Ultrasonographic Contrast and Therapeutic Effects of Hydrogen Peroxide-Responsive Nanoparticles in a Rat Model with Sciatic Neuritis.

Purpose: Peripheral nerve damage lacks an appropriate diagnosis consistent with the patient's symptoms, despite expensive magnetic resonance imaging or electrodiagnostic assessments, which cause discomfort. Ultrasonography is valuable for diagnosing and treating nerve lesions; however, it is unsuitable for detecting small lesions. Poly(vanillin-oxalate) (PVO) nanoparticles are prepared from vanillin, a phytochemical with antioxidant and anti-inflammatory properties. Previously, PVO nanoparticles were cleaved by H2O2 to release vanillin, exert therapeutic efficacy, and generate CO2 to increase ultrasound contrast. However, the role of PVO nanoparticles in peripheral nerve lesion models is still unknown. Herein, we aimed to determine whether PVO nanoparticles can function as contrast and therapeutic agents for nerve lesions. Methods: To induce sciatic neuritis, rats were administered a perineural injection of carrageenan using a nerve stimulator under ultrasonographic guidance, and PVO nanoparticles were injected perineurally to evaluate ultrasonographic contrast and therapeutic effects. Reverse transcription-quantitative PCR was performed to detect mRNA levels of pro-inflammatory cytokines, ie, tumor necrosis factor-α, interleukin-6, and cyclooxygenase-2. Results: In the rat model of sciatic neuritis, PVO nanoparticles generated CO2 bubbles to increase ultrasonographic contrast, and a single perineural injection of PVO nanoparticles suppressed the expression of tumor necrosis factor-α, interleukin-6, and cyclooxygenase-2, reduced the expression of F4/80, and increased the expression of GAP43. Conclusion: The results of the current study suggest that PVO nanoparticles could be developed as ultrasonographic contrast agents and therapeutic agents for nerve lesions.

The Pulsed Nd:YAG Laser Therapy Enhanced Nerve Regeneration via Apoptosis Inhibition in a Rat Crushed Sciatic Nerve Model.

The study was aimed to validate the efficacy of the pulsed Nd:YAG laser on nerve regeneration in a rat sciatic nerve crushed model. 54 Wistar rats were randomly assigned into three groups: shame control, crush control, and laser treated group. For the laser treated group, the pulsed Nd:YAG laser (10 Hz) with 350 mJ per pulse in energy density and 50 J/cm2 in fluence was applied extracorporeally at the lesion site for 12 min to daily deliver 500 J immediately and consecutive 9 days following the crush injury. At week 1, the apoptosis-related activities in the injured nerve were examined (n = 8/each group). The sciatic functional index (SFI) was measured preoperatively and weekly until 4 weeks after the index procedure. The injured nerve and the innervated gastrocnemius muscle histology were assessed at week 4 (n = 10/each group). At week 1, the laser group showed the significant less TUNEL-positive ratio (P < 0.05), and the lower expression of cleaved caspase3/procaspase-3 and beclin-2/beclin-2-associated protein X ratios compared with the crush control. Furthermore, the laser group revealed significantly better SFI since week 1 and throughout the study (P < 0.05, all) compared with the crush control. At week 4, the laser group showed significantly higher axon density, lower myelin g-ratio, and the corresponding higher glycogen expression (P < 0.05, all) in the gastrocnemius muscle compared with those in the crush control. The pulsed Nd:YAG might enhance the injured nerve regeneration via apoptosis inhibition.

Enhancement of nerve regeneration through schwann cell-mediated healing in a 3D printed polyacrylonitrile conduit incorporating hydrogel and graphene quantum dots: a study on rat sciatic nerve injury model.

Despite recent technological advancements, effective healing from sciatic nerve damage remains inadequate. Cell-based therapies offer a promising alternative to autograft restoration for peripheral nerve injuries, and 3D printing techniques can be used to manufacture conduits with controlled diameter and size. In this study, we investigated the potential of Wharton's jelly-derived mesenchymal stem cells (WJMSCs) differentiated into schwann cells, using a polyacrylonitrile (PAN) conduit filled with fibrin hydrogel and graphene quantum dots (GQDs) to promote nerve regeneration in a rat sciatic nerve injury model. We investigated the potential of WJMSCs, extracted from the umbilical cord, to differentiate into schwann cells and promote nerve regeneration in a rat sciatic nerve injury model. WJMSCs were 3D cultured and differentiated into schwann cells within fibrin gel for two weeks. A 3 mm defect was created in the sciatic nerve of the rat model, which was then regenerated using a conduit/fibrin, conduit covered with schwann cells in fibrin/GQDs, GQDs in fibrin, and a control group without any treatment (n= 6/group). At 10 weeks after transplantation, motor and sensory functions and histological improvement were assessed. The WJMSCs were extracted, identified, and differentiated. The differentiated cells expressed typical schwann cell markers, S100 and P75.In vivoinvestigations established the durability and efficacy of the conduit to resist the pressures over two months of implantation. Histological measurements showed conduit efficiency, schwann cell infiltration, and association within the fibrin gel and lumen. Rats treated with the composite hydrogel-filled PAN conduit with GQDs showed significantly higher sensorial recovery than the other groups. Histological results showed that this group had significantly more axon numbers and remyelination than others. Our findings suggest that the conduit/schwann approach has the potential to improve nerve regeneration in peripheral nerve injuries, with future therapeutic implications.

Evaluation of Stem Cell Laden Collagen + Polycaprolactone + Multi-Walled Carbon Nano-Tubes Nano-Neural Scaffold with and Without Insulin Like Growth Factor-I For Sciatic Nerve Regeneration Post Crush Injury in Wistar Rats.

BACKGROUND/AIMS: All body functions are activated, synchronized and controlled by a substantial, complex network, the nervous system. Upon injury, pathophysiology of the nerve injury proceeds through different paths. The axon may undergo a degenerative retraction from the site of injury for a short distance unless the injury is near to the cell body, in which case it continues to the soma and undergoes retrograde neuronal degeneration. Otherwise, the distal section suffers from Wallerian degeneration, which is marked by axonal swelling, spheroids, and cytoskeleton degeneration. The objective of the study was to evaluate the potential of mesenchymal stem cell laden neural scaffold and insulin-like growth factor I (IGF-I) in nerve regeneration following sciatic nerve injury in a rat model. METHODS: The animals were anaesthetized and a cranio-lateral incision over left thigh was made. Sciatic nerve was exposed and crush injury was introduced for 90 seconds using haemostat at second locking position. The muscle and skin were sutured in routine fashion and thus the rat model of sciatic crush injury was prepared. The animal models were equally distributed into 5 different groups namely A, B, C, D and E and treated with phosphate buffer saline (PBS), carbon nanotubes based neural scaffold only, scaffold with IGF-I, stem cell laden scaffold and stem cell laden scaffold with IGF-I respectively. In vitro scaffold testing was performed. The nerve regeneration was assessed based on physico-neuronal, biochemical, histopathological examination, and relative expression of NRP-1, NRP-2 and GAP-43 and scanning electron microscopy. RESULTS: Sciatic nerve injury model with crush injury produced for 90 seconds was standardized and successfully used in this study. All the biochemical parameters were in normal range in all the groups indicating no scaffold related changes. Physico-neuronal, histopathological, relative gene expression and scanning electron microscopy observations revealed appreciable nerve regeneration in groups E and D, followed by C and B. Restricted to no regeneration was observed in group A. CONCLUSION: Carbon nanotubes based scaffold provided electro-conductivity for proper neuronal regeneration while rat bone marrow-derived mesenchymal stem cells were found to induce axonal sprouting, cellular transformation; whereas IGF-I induced stem cell differentiation, myelin synthesis, angiogenesis and muscle differentiation.

Betulinic acid alleviates neuropathic pain induced by chronic constriction injury of the sciatic nerve in mice.

Neuropathic pain refers to a type of pain that arises from primary damage and dysfunction within the nervous system. Addressing this condition presents significant challenges and complexities. Betulinic acid (BA), known for its potent antioxidative and anti-inflammatory properties, has garnered extensive attention; nevertheless, the impact upon neuropathic pain induced by CCI is still uncertain. This paper explores the analgesic effects concerning BA on mice experiencing neuropathic pain due to sciatic nerve injury. Throughout the experiment, mice with CCI received oral gavage of BA at dosages of 3, 10, and 30 mg/kg for consecutively 8 days from the 7th day post-surgery. To assess their responses, behavioral tests and sciatic functional index (SFI) evaluations were conducted on zeroth, seventh, eighth, tenth, twelveth and fourteenth day post-CCI. On day 14, histopathological examinations and measurements of biochemical markers were performed. Immunofluorescence techniques were employed to detect Nrf2 and glial cell activation, while the Western blot method was utilized to evaluate Nrf2/HO-1 protein levels and pro-inflammatory cytokine expression. The results elucidated that BA significantly alleviated hyperalgesia and allodynia, demonstrating a dose-dependent enhancement in sciatic nerve function and facilitating the recovery of sciatic nerve injury. Furthermore, BA prominently augmented the entire antioxidative capacity (T-AOC) and T-SOD levels, concomitantly reducing MDA concentrations. Notably, BA activated the Nrf2/HO-1 signaling pathway, inhibited glial cell activation, and downregulation of the expression levels of pro-inflammatory cytokines, specifically, TNF-α, IL-1ß, and IL-6 were observed. As such, this study provides a basis to support BA as a candidate drug for the treatment of neuropathic pain, attributing its analgesic effects to its anti-inflammatory, antioxidative, and neuroprotective properties.

Effect of Hesperidin on Sciatic Nerve Damage in STZ-Induced Diabetic Neuropathy: Modulation of TRPM2 Channel.

Diabetic neuropathy (DNP) is a severe complication of diabetes mellitus. In this study, we examined the potential of hesperidin (HES) to attenuate DNP and the involvement of the TRPM2 channel in this process. The rats were given a single dose of 45 mg/kg of streptozotocin (STZ) intraperitoneally to induce diabetic neuropathic pain. On the third day, we confirmed the development of diabetes in the DNP and DNP + HES groups. The HES groups were treated with 100 mg/kg and intragastric gavage daily for 14 days. The results showed that treatment with HES in diabetic rats decreased STZ-induced hyperglycemia and thermal hyperalgesia. Furthermore, in the histopathological examination of the sciatic nerve, HES treatment reduced STZ-induced damage. The immunohistochemical analysis also determined that STZ-induced increased TRPM2 channel, type-4 collagen, and fibrinogen immunoactivity decreased with HES treatment. In addition, we investigated the TRPM2 channel activation in the sciatic nerve damage mechanism of DNP model rats created by STZ application using the ELISA method. We determined the regulatory effect of HES on increased ROS, and PARP1 and TRPM2 channel activation in the sciatic nerves of DNP model rats. These findings indicated that hesperidin treatment could attenuate diabetes-induced DNP by reducing TRPM2 channel activation.

Therapeutic effects of cinnamon bark oil on sciatic nerve injury in rats.

OBJECTIVE: The aim of this study was to investigate the effects of cinnamon bark essential oil (CBO) on analgesia, motor activity, balance, and coordination in rats with sciatic nerve damage. MATERIALS AND METHODS: Rats were divided into three groups as simply randomized. The right sciatic nerve (RSN) of the Sham group was explored. Only vehicle solution was applied for 28 days. The RSN of the sciatic nerve injury (SNI) group was explored. Damage was created by unilateral clamping, and vehicle solution was applied for 28 days. The RSN of the sciatic nerve injury+cinnamon bark essential oil (SNI+CBO) group was explored. SNI was created by unilateral clamping and CBO was applied for 28 days. In the experiment study, motor activity, balance, and coordination measurements were made with rotarod and accelerod tests. A hot plate test was performed for analgesia measurements. Histopathology studies were carried out with the sciatic nerve tissues. RESULTS: In the rotarod test, there was a statistically significant difference between the SNI group and the SNI+CBO group (p<0.05). According to the accelerod test findings, there was a statistically significant difference between the SNI group with the Sham and SNI+CBO groups. In the hot plate test, there was a statistically significant difference between the SNI group with the Sham and SNI+CBO groups (p<0.05). In comparison to the Sham group and the SNI group, the SNI+CBO group was shown to have the greatest expression level of vimentin. CONCLUSIONS: We have concluded that CBO can be used as an adjuvant treatment in cases of SNI, increased pain, nociception, impaired balance, motor activity, and coordination. Our results will be supported by further studies.

Effect of Azithromycin on Sciatic Nerve Injury in the Wistar Rats.

After a severe peripheral nerve injury, complete functional recovery is rare. Modulating the inflammatory response could be an effective way to enhance peripheral nerve regeneration. The present study aimed to determine the effect of azithromycin on functional recovery following sciatic nerve crush in Wistar rats. 40 male Wistar rats were used in four groups, including: the negative control, sham, and two groups of azithromycin (15 and 150 mg/kg/day) (n = 10).The rats' right sciatic nerve was crushed using a non-serrated clamp. In experimental groups, animals were treated with azithromycin (15 and 150 mg/kg/day) for 7 days. Then, sensory-motor functions were evaluated over eight weeks. Real-time PCR was used to measure the expression of NGF and BDNF genes. At the end of the 4th week, the sensory recovery accelerated in the azithromycin-treated rats so that the reaction times in the groups treated with 15 mg/kg and 150 mg/kg doses of azithromycin reached 5.14 s and 6.61 s, respectively, which were significantly lower than the 12 s in the negative control group (P < 0.05).Eventually, the mean SFI values in the negative control and both azithromycin-treated groups recovered to preoperative levels in the 8th week, with no significant difference between the sciatic lesion groups. Findings showed a seven-day course of azithromycin administered immediately after a sciatic nerve crush could accelerate regeneration and improve motor and sensory function recovery compared to negative controls. These significant effects were observed in both the azithromycin 15 mg/kg and the azithromycin 150 mg/kg treatment groups. Azithromycin treatment upregulated the expression of NGF and BDNF genes in crushed sciatic nerve. Our findings suggest that a seven-day treatment of azithromycin after a sciatic nerve injury could accelerate the regeneration process and improve functional recovery.

Enhancement of nerve regeneration with nimodipine treatment after sciatic nerve injury.

Peripheral nerve injuries (PNI/s) are common orthopedic conditions, characterized by motor and sensory deficits in the damaged region. There is growing evidence that the L-type calcium channel antagonist nimodipine has neuroprotective and neuroregenerative effects in animal models of neurological disorders. The efficacy of nimodipine on improving motor function and sensation following a sciatic nerve crush model was investigated in male Wistar rats as a model of PNI. At different time periods following damage, we evaluated motor function, sensory recovery, electrophysiology, histomorphometry, and gene expression. Moreover, we used histological and mass ratio analysis of the gastrocnemius muscle to assess atrophy. Our findings suggest that the nimodipine improves motor and sensory function more quickly in the damaged region 2, 4, and 6 weeks after 1 week of treatment. Nimodipine treatment also increased the number of myelinated fibers while decreasing their thickness, as shown by histomorphometry. Additionally, nimodipine treatment increases the mRNA levels of neurotrophic factors (BDNF and NGF), which are known to contribute to the regeneration of injured neurons. The impact of nimodipine in PNI recovery may be due to its stimulation of the CREB signaling pathway and suppression of pro-inflammatory factor production.

A Sciatic Neuralgia Case of an Entrapment Neuropathy Mimicking Piriformis Syndrome Due to Soft Tissue Hemangioma.

BACKGROUND: Lumbosacral pain is commonly seen in daily clinical practice. In fact, entrapment of the part of the sciatic nerve after the sacral foramen causes some of these pains, which should not be overlooked. The sciatic nerve may be compressed during its course after the sacral foramen for a variety of reasons. We aimed in this article to review extra-spinal compressive sciatic neuropathy reasons and abnormal magnetic resonance imaging (MRI) by presenting a sciatic neuralgia case of an entrapment neuropathy mimicking piriformis syndrome due to soft tissue hemangioma. CASE PRESENTATION: A 30-year-old male patient was admitted with complaints of lumbosacral pain spreading to the leg that had been worsening over the previous 10 days. With the preliminary diagnosis of labral damage and piriformis syndrome, the patient was referred to the radiology clinic for a hip MRI. In the hip MR images, a mass lesion suggestive of heterogeneously enhanced soft tissue hemangioma after the injection of paramagnetic contrast material was observed in the proximal left thigh. The soft tissue hemangioma extends towards the obturator foramen and compresses the sciatic nerve proximal to the femur after the sciatic foramen. CONCLUSION: The diagnosis of lower extremity entrapment neuropathy is frequently misdiagnosed. In these cases, MRI becomes more important for accurate diagnosis. The radiologists' knowledge of the sciatic nerve in MRI, regional anatomy during the course of the sciatic nerve, and abnormal nerve imaging findings will aid in the diagnosis.

Effects of apocynin on sciatic nerve injury in rabbits.

We investigated the effects of apocynin (APO) on experimental sciatic nerve compression injury in rabbits. We used 21 male rabbits divided randomly into three groups of seven. The control group was subjected to sciatic nerve compression with no further intervention. The APO treated group was subjected to compression injury and 20 mg/kg APO was administered daily for 21 days by intraperitoneal injection beginning the day after the injury. The sham group was treated with APO without injury. The control group exhibited shrinkage of axons, disruption of myelin sheaths and loss of nerve fibers. The damage for the control group was significantly greater than for the sham group. The severity of histopathology was decreased in the APO treated group compared to the control group, as was the oxidative stress index. Our findings suggest that APO treatment may contribute to healing of sciatic nerve damage.

Electrical stimulation accelerates Wallerian degeneration and promotes nerve regeneration after sciatic nerve injury.

Following peripheral nerve injury (PNI), Wallerian degeneration (WD) in the distal stump can generate a microenvironment favorable for nerve regeneration. Brief low-frequency electrical stimulation (ES) is an effective treatment for PNI, but the mechanism underlying its effect on WD remains unclear. Therefore, we hypothesized that ES could enhance nerve regeneration by accelerating WD. To verify this hypothesis, we used a rat model of sciatic nerve transection and provided ES at the distal stump of the injured nerve. The injured nerve was then evaluated after 1, 4, 7, 14 and 21 days post injury (dpi). The results showed that ES significantly promoted the degeneration and clearance of axons and myelin, and the dedifferentiation of Schwann cells. It upregulated the expression of BDNF and NGF and increased the number of monocytes and macrophages. Through transcriptome sequencing, we systematically investigated the effect of ES on the molecular processes involved in WD at 4 dpi. Evaluation of nerves bridged using silicone tubing after transection showed that ES accelerated early axonal and vascular regeneration while delaying gastrocnemius atrophy. These results demonstrate that ES promotes nerve regeneration by accelerating WD and upregulating the expression of neurotrophic factors.

Spinal Irisin Gene Delivery Attenuates Burn Injury-Induced Muscle Atrophy by Promoting Axonal Myelination and Innervation of Neuromuscular Junctions.

Muscle loss and weakness after a burn injury are typically the consequences of neuronal dysregulation and metabolic change. Hypermetabolism has been noted to cause muscle atrophy. However, the mechanism underlying the development of burn-induced motor neuropathy and its contribution to muscle atrophy warrant elucidation. Current therapeutic interventions for burn-induced motor neuropathy demonstrate moderate efficacy and have side effects, which limit their usage. We previously used a third-degree burn injury rodent model and found that irisin-an exercise-induced myokine-exerts a protective effect against burn injury-induced sensory and motor neuropathy by attenuating neuronal damage in the spinal cord. In the current study, spinal irisin gene delivery was noted to attenuate burn injury-induced sciatic nerve demyelination and reduction of neuromuscular junction innervation. Spinal overexpression of irisin leads to myelination rehabilitation and muscular innervation through the modulation of brain-derived neurotrophic factor and glial-cell-line-derived neurotrophic factor expression along the sciatic nerve to the muscle tissues and thereby modulates the Akt/mTOR pathway and metabolic derangement and prevents muscle atrophy.

Evaluation of the therapeutic effects of calcium dobesilate in sciatic nerve crush injury in rats.

INTRODUCTION: Proinflammatory cytokines released from nerve endings and surrounding injured tissue after nerve damage can prolong the inflammation process, delay nerve healing or result in poor quality nerve healing. In this case, due to the loss of function in the muscles innervated by the damaged nerve, the patient may have neurological and functional difficulties which may reduce the patient's quality of life and create an economic burden. Although the attempts of many pharmacological agents to heal crush injury of peripheral nerves have been recorded in literature, a drug that can provide adequate recovery of the crushed nerve and can be applied in daily life has not been defined as yet. This study aimed to assess the effects of calcium dobesilate on sciatic nerve crush injury in a rat model. METHODS: A total of 26 male Wistar albino rats were separated into four groups as follows: CONTROL group (healthy subjects, n=6); SHAM group (crush injury was created, n=6); MP group (after created crush injury, methylprednisolone was administered, n=7); and CAD group (after created crush injury, calcium dobesilate was administered, n=7). A crush injury was created, then the electrophysiological findings and sciatic nerve functional index (SFI) were recorded before euthanasia. After the euthanasia of all the rats, samples of the crushed nerve and gastrocnemius muscle were evaluated histopathologically, immunohistochemically, and biochemically. RESULTS: Both pharmacological agents were histopathologically effective in axon regeneration and repair. Calcium dobesilate did not preserve total muscle mass but was seen to prevent atrophy microscopically. Immunohistochemistry and biochemistry results showed that calcium dobesilate and methylprednisolone had anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-autophagic activity in the crushed sciatic nerve. Neither calcium dobesilate nor methylprednisolone improved the nerve conductance level. SFI values obtained on day 30 from the CAD group were numerically closer to the values of the healthy animals but not at a statistically significant level. CONCLUSION: The study results demonstrated that calcium dobesilate could suppress inflammatory processes and provide histopathological and functional improvements in the injured nerve in rats. Therefore, further clinical studies are recommended to investigate in detail the therapeutic effects of calcium dobesilate on peripheral nerve crush injury.

Human Multipotent Mesenchymal Stromal Cell-Derived Extracellular Vesicles Enhance Neuroregeneration in a Rat Model of Sciatic Nerve Crush Injury.

Peripheral nerve injury remains a serious problem for medicine, with no effective method of treatment at the moment. The most prominent example of this problem is neonatal brachial plexus palsy, which results from the stretching of the brachial plexus nerves in the birth or perinatal period. Multipotent mesenchymal cells (MSCs) and the extracellular vesicles (EVs) they produce are known to have a marked neuroprotective effect in central nervous system injuries. We suggested that the use of MSCs-derived EVs may be an effective approach to the regeneration of peripheral nerves after injury. Sciatic nerve injury was modeled in rats via crushing, and then a gel containing MSCs-EVs was applied to the injured area. After 15 and 30 days, a histological, physiological, and functional assessment of nerve, dorsal root ganglia (DRG), and innervated muscles' recovery was performed. Transplantation of EVs to the area of sciatic nerve injury significantly reduced muscle atrophy as compared to the control group. Functional recovery of the innervated muscles, as measured by the extensor postural thrust test, was revealed 30 days after the surgery. We associate the obtained results with EVs-induced neuroprotective mechanisms, which were expressed in a decrease in apoptotic neuronal death and an increase in regeneration-associated proteins NF-200 and GAP-43, as well as in DRG and damaged nerve. We suggest that the therapeutic scheme we used is efficient for the treatment of acute peripheral nervous system injuries and can be transferred to the clinics. However, additional studies are required for a more detailed analysis of neuroprotection mechanisms.

Raman spectroscopy and sciatic functional index (SFI) after low-level laser therapy (LLLT) in a rat sciatic nerve crush injury model.

Axonotmesis causes sensorimotor and neurofunctional deficits, and its regeneration can occur slowly or not occur if not treated appropriately. Low-level laser therapy (LLLT) promotes nerve regeneration with the proliferation of myelinating Schwann cells to recover the myelin sheath and the production of glycoproteins for endoneurium reconstruction. This study aimed to evaluate the effects of LLLT on sciatic nerve regeneration after compression injury by means of the sciatic functional index (SFI) and Raman spectroscopy (RS). For this, 64 Wistar rats were divided into two groups according to the length of treatment: 14 days (n = 32) and 21 days (n = 32). These two groups were subdivided into four sub-groups of eight animals each (control 1; control 2; laser 660 nm; laser 808 nm). All animals had surgical exposure to the sciatic nerve, and only control 1 did not suffer nerve damage. To cause the lesion in the sciatic nerve, compression was applied with a Kelly clamp for 6 s. The evaluation of sensory deficit was performed by the painful exteroceptive sensitivity (PES) and neuromotor tests by the SFI. Laser 660 nm and laser 808 nm sub-groups were irradiated daily (100 mW, 40 s, energy density of 133 J/cm2). The sciatic nerve segment was removed for RS analysis. The animals showed accentuated sensory and neurofunctional deficit after injury and their rehabilitation occurred more effectively in the sub-groups treated with 660 nm laser. Control 2 sub-group did not obtain functional recovery of gait. The RS identified sphingolipids (718, 1065, and 1440 cm-1) and collagen (700, 852, 1004, 1270, and 1660 cm-1) as biomolecular characteristics of sciatic nerves. Principal component analysis revealed important differences among sub-groups and a directly proportional correlation with SFI, mainly in the sub-group laser 660 nm treated for 21 days. In the axonotmesis-type lesion model presented herein, the 660 nm laser was more efficient in neurofunctional recovery, and the Raman spectra of lipid and protein properties were attributed to the basic biochemical composition of the sciatic nerve.

Glibenclamide promoted functional recovery following sciatic nerve injury in male Wistar rats.

The impact of peripheral nerve damage on a patient's quality of life is severe. The most frequent peripheral nerve crush damage is a sciatic nerve injury. Previous research has shown that glibenclamide (GB) has neuroprotective properties in a variety of oxidative stress-related disorders, including Alzheimer and Parkinson. The goal of this study was to see how GB affected nerve regeneration and improved function of the sciatic nerve in a rat model following a crush injury. We evaluated motor function, sensory recovery, gene expression, and histomorphometry following damage at different time points. Additionally, we assessed atrophy in the gastrocnemius muscle using histology and mass ratio analyses. Our results suggest that 2, 4, 6, and 8 weeks following glibenclamide therapy, promotes the recovery of motor and sensory function in the injured site. Following glibenclamid injection, the mRNA levels of neurotrophic factors (NGF and BDNF) are raised. According to histomorphometry assessment, glibenclamide injection also increased the number of myelinated fibers while decreasing their thickness. These results showed that glibenclamide therapy by decreasing the proinflammatory and oxidant factors may enhance the nerve regeneration. It is clear that more research is needed to confirm these findings.

Thyroxine Accelerates Functional Recovery in a Rat Model of Sciatic Nerve Crush.

AIM: To see how thyroxine affects the sensory and motor function of a damaged sciatic nerve in male rats. MATERIAL AND METHODS: Forty adult male Wistar rats were allocated to four groups, 10 individuals each. Then, crush injury was done on the right sciatic nerve in all the groups using a vessel clamp. In thyroxine-treated groups and after the crush, the rats were given regular doses of thyroxine (5 and 10 ?g/kg) for one week intraperitoneally. Negative control group was treated intraperitoneally with distilled water as a vehicle. In sham operated group, only surgical procedures were performed without nerve crush. Then, behavioral, histological, and morphometric parameters were assessed at the regeneration time. RESULTS: After one week of treatment with thyroxine, the motor function improved significantly following a sciatic nerve crush (P ? 0.05). Also, morphometric parameters and sensory restoration improved in thyroxine-treated groups. CONCLUSION: Findings of this study showed that neuro-protective effects of thyroxine can be due to the stimulatory effects of thyroxine in myelin sheath formation and increasing the expression of SCG10 protein which is required for the development of growth cones.

Comparing effects of L-carnitine and sildenafil citrate on histopathologic recovery from sciatic nerve crush injury in female albino rats.

BACKGROUND: The sciatic nerve is a peripheral nerve and is more vulnerable to compression with subsequent short- or long-term neuronal dysfunction. The current study was designed to elucidate the possible ameliorative effect of L-carnitine and sildenafil (SIL) on sciatic nerve crush injury. We sought to determine the effects of L-carnitine, a neuroprotective and a neuro-modulatory agent, and SIL citrate, a selective peripheral phosphodiesterases inhibitor, on modulating neuro-degenerative changes due to sciatic nerve compression. MATERIALS AND METHODS: The comparative effect of L-carnitine (at an oral dose of 20 mg/kg/day) or SIL citrate (20 mg/kg/day orally) administration for 21 days was studied in a rat model of sciatic nerve compression. Sciatic nerve sections were subjected to biochemical, histological, ultrastructure, and immunohistochemical studies to observe the effects of these treatments on neurofilament protein. RESULTS: The sciatic nerve crush injury group (group II) showed a significant decrease in tissue catalase (CAT), superoxide dismutase (SOD) and increase in malondialdehyde (MDA) as compared to control group (p < 0.01). Histological changes in the form of degenerated and vacuolated axoplasm with areas of nerve fibre loss and pyknotic nuclei were reported. The blood vessels were dilated, congested with areas of haemorrhage and mononuclear cell infiltration. Histo-morphometrically, a statistically significant reduction in the nerve fibres' number, mean axon cross-sectional area, myelin sheath thickness and a significant increase in collagen fibres' percentage (p < 0.05) as compared to control group. Immunohistochemically, neurofilament protein was significantly downregulated as proved by a significant reduction in mean area per cent of neurofilament expression. L-carnitine ameliorated the studied parameters through its neuroprotective effect while SIL, a selective peripheral phosphodiesterases (PDE-5) inhibitor, improved crush injury parameters but with less extent than L-carnitine. CONCLUSIONS: These findings indicate the valuable effects of L-carnitine administration compared to that of SIL citrate in alleviating the serious debilitating effects of sciatic nerve crush injury. Our results provide a new insight into the scope of neuroprotective and neuro-regenerative effects of L-carnitine in a sciatic nerve compression model.

Effect of decorin protein administration on rat sciatic nerve injury: an experimental study.

INTRODUCTION: Peripheral nerve traumas are common injuries in young adult population. The myriad of techniques and medications have been defined to obtain better recovery but none of them was proved to have superior effect. This study aims to determine the anti-fibrotic effect of the decorin on sciatic nerve injury in order to enhance functional outcome. MATERIALS AND METHODS: 24 12-week-old male Sprague-Dawley rats (350-400 gr) were divided into four groups. The sciatic nerve was dissected and exposed; a full-thickness laceration was created 1.5 cm proximal to the bifurcation point and 1.5 cm distal to where it originated from the lumbosacral plexus. Motor and sensory tests were conducted before and after the operations for evaluating the nerve healing. RESULTS: There was a statistically significant difference between DCN bolus and PBS bolus group. (p<0.0001, p<0.05) in neuromotor tests. Increase of the latency was significantly lower in DCN bolus and infusion group when compared with the PBS bolus group. (p<0,001). All operated gastrocnemius muscles were atrophic compared with the contralateral side. The differences between the averages in the sciatic functional index, the improvement of the DCN infusion group was 8.6 units better than the PBS group and 4.4 units better than the DCN bolus group. When the amount of stimulation was 10 mV at the proximal segment in electromyography, there was no significant difference between the DCN bolus and sham groups. (p> 0.05, p = 0.6623). CONCLUSION: Decorin protein reduces the fibrosis and enhances the motor and sensory recovery both clinically and histologically. Despite the high cost, short half-life and production issues, this protein could be administered after the microsurgical repair but more studies are required to overcome the limitations.