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      Thiazolidine Derivatives Attenuate Carrageenan-Induced Inflammatory Pain in Mice

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          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.


          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.


          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.


          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.

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          Most cited references 65

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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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            Quantitative assessment of tactile allodynia in the rat paw

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              Current challenges in glia-pain biology.

              A remarkable series of findings over the last decade or so has demonstrated a previously unrecognized role for CNS glia in many aspects of neuronal functioning including pain processing. In addition to their recruitment to sites of CNS damage, these cells also appear to be capable of "action at a distance," playing functional roles in areas of CNS that are quite remote from the focus of injury or disease. The implication is that the nervous system is able to initiate signals that alter the function of these glial cells, and these cells in turn release factors that regulate neuronal function. This idea has taken root, resulting in an explosion of research interest, and here we look critically at what has been reported in order to assess where knowledge is missing or uncertain.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                04 February 2021
                : 15
                : 369-384
                [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
                © 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).

                Page count
                Figures: 6, Tables: 6, References: 65, Pages: 16
                Original Research


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