Testosterone signaling pathways for reducing neuropathic pain in a rat model of spinothalamic tract lesion.

Objectives: Most individuals who suffer from spinal cord injury (SCI) experience neuropathic pain, which currently has no effective treatment. In this study, we examined how testosterone affects neuropathic pain resulting from SCI.

Materials And Methods: We administered three different doses of testosterone (4, 8, 16 mg/kg, intraperitoneal) to male rats after an electrolytic lesion of the spinothalamic tract.

The Role of Vitamins in Spinal Cord Injury: Mechanisms and Benefits.

Spinal cord injury (SCI) is a common neurological disease worldwide, often resulting in a substantial decrease in quality of life, disability, and in severe cases, even death. Unfortunately, there is currently no effective treatment for this disease. Nevertheless, current basic and clinical evidence suggests that vitamins, with their antioxidant properties and biological functions, may play a valuable role in improving the quality of life for individuals with SCI.

Astaxanthin ameliorates spinal cord edema and astrocyte activation via suppression of HMGB1/TLR4/NF-κB signaling pathway in a rat model of spinal cord injury.

Spinal cord edema is a quick-onset phenomenon with long-term effects. This complication is associated with inflammatory responses, as well as poor motor function. No effective treatment has been developed against spinal edema, which urges the need to provide novel therapies.

Intra-arterial verapamil improves functional outcomes of thrombectomy in a preclinical model of extended hyperglycemic stroke.

The abrupt hyperglycemic reperfusion following thrombectomy has been shown to harm the efficacy of the intervention in stroke patients with large vessel occlusion. Studies of ours and others have shown thioredoxin-interacting protein (TXNIP) is critically involved in hyperglycemic stroke injury. We recently found verapamil ameliorates cerebrovascular toxicity of tissue plasminogen activators in hyperglycemic stroke.

Estrogen as a key regulator of energy homeostasis and metabolic health.

Over the last two decades, it has become evident that estrogens preserve the integrity of energy homeostasis at central and peripheral levels. Estrogen deficiency, such as that caused by menopause or ovariectomy, has been linked to obesity and metabolic disorders that can be resolved or reversed by estrogen therapy. 17β-estradiol (E2), as the major estrogen in the body, primarily regulates energy balance via estrogen receptor alpha (ERα).

Astaxanthin ameliorates serum level and spinal expression of macrophage migration inhibitory factor following spinal cord injury.

Astaxanthin (AST) is a lipid-soluble carotenoid with antioxidant and anti-inflammatory properties. Previous reports demonstrated the promising effects of AST on spinal cord injury (SCI)-induced inflammation and sensory-motor dysfunction. Macrophage migration inhibitory factor (MIF), as a cytokine, plays a critical role in the inflammatory phase of SCI.

Synergistic effects of Nepeta menthoides and Melissa officinalis aqueous extracts on reserpine-induced depressive-like behaviors in mice.

Nepeta menthoides Boiss. & Buhse and Melissa officinalis are extensively used in Persian medicine for the treatment of depression. Considering the active ingredients and main phenolic compounds of these plants and possible synergistic effects, this study examined the antidepressant and antioxidant activities of aqueous extract of N.

Astaxanthin Modulates Autophagy, Apoptosis, and Neuronal Oxidative Stress in a Rat Model of Compression Spinal Cord Injury.

The effects of astaxanthin (AST) were evaluated on oxidative mediators, neuronal apoptosis, and autophagy in functional motor recovery after spinal cord injury (SCI). Rats were divided into three groups of sham, SCI + DMSO (dimethyl sulfoxide), and SCI + AST. Rats in the sham group only underwent a laminectomy at thoracic 8-9.

Anti-inflammatory and antioxidant effects of astaxanthin following spinal cord injury in a rat animal model.

Spinal cord injury (SCI) is a severely debilitating problem leading to substantial decrease in the quality of life. After spinal cord injury, inflammation and oxidative stress plays a key role in initiating the secondary injury cascades leading to progressive tissue degradation and extreme functional deficits. Given that the primary mechanical injuries to spinal cord are rarely repaired, the pharmacological interventions may improve the neurological outcomes caused by secondary injury.

On the therapeutic targets and pharmacological treatments for pain relief following spinal cord injury: A mechanistic review.

Spinal cord injury (SCI) is globally considered as one of the most debilitating disorders, which interferes with daily activities and life of the affected patients. Despite many developments in related recognizing and treating procedures, post-SCI neuropathic pain (NP) is still a clinical challenge for clinicians with no distinct treatments. Accordingly, a comprehensive search was conducted in PubMed, Medline, Scopus, Web of Science, and national database (SID and Irandoc).

The role of ERα36 in cell type-specific functions of estrogen and cancer development.

Exploring the regulatory effects of estrogen on different body organs via its receptors is largely of interest. Recently, the expression, signaling and the clinical significance of ERα36, the newly identified isoform of ERα, mediating non-genomic signaling of estrogen, have been studied in a wide range of organs and tumors. ERα36 is expressed highly in the CNS and actively involved in neuroprotection.

Fingolimod increases oligodendrocytes markers expression in epidermal neural crest stem cells.

Epidermal neural crest stem cells (EPI-NCSCs) are propitious candidates for cell replacement therapy and supplying neurotrophic factors in the neurological disorders. Considering the potential remyelinating and regenerative effects of fingolimod, in this study, we evaluated its effects on EPI-NCSCs viability and the expression of neurotrophic and oligodendrocyte differentiation factors. EPI-NCSCs, extracted from the bulge of rat hair follicles, were characterized and treated with fingolimod (0, 50, 100, 200, 400, 600, 1000, and 5000 nM).

Combination therapy with astaxanthin and epidermal neural crest stem cells improves motor impairments and activates mitochondrial biogenesis in a rat model of spinal cord injury.

Spinal cord injury (SCI), a multifactorial disease, can lead to irreversible motor and sensory disabilities. Cell therapy in combination with pharmacological agents can be a promising approach to attenuate SCI damages. Epidermal neural crest stem cells (EPI-NCSCs) extracted from bulge hair follicle in adults are attractive candidates due to the possibility of autologous transplantation.

Expression patterns of ERα66 and its novel variant isoform ERα36 in lactotroph pituitary adenomas and associations with clinicopathological characteristics.

Purpose: The regulatory effects of estradiol on pituitary homeostasis have been well documented. However, the expression patterns of ERα66 and ERα36 and their correlations with the clinical course of postoperative prolactinoma tumors remain unclear.

Methods: The expression of ERα36, ERα66, Ki67, p53, and CD31 were determined by immunohistochemistry in 62 prolactinoma patients.

The effects of anticancer medicinal herbs on vascular endothelial growth factor based on pharmacological aspects: a review study.

As a complicated process of forming new blood vessels from the present vasculature endothelium, angiogenesis plays a critical role in the progression of cancer, through developing new blood vessels in tumor cells. Angiogenesis is regulated by proteins known as inhibitor or activator molecules, affected by different medicinal herbs and small molecules. In the present review, the molecular mechanisms of tumor angiogenesis are outlined, focusing on the pharmacological aspects and molecular mechanisms of natural compounds used in chemotherapy and their effects on angiogenesis, focusing on vascular endothelial growth factor (VEGF).

Urogenital chlamydia trachomatis treatment failure with azithromycin: A meta-analysis.

Background: Chlamydia Trachomatis is one of the most common pathogens transmitted through the genital tract in humans that leads to urogenital infection.

Objective: Given the high prevalence of chlamydia infection and its adverse effects on the health of women and men, the present meta-analysis was conducted to determine the rate of treatment failure with azithromycin.

Materials And Methods: Databases including MEDLINE, ISI - Web of Science, PubMed, EMBASE, Scopus, ProQuest, and Science Direct were searched for articles published between 1991 and 2018.

Sex Differences and Role of Gonadal Hormones on Glutamate LevelAfter Spinal Cord Injury in Rats: A Microdialysis Study.

Introduction: Sex differences in outcomes of Spinal Cord Injury (SCI) suggest a sex-hormone-mediated effect on post-SCI pathological events, including glutamate excitotoxicity. This study aimed to investigate the importance of gonadal hormones on glutamate release subsequent to SCI in rats.

Methods: After laminectomy at T8-T9, an electrolytic lesion was applied to the spinothalamic tracts of male and female rats.

Effects of astaxanthin on sensory-motor function in a compression model of spinal cord injury: Involvement of ERK and AKT signalling pathway.

Background: Spinal cord injury (SCI) causes continuous neurological deficits and major sensory-motor impairments. There is no effective treatment to enhance sensory-motor function following SCI. Thus, it is crucial to develop novel therapeutics for this particular patient population.

Astaxanthin attenuates neuroinflammation contributed to the neuropathic pain and motor dysfunction following compression spinal cord injury.

Spinal cord injury (SCI) is a debilitating condition in which inflammatory responses in the secondary phase of injury leads to long lasting sensory-motor dysfunction. The medicinal therapy of SCI complications is still a clinical challenge. Understanding the molecular pathways underlying the progress of damage will help to find new therapeutic candidates.

Astaxanthin: A mechanistic review on its biological activities and health benefits.

Astaxanthin (AST) is a potent lipid-soluble keto-carotenoid with auspicious effects on human health. It protects organisms against a wide range of diseases with excellent safety and tolerability. Various imperative biological activities in vitro and in vivo models have been suggested for AST.

How Nitric Oxide Increases in Diabetic Morphine Tolerated Male Rats.

Neuropathic pain is a complication of inflammation, infection or some diseases such as diabetes. Opioids are used as a salvage therapy for neuropathic pain but tolerance restricts their use. In our previous study, we have observed an increase of Nitric Oxide in diabetes and in morphine tolerance.

Neuroprotective effects of astaxanthin in a rat model of spinal cord injury.

Spinal cord injury (SCI) often leads to constant neurological deficits and long-term unalterable disability. Apoptosis plays an important role in the initiation of the secondary injury cascades leading to progressive tissue damage and severely functional deficits after SCI. Although the primary mechanical destructive events cannot be reversed, a therapeutic intervention could be carried out in order to moderate the secondary injury damage several hours to weeks after injury.

Effect of WR-1065 on 6-hydroxydopamine-induced catalepsy and IL-6 level in rats.

Objectives: Neuroinflammation and oxidative stress play a key role in pathogenesis of Parkinson's disease (PD). In the present study we investigated the effect of reactive oxygen species (ROS) scavenger WR-1065 on catalepsy and cerebrospinal fluid (CSF) level of interleukin 6(IL-6) and striatum superoxide dismutase (SOD) activity in 6-hydroxydopamine (6-OHDA) induced experimental model of PD.

Materials And Methods: Seventy two male Wistar rats were divided into 9 equal groups and 6-OHDA (8 μg/2 μl/rat) was infused unilaterally into substantia nigra pars copmacta (SNc) to induce PD.