Publications by authors named "Julia Borges Paes Lemes"

Platelet-rich plasma (PRP) is a biological blood-derived therapeutic obtained from whole blood that contains higher levels of platelets. PRP has been primarily used to mitigate joint degeneration and chronic pain in osteoarthritis (OA). This clinical applicability is based mechanistically on the release of several proteins by platelets that can restore joint homeostasis.

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Background: Pannexin1 (Panx1) is a membrane channel expressed in different cells of the nervous system and is involved in several pathological conditions, including pain and inflammation. At the central nervous system, the role of Panx1 is already well-established. However, in the periphery, there is a lack of information regarding the participation of Panx1 in neuronal sensitization.

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Activation of neuraxial nociceptive linkages leads to a high level of encoding of the message that is transmitted to the brain and that can initiate a pain state with its attendant emotive covariates. As we review here, the encoding of this message is subject to a profound regulation by pharmacological targeting of dorsal root ganglion and dorsal horn systems. Though first shown with the robust and selective modulation by spinal opiates, subsequent work has revealed the pharmacological and biological complexity of these neuraxial systems and points to several regulatory targets.

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Unsuccessful anesthesia often occurs under an inflammatory tissue environment, making dentistry treatment extremely painful and challenging. Articaine (ATC) is a local anesthetic used at high (4%) concentrations. Since nanopharmaceutical formulations may improve the pharmacokinetics and pharmacodynamics of drugs, we encapsulated ATC in nanostructured lipid carriers (NLCs) aiming to increase the anesthetic effect on the inflamed tissue.

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Nociceptive afferent signaling evoked by inflammation and nerve injury is mediated by the opening of ligand-gated and voltage-gated receptors or channels localized to cholesterol-rich lipid raft membrane domains. Dorsal root ganglion (DRG) nociceptors express high levels of toll-like receptor 4 (TLR4), which also localize to lipid rafts. Genetic deletion or pharmacologic blocking of TLR4 diminishes pain associated with chemotherapy-induced peripheral neuropathy (CIPN).

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Millions of people suffer from arthritis worldwide, consistently struggling with daily activities due to debilitating pain evoked by this disease. Perhaps the most intensively investigated type of inflammatory arthritis is rheumatoid arthritis (RA), where, despite considerable advances in research and clinical management, gaps regarding the neuroimmune interactions that guide inflammation and chronic pain in this disease remain to be clarified. The pain and inflammation associated with arthritis are not isolated to the joints, and inflammatory mechanisms induced by different immune and glial cells in other tissues may affect the development of chronic pain that results from the disease.

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Several recent studies have established the efficacy of photobiomodulation therapy (PBMT) in painful clinical conditions. Diabetic neuropathy (DN) can be related to activating mitogen-activated protein kinases (MAPK), such as p38, in the peripheral nerve. MAPK pathway is activated in response to extracellular stimuli, including interleukins TNF-α and IL-1β.

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Inflammation is a vital process for the injured tissue restoration and one of its hallmarks is inflammatory hyperalgesia. The cyclooxygenase (COX) pathway is strongly related to the inflammatory and painful process. Usually, the COX-1 isoform is described as homeostatic, while COX-2 is characterized as inducible in inflammatory conditions.

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Previous data indicate that the diabetogenic substance streptozotocin might act in nociceptive neurons changing the sensory signal, regardless of hyperglycemia. In the present article the effects of streptozotocin were compared with another diabetogenic drug, alloxan, for diabetes induction in rats. A possible direct effect of these drugs was tested by means of in vivo experiments and in vitro assays using cultured primary nociceptive neurons.

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Background And Purpose: While dipyrone is a widely used analgesic, its mechanism of action is not completely understood. Recently, we have reported that the dipyrone metabolite 4-aminoantipyrine (4-AA) reduces PGE -induced pain-related behaviour through cannabinoid CB receptors. Here, we ascertained, in naive and PGE -induced "inflamed" conditions, both in vivo and in vitro, the molecular mechanisms involved in the 4-AA-induced analgesic effects.

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Article Synopsis
  • Recent research is focusing on voltage-gated sodium (Nav) channels as potential targets for pain relief medications, specifically targeting Nav 1.8 for conditions like neuropathies and fibromyalgia.
  • The study explored the impact of chronic social defeat stress (SDS) on pain sensitivity in mice, revealing that SDS led to behaviors associated with depression and increased pain sensitivity to both mechanical and chemical stimuli.
  • By using an intrathecal injection of Nav 1.8 antisense, the study found that it successfully reduced the pain sensitivity associated with SDS, demonstrating the role of Nav 1.8 nociceptive fibers in this process.
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The aim of this study was to determine whether maternal diabetes induced by alloxan injection in the first gestational day of female Wistar rats interferes with the development of the nociceptive peripheral system of the offspring. Behavioral and histologic analysis was performed using the adult offspring of diabetic and control rats. It was found that the offspring of diabetic rats were more sensitive to thermal stimulation and showed an altered response to carrageenan-induced inflammatory hyperalgesia.

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Article Synopsis
  • Burn injuries cause significant inflammation and can severely impact survival and quality of life.
  • In a study on rats, levels of leptin and fractalkine increased significantly after burn injuries, correlating with tissue swelling and changes in gene expression.
  • The findings suggest that these cytokines contribute to pain and inflammation, indicating they could be potential targets for new treatments in burn care.
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Cumulating data suggests that ion channel alterations in nociceptive neurons might be involved in the development of diabetic painful neuropathy. In the present study we investigated the involvement of ATP-sensitive potassium (K) channels in the acute effect of high glucose solution in vitro and in vivo. High glucose concentrations depolarized cultured nociceptive neurons and depolarization was blocked by the K opener, diazoxide or by insulin.

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At dorsal root ganglia, neurons and satellite glial cells (SGC) can communicate through ATP release and P2X7 receptor activation. SGCs are also interconnected by gap junctions and have been previously implicated in modulating inflammatory and chronic pain.We now present evidence that SGCs are also involved in processing acute nociception in rat dorsal root ganglia.

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