Anti-allodynic effect induced by curcumin in neuropathic rat is mediated through the NO-cyclic-GMP-ATP sensitive K+ channels pathway

Maier

2021

IJMS

Lesion or disease of the somatosensory system leads to the development of neuropathic pain. Peripheral neuropathic pain encompasses damage or injury of the peripheral nervous system. On the other hand, 10–15% of individuals suffer from acute postoperative pain followed by persistent pain after undergoing surgeries. Antidepressants, anticonvulsants, baclofen, and clonidine are used to treat peripheral neuropathy, whereas opioids are used to treat postoperative pain. The negative effects associated with these drugs emphasize the search for alternative therapeutics with better efficacy and fewer side effects. Curcumin, a polyphenol isolated from the roots of Curcuma longa, possesses antibacterial, antioxidant, and anti-inflammatory properties. Furthermore, the low bioavailability and fast metabolism of curcumin have led to the advent of various curcumin formulations. The present review provides a comprehensive analysis on the effects of curcumin and its formulations in preclinical and clinical studies of neuropathic and postoperative pain. Based on the positive outcomes from both preclinical and clinical studies, curcumin holds the promise of mitigating or preventing neuropathic and postoperative pain conditions. However, more clinical studies with improved curcumin formulations are required to involve its use as adjuvant to neuropathic and postoperative drugs.

Section: Curcumin and Neuropathic Pain—preclinical Studiesmentioning

confidence: 99%

Effects of Curcumin and Its Different Formulations in Preclinical and Clinical Studies of Peripheral Neuropathic and Postoperative Pain: A Comprehensive Review

Maier

2021

IJMS

“…In these models, animals develop chronic inflammatory pain. Thus, in particular by its anti-inflammatory action, curcumin reduced mechanical and thermal hypersensitivity in the CCI model in SD rats [ 53 , 54 , 55 ], in Wistar rats [ 56 ], in male C57BL/6J mice [ 57 ], and in nerve ligature model in female Wistar rats [ 58 ] and in BALB/c mice [ 59 ]. Finally, curcumin also showed antinociceptive properties in SD rats in models of brachial plexus avulsion [ 60 ], alcohol-induced neuropathy in male and female Wistar rats [ 61 , 62 ], opioid-induced hyperalgesia in C57-BL/6J mice [ 63 ], HIV-gp120-induced neuropathic pain in male SD rats [ 64 ], and complete Freund’s adjuvant-induced inflammatory pain in Charles-Foster strain rats [ 65 ].…”

Section: Curcumin Studies In Animal Models Of Pnmentioning

confidence: 99%

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

et al. 2020

Peripheral neuropathies (PN) can be triggered after metabolic diseases, traumatic peripheral nerve injury, genetic mutations, toxic substances, and/or inflammation. PN is a major clinical problem, affecting many patients and with few effective therapeutics. Recently, interest in natural dietary compounds, such as polyphenols, in human health has led to a great deal of research, especially in PN. Curcumin is a polyphenol extracted from the root of Curcuma longa. This molecule has long been used in Asian medicine for its anti-inflammatory, antibacterial, and antioxidant properties. However, like numerous polyphenols, curcumin has a very low bioavailability and a very fast metabolism. This review addresses multiple aspects of curcumin in PN, including bioavailability issues, new formulations, observations in animal behavioral tests, electrophysiological, histological, and molecular aspects, and clinical trials published to date. The, review covers in vitro and in vivo studies, with a special focus on the molecular mechanisms of curcumin (anti-inflammatory, antioxidant, anti-endoplasmic reticulum stress (anti-ER-stress), neuroprotection, and glial protection). This review provides for the first time an overview of curcumin in the treatment of PN. Finally, because PN are associated with numerous pathologies (e.g., cancers, diabetes, addiction, inflammatory disease...), this review is likely to interest a large audience.

“…Several studies have evaluated the potential analgesic effects of glibenclamide and other SUR agonists/antagonists in conjunction with other analgesics vis-à-vis K ATP channels in neuropathic pain [ 193 , 194 , 195 , 196 , 197 , 198 , 199 , 200 ]. In these studies, single doses of glibenclamide did not influence pain thresholds but they did blunt the anesthetic effects of the analgesic being tested.…”

Section: Sur1-trpm4 Expression and Inhibition In Other Neurological Conditionsmentioning

confidence: 99%

Sulfonylurea Receptor 1 in Central Nervous System Injury: An Updated Review

Jha

Rani

Desai

et al. 2021

IJMS

Sulfonylurea receptor 1 (SUR1) is a member of the adenosine triphosphate (ATP)-binding cassette (ABC) protein superfamily, encoded by Abcc8, and is recognized as a key mediator of central nervous system (CNS) cellular swelling via the transient receptor potential melastatin 4 (TRPM4) channel. Discovered approximately 20 years ago, this channel is normally absent in the CNS but is transcriptionally upregulated after CNS injury. A comprehensive review on the pathophysiology and role of SUR1 in the CNS was published in 2012. Since then, the breadth and depth of understanding of the involvement of this channel in secondary injury has undergone exponential growth: SUR1-TRPM4 inhibition has been shown to decrease cerebral edema and hemorrhage progression in multiple preclinical models as well as in early clinical studies across a range of CNS diseases including ischemic stroke, traumatic brain injury, cardiac arrest, subarachnoid hemorrhage, spinal cord injury, intracerebral hemorrhage, multiple sclerosis, encephalitis, neuromalignancies, pain, liver failure, status epilepticus, retinopathies and HIV-associated neurocognitive disorder. Given these substantial developments, combined with the timeliness of ongoing clinical trials of SUR1 inhibition, now, another decade later, we review advances pertaining to SUR1-TRPM4 pathobiology in this spectrum of CNS disease—providing an overview of the journey from patch-clamp experiments to phase III trials.