity in the corpus cavernosum, increased smooth muscle content, and enhanced nerve myelination. Immunofluorescence staining showed elevated expression of neuronal markers, including nNOS and β-III-tubulin, in the major pelvic ganglion (0.42 ± 0.01%) and dorsal penile nerve (0.46 ± 0.01%). No significant differences were observed in vWF expression between the BCNC and BCNC + secretome groups in some regions (0.07 ± 0.009%). However, Western blot analysis revealed restored expression of endothelial markers CD31 and eNOS in penile tissue. Conclusion: hAFSC-S therapy enhanced nerve regeneration and penile tissue restoration, leading to improved erectile function in a BCNC rat model. These findings highlight its potential as a therapeutic option for ED.

Objective: Traumatic brain injuries (TBIs) are a prime public health challenge with a high incidence of mortality, and also reflect severe economic impacts. One of their severe symptoms is bladder dysfunction. Conventional therapeutic methods are not effective in managing bladder dysfunction. Henceforth, a research endeavor was attempted to explore a new therapeutic approach for bladder dysfunction through deep brain stimulation (DBS) procedures in a TBI animal model. Methods: TBI in this animal model was induced by the weight-drop method. All rats with an induced TBI were housed for 4 weeks to allow severe bladder dysfunction to develop. Subsequently, an initial urodynamic measurement, the simultaneous recording of cystometric (CMG) and external urethral sphincter electromyography (EUS-EMG) activity was conducted to evaluate bladder function. Further, standard DBS procedures with varying electrical stimulation parameters were executed in the target area of the pedunculopontine tegmental nucleus (PPTg). Simultaneously, urodynamic measurements were re-established to compare the effects of DBS interventions on bladder functions. Results: From the variable combinations of electrical stimulation, DBS at 50 Hz and 2.0 V, significantly reverted the voiding efficiency from 39% to 69% in TBI rats. Furthermore, MRI studies revealed the precise localization of the DBS electrode in the target area. Conclusions: The results we obtained showed an insightful understanding of PPTg-DBS and its therapeutic applications in alleviating bladder dysfunction in rats with a TBI. Hence, the present study suggests that PPTg-DBS is an effective therapeutic strategy for treating bladder dysfunction.