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      Thiazolidine Derivatives Attenuate Carrageenan-Induced Inflammatory Pain in Mice

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          Abstract

          Background

          Peripheral inflammation leads to the development of persistent thermal hyperalgesia and mechanical allodynia associated with increased expression of interleukin-1β (IL-1β) in the spinal cord. The aim of the present study was to investigate the effects of thiazolidine derivatives, 1b ([2-(2-hydroxyphenyl)-1,3-thiazolidin-4-yl](morpholin-4-yl)methanone) and 1d (2-hydroxy-4-{[2-(2-hydroxyphenyl)-1,3-thiazolidine-4-carbonyl]amino}benzoic acid), on thermal hyperalgesia, mechanical allodynia and on IL-1β expression during carrageenan-induced inflammation in the spinal cord in mice. Inflammatory pain was induced by injecting 1% carrageenan into the right hind paw of the mice.

          Methods

          The animals were administered thiazolidine derivatives, 1b and 1d (1 mg/kg, 3 mg/kg, or 10 mg/kg), intraperitoneally 30 minutes before carrageenan administration. The animals’ behavior was evaluated by measuring thermal hyperalgesia, mechanical allodynia, and motor coordination. The IL-1β expression was measured by enzyme-linked immunosorbent assay. Acute and sub-acute toxicity studies were conducted to evaluate the toxicity profile of compounds.

          Results

          Treatment with the thiazolidine derivative, 1b and 1d, attenuated carrageenan-induced thermal hyperalgesia and mechanical allodynia at doses of 1 mg/kg, 3 mg/kg, and 10 mg/kg. No motor coordination deficits were observed in animals. The compounds also reduced IL-1β expression in the spinal cord of mice. Acute and sub-acute toxicity studies revealed that both compounds were safe.

          Conclusion

          The compounds exhibit promising activity against inflammatory pain due to their ability to produce anti-hyperalgesic and anti-allodynic effects and to inhibit IL-1β expression in the spinal cord.

          Most cited references65

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          Quantitative assessment of tactile allodynia in the rat paw

          We applied and validated a quantitative allodynia assessment technique, using a recently developed rat surgical neuropathy model wherein nocifensive behaviors are evoked by light touch to the paw. Employing von Frey hairs from 0.41 to 15.1 g, we first characterized the percent response at each stimulus intensity. A smooth log-linear relationship was observed, with a median 50% threshold at 1.97 g (95% confidence limits, 1.12-3.57 g). Subsequently, we applied a paradigm using stimulus oscillation around the response threshold, which allowed more rapid, efficient measurements. Median 50% threshold by this up-down method was 2.4 g (1.81-2.76). Correlation coefficient between the two methods was 0.91. In neuropathic rats, good intra- and inter-observer reproducibility was found for the up-down paradigm; some variability was seen in normal rats, attributable to extensive testing. Thresholds in a sizable group of neuropathic rats showed insignificant variability over 20 days. After 50 days, 61% still met strict neuropathy criteria, using survival analysis. Threshold measurement using the up-down paradigm, in combination with the neuropathic pain model, represents a powerful tool for analyzing the effects of manipulations of the neuropathic pain state.
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            Persistent postsurgical pain: risk factors and prevention.

            Acute postoperative pain is followed by persistent pain in 10-50% of individuals after common operations, such as groin hernia repair, breast and thoracic surgery, leg amputation, and coronary artery bypass surgery. Since chronic pain can be severe in about 2-10% of these patients, persistent postsurgical pain represents a major, largely unrecognised clinical problem. Iatrogenic neuropathic pain is probably the most important cause of long-term postsurgical pain. Consequently, surgical techniques that avoid nerve damage should be applied whenever possible. Also, the effect of aggressive, early therapy for postoperative pain should be investigated, since the intensity of acute postoperative pain correlates with the risk of developing a persistent pain state. Finally, the role of genetic factors should be studied, since only a proportion of patients with intraoperative nerve damage develop chronic pain. Based on information about the molecular mechanisms that affect changes to the peripheral and central nervous system in neuropathic pain, several opportunities exist for multimodal pharmacological intervention. Here, we outline strategies for identification of patients at risk and for prevention and possible treatment of this important entity of chronic pain.
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              The PPARalpha-leukotriene B4 pathway to inflammation control.

              Inflammation is a local immune response to 'foreign' molecules, infection and injury. Leukotriene B4, a potent chemotactic agent that initiates, coordinates, sustains and amplifies the inflammatory response, is shown to be an activating ligand for the transcription factor PPARalpha. Because PPARalpha regulates the oxidative degradation of fatty acids and their derivatives, like this lipid mediator, a feedback mechanism is proposed that controls the duration of an inflammatory response and the clearance of leukotriene B4 in the liver. Thus PPARalpha offers a new route to the development of anti- or pro-inflammatory reagents.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                dddt
                dddt
                Drug Design, Development and Therapy
                Dove
                1177-8881
                04 February 2021
                2021
                : 15
                : 369-384
                Affiliations
                [1 ]Riphah Institute of Pharmaceutical Sciences, Riphah International University , Islamabad, Pakistan
                [2 ]Faculty of Pharmacy, Capital University of Science and Technology , Islamabad, Pakistan
                [3 ]College of Natural and Health Sciences, Zayed University , Abu Dhabi, United Arab Emirates
                [4 ]Laboratory Medicine Department, Faculty of Applied Medical Sciences, Umm Al-Qura University , Mecca, Saudi Arabia
                [5 ]Department of Pharmacy, Sarhad University of Science and Information Technology , Peshawar, KPK, Pakistan
                [6 ]State Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Peking University , Shenzhen, People’s Republic of China
                Author notes
                Correspondence: Muzaffar Abbas Faculty of Pharmacy, Capital University of Science and Technology , Islamabad Expressway, Kahuta Road, Zone-V, Islamabad, PakistanTel +92-51-111555666Fax +92-51-4486705 Email Muzaffar.abbas@cust.edu.pk
                Shupeng Li State Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School , Shenzhen, 518055, People's Republic of ChinaEmail lisp@pku.edu.cn
                Author information
                http://orcid.org/0000-0003-0882-5480
                http://orcid.org/0000-0003-1915-3480
                http://orcid.org/0000-0002-8338-7655
                http://orcid.org/0000-0002-5415-2179
                http://orcid.org/0000-0003-4532-9128
                http://orcid.org/0000-0002-9768-4255
                Article
                281559
                10.2147/DDDT.S281559
                7871178
                33574656
                71947231-8f2e-4e5d-b130-7de33b0eac96
                © 2021 Malik et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 14 October 2020
                : 18 December 2020
                Page count
                Figures: 6, Tables: 6, References: 65, Pages: 16
                Categories
                Original Research

                Pharmacology & Pharmaceutical medicine
                inflammatory pain,il-1β,thiazolidine derivatives,mechanical allodynia,thermal hyperalgesia

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