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Neurodegenerative disorders, which are defined by the breakdown of neurons over time, are affecting an increasing number of people. Stroke, Alzheimer's, Parkinson's, Multiple Sclerosis, Migraine, and Amyotrophic Lateral Sclerosis are just a few examples of brain disorders that have no cure. Besides, there is a huge demand for drugs that can cure the diseases mentioned above because the majority of the medications we use to treat them only alleviate diseases. Different neurological disorders have responded satisfactorily to the pharmacological effects of medicinal plants. Despite the numerous multiple types of plants in the world, only a small number of them have been investigated for neurological disorders. As a result, there are many opportunities in this area for further research on plants and their bioactive chemicals. The search for natural therapeutic alternatives that promote faster healing and adverse effects avoidance has gained popularity in recent years. The aim of this mini-review is to explore some natural products that have strong therapeutic effects on neurodegenerative disorders such as Stroke, Alzheimer's Disease, Parkinson's Disease, Multiple Sclerosis, Migraine, Amyotrophic Lateral Sclerosis, and others. We have also shown the safety of natural products to improve their appropriate usage in neurological disorders from recent literature.
Learn More >MiR-204-5p Alleviates Neuropathic Pain by Targeting BRD4 in a Rat Chronic Constrictive Injury Model.
The pathogenesis of neuropathic pain is complex, and previous studies have found that microRNAs are important regulators of neuropathic pain and are associated with the progression of neuropathic pain. This study aims to explore the level and role of miR-204-5p in the chronic constrictive injury (CCI) model of rats.
Learn More >Chronic pain interferes with daily functioning and is frequently accompanied by depression. Currently, traditional clinic treatments do not produce satisfactory analgesic effects and frequently result in various adverse effects. Pathogen recognition receptors (PRRs) serve as innate cellular sensors of danger signals, sense invading microorganisms, and initiate innate and adaptive immune responses. Among them, cGAS-STING alerts on the presence of both exogenous and endogenous DNA in the cytoplasm, and this pathway has been closely linked to multiple diseases, including auto-inflammation, virus infection, and cancer. An increasing numbers of evidence suggest that cGAS-STING pathway involves in the chronic pain process; however, its role remains controversial. In this narrative review, we summarize the recent findings on the involvement of the cGAS-STING pathway in chronic pain, as well as several possible mechanisms underlying its activation. As a new area of research, this review is unique in considering the cGAS-STING pathway in sensory neurons and glial cells as a part of a broader understanding of pain, including potential mechanisms of inflammation, immunity, apoptosis, and autophagy. It will provide new insight into the treatment of pain in the future.
Learn More >Peripheral nerve injury (PNI) induces neuronal hyperexcitability, which underlies neuropathic pain. The emergence of RNA sequencing technologies has enabled profiling of transcriptional changes in pathological conditions. However, these approaches do not provide information regarding metabolites such as lipids that are not directly encoded by genes. Fatty acids (FAs) are some of the essential lipids in mammalian organisms and are mainly stored as membrane phospholipids. In response to various biological stimuli, FAs are rapidly released and converted into several mediators, such as eicosanoids and docosanoids. FAs themselves or their metabolites play important roles in physiology and pathology. In this study, using a comprehensive lipidomic analysis of FA metabolites, 152 species were measured in the dorsal root ganglia of mice at multiple time points after PNI. We found that PNI increased the ω-6 FA metabolites produced by cyclooxygenases but not those produced by lipoxygenases or cytochrome P450 enzymes in the dorsal root ganglia. In contrast, ω-3 FA metabolites biosynthesized by any enzyme transiently increased after nerve injury. Overall, these findings provide a new resource and valuable insights into PNI pathologies, including pain and nerve regeneration.
Learn More >Acetaminophen is an important component of a multimodal analgesia strategy to reduce opioid consumption and pain intensity after an orthopedic surgery. The opioid-sparing efficacy of intravenous acetaminophen has been established at a daily dose of 4 g. However, it is still unclear for the daily dose of 2 g of acetaminophen, which is recommended by the China Food and Drug Administration Center for Drug Evaluation, in terms of its efficacy and safety. This study aimed to evaluate the efficacy and safety of intravenous acetaminophen at a daily dose of 2 g for reducing opioid consumption and pain intensity after orthopedic surgery. In this multicenter, randomized, double-blind, placebo-controlled phase III trial, 235 patients who underwent orthopedic surgery were randomly assigned to receive intravenous acetaminophen 500 mg every 6 h or placebo. Postoperative morphine consumption, pain intensity at rest and during movement, and adverse events were analysed. For the mean (standard deviation) morphine consumption within 24 h after surgery, intravenous acetaminophen was superior to placebo both in the modified intention-to-treat analysis [8.7 (7.7) mg vs. 11.2 (9.2) mg] in the acetaminophen group and the placebo group, respectively. Difference in means: 2.5 mg; 95% confidence interval, 0.25 to 4.61; = 0.030), and in the per-protocol analysis (8.3 (7.0) mg and 11.7 (9.9) mg in the acetaminophen group and the placebo group, respectively. Difference in means: 3.4 mg; 95% confidence interval: 1.05 to 5.77; = 0.005). The two groups did not differ significantly in terms of pain intensity and adverse events. Our results suggest that intravenous acetaminophen at a daily dose of 2 g can reduce morphine consumption by Chinese adults within the first 24 h after orthopedic surgery, but the extent of reduction is not clinically relevant. : [ClinicalTrials.gov], identifier [NCT02811991].
Learn More >The purposes of this study are to explore (1) whether comorbid depressive symptoms in patients with chronic back pain (CBP) affect the pain matrix. And (2) whether the interaction of depression and CBP exacerbates impaired brain function.
Learn More >Diabetes mellitus (DM) is one of the leading causes of morbidity and mortality worldwide. DM patients with diabetic neuropathy (DN) usually present with distal pain, sensorimotor polyneuropathy, postural hypotension, or erectile dysfunction. They also may present with other nerve pathologies such as inflammatory neuropathies and carpal tunnel syndrome. We conducted a systematic review and meta-analysis to assess the benefits of using sodium-glucose co-transporter-2 inhibitors (SGLT2Is) to manage DN. An extensive systematic literature review was conducted to include all articles published up to 24 February 2022. All clinical studies included patients with DM and reported the outcomes of SGLT2I on diabetes-associated neuropathy. Six studies were identified for meta-analysis, including a total of 5312 diabetic patients. The average age of the included patients ranged from 41 to 74 years and 34-73 years in the SGLT2I treatment and control groups, respectively. SGLT2I moderately improved the manifestations of diabetic peripheral neuropathy events and nerve conduction velocity. Furthermore, the SGLT2I treatment group had a statistically significant higher mean heart-to-mediastinum ratio (MD 0.41; 95% 0.17, 0.64; = 0.0006). However, the mean heart rates (MD -4.51; 95% -10.05, 1.04; = 0.11) and wash out rates (MD 2.13; 95% -8.48, 12.75; = 0.69) were not significantly different between the two groups. SGLT2Is could therefore be considered neuroprotective in patients with DN, possibly by considerably increasing the sensory and motor nerve conduction velocity, improving the clinical manifestations of DPN, and reducing sympathetic nervous system activity. http://www.crd.york.ac.uk/prospero/, identifier CRD42022312828.
Learn More >Chronic pain is a long-standing unpleasant sensory and emotional feeling that has a tremendous impact on the physiological functions of the body, manifesting itself as a dysfunction of the nervous system, which can occur with peripheral and central sensitization. Many recent studies have shown that a variety of common immune cells in the immune system are involved in chronic pain by acting on the peripheral or central nervous system, especially in the autoimmune diseases. This article reviews the mechanisms of regulation of the sensory nervous system by neutrophils, macrophages, mast cells, B cells, T cells, and central glial cells. In addition, we discuss in more detail the influence of each immune cell on the initiation, maintenance, and resolution of chronic pain. Neutrophils, macrophages, and mast cells as intrinsic immune cells can induce the transition from acute to chronic pain and its maintenance; B cells and T cells as adaptive immune cells are mainly involved in the initiation of chronic pain, and T cells also contribute to the resolution of it; the role of glial cells in the nervous system can be extended to the beginning and end of chronic pain. This article aims to promote the understanding of the neuroimmune mechanisms of chronic pain, and to provide new therapeutic ideas and strategies for the control of chronic pain at the immune cellular level.
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