Transmission pathways and mediators as the basis for clinical pharmacology of pain

Kirkpatrick, Daniel R.; McEntire, Dan; Smith, Tyler A.; Dueck, Nicholas P; Kerfeld, Mitchell J.; Hambsch, Zakary J.; Nelson, Taylor J.; Reisbig, Mark D.; Agrawal, Devendra K.

doi:10.1080/17512433.2016.1204231

Cited by 14 publications

(11 citation statements)

References 187 publications

(366 reference statements)

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“…The potential effect of curcumin supplementation in reducing muscle pain could be due to the effect it has on suppressing the induction of expression of the isoform COX-2 [25], thus avoiding the production of mediating substances, such as prostaglandin E2 (PGE2), histamine, bradykinin, and serotonin derived from COX-2 that activate nerve endings [19]. The action of curcumin decreasing these mediators, especially PGE2, would provide the attenuation of the phenomenon of long-lasting hyperalgesia that occurs in afferent sensory fibers of type C [42].…”

Section: Effect On Muscle Painmentioning

confidence: 99%

Modulation of Exercise-Induced Muscle Damage, Inflammation, and Oxidative Markers by Curcumin Supplementation in a Physically Active Population: A Systematic Review

et al. 2020

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Physical activity, particularly high-intensity eccentric muscle contractions, produces exercise-induced muscle damage (EIMD). The breakdown of muscle fibers and the consequent inflammatory responses derived from EIMD affect exercise performance. Curcumin, a natural polyphenol extracted from turmeric, has been shown to have mainly antioxidant and also anti-inflammatory properties. This effect of curcumin could improve EIMD and exercise performance. The main objective of this systematic review was to critically evaluate the effectiveness of curcumin supplementation on EIMD and inflammatory and oxidative markers in a physically active population. A structured search was carried out following Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines in the databases SCOPUS, Web of Science (WOS), and Medline (PubMed) from inception to October 2019. The search included original articles with randomized controlled crossover or parallel design in which the intake of curcumin administered before and/or after exercise was compared with an identical placebo situation. No filters were applied to the type of physical exercise performed, the sex or the age of the participants. Of the 301 articles identified in the search, 11 met the established criteria and were included in this systematic review. The methodological quality of the studies was assessed using the McMaster Critical Review Form. The use of curcumin reduces the subjective perception of the intensity of muscle pain; reduces muscle damage through the decrease of creatine kinase (CK); increases muscle performance; has an anti-inflammatory effect by modulating the pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-8; and may have a slight antioxidant effect. In summary, the administration of curcumin at a dose between 150–1500 mg/day before and during exercise, and up until 72 h’ post-exercise, improved performance by reducing EIMD and modulating the inflammation caused by physical activity. In addition, humans appear to be able to tolerate high doses of curcumin without significant side-effects.

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Section: Effect On Muscle Painmentioning

confidence: 99%

Modulation of Exercise-Induced Muscle Damage, Inflammation, and Oxidative Markers by Curcumin Supplementation in a Physically Active Population: A Systematic Review

et al. 2020

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“…На сьогодні велике значення в механізмах сенситизації ноцицептивних нейронів задніх рогів спинного мозку мають збуджуючі амінокислоти і нейропептиди. За допомогою імуногістохімічних методів дослідження було встановлено, що синаптичні терміналі багатьох тонких високопорогових аферентних волокон містять як нейромедіатор глутамат, аспартат і низку нейропептидів, таких як субстанція Р, ней рокінін А, кальцитонін-генродинний пептид та багато інших, що вивільняються з пресинаптичних терміналей під дією ноцицептивних імпульсів [17]. Звільнення глутамату із пресинаптичних терміналей відбувається за будь-якої ноцицептивної дії.…”

Section: науковий оглядunclassified

“…Крім сенситизації ноцицептивних нейронів заднього рогу спинного мозку пошкодження тканин викликає також підвищення збудливості і реактивності ноцицептивних нейронів вищерозташованих центрів, включаючи ядра таламуса і соматосенсорну кору великих півкуль головного мозку [17].…”

Section: рисунок 2 механізми опіоїдіндукованої антиноцицепції примітunclassified

Малоопиоидная Общая Анестезия: Компоненты И Механизмы Формирования

Лоскутов¹,

Bondar²,

Ovsienko³

2021

ЕМ

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Мультимодальна малоопіоїдна анестезія: компоненти й механізми формування Резюме. В роботі висвітлені сучасні уявлення про компоненти мультимодальної малоопіоїдної загальної анестезії та їх механізми дії з урахуванням більпровідних трактів організму та механізмів формування антиноцицептивної дії препаратів, що використовуються для проведення анестезії. Подано досліджувану нами методику мультимодальної малоопіоїдної загальної анестезії при проведенні лапароскопічних оперативних втручань на нирках і препарати, що найбезпечніше використовувати у хворих з патологією нирок, щоб уникнути погіршення їх функцій.

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“…that these guidelines will stifle the optimum treatment of chronic pain. The one area in which pain experts agree is that pain needs to be controlled and the best option is the development of new non-opioid medications based on scientific knowledge of chronic pain etiology, including persistence, initiation, conduction, transduction and perception [ 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

Controlling the “Opioid Epidemic”: A Novel Chemical Entity (NCE) to Reduce or Supplant Opiate Use for Chronic Pain

Tabakoff

Hoffman

2020

J Psychiatry Brain Sci

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We report on the ongoing project "A Novel Therapeutic to Ameliorate Chronic Pain and Reduce Opiate Use." Over 100 million adults in the U.S. suffer from intermittent or constant chronic pain, and chronic pain affects at least 10% of the world's population. The primary pharmaceuticals for treatment of chronic pain have been natural or synthetic opioids and the use of opioids for pain treatment has resulted in what has been called an "epidemic" of opioid abuse, addiction and lethal overdoses. We have, through a process of rational drug design, generated a novel chemical entity (NCE) and have given it the name Kindolor. Kindolor is a non-opiate, non-addicting molecule that was developed specifically to simultaneously control the aberrant activity of three targets on the peripheral sensory system that are integral in the development and propagation of chronic pain. In our initial preclinical studies, we demonstrated the efficacy of Kindolor to reduce or eliminate chronic pain in five animal models. The overall goal of the project is to complete the investigational new drug (IND)-enabling preclinical studies of Kindolor, and once IND approval is gained, we will proceed to the clinical Phase Ia and 1b safety studies and a Phase 2a efficacy study. The work is in its second year, and the present report describes progress toward our overall goal of bringing our compound to a full Phase 2 ready stage.

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Transmission pathways and mediators as the basis for clinical pharmacology of pain

Cited by 14 publications

References 187 publications

Modulation of Exercise-Induced Muscle Damage, Inflammation, and Oxidative Markers by Curcumin Supplementation in a Physically Active Population: A Systematic Review

Modulation of Exercise-Induced Muscle Damage, Inflammation, and Oxidative Markers by Curcumin Supplementation in a Physically Active Population: A Systematic Review

Малоопиоидная Общая Анестезия: Компоненты И Механизмы Формирования

Controlling the “Opioid Epidemic”: A Novel Chemical Entity (NCE) to Reduce or Supplant Opiate Use for Chronic Pain

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