Mina Gholami, Zahra Ghelichkhani, Reza Aghakhani, Daniel J Klionsky, Ozra Motaghinejad, Majid Motaghinejad, Mohammad Kazem Koohi, Jalal Hassan
{"title":"米诺环素是一种神经保护剂，可防止曲马多诱发的神经退行性变：行为和分子证据。","authors":"Mina Gholami, Zahra Ghelichkhani, Reza Aghakhani, Daniel J Klionsky, Ozra Motaghinejad, Majid Motaghinejad, Mohammad Kazem Koohi, Jalal Hassan","doi":"10.4103/ijpvm.ijpvm_10_24","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Previous evidence indicates that tramadol (TRA) can lead to neurodegenerative events and minocycline (MIN) has neuroprotective properties.</p><p><strong>Aim of the study: </strong>The current research evaluated the neuroprotective effects of MIN for TRA-promoted neurodegeneration.</p><p><strong>Methods: </strong>Sixty adult male rats were placed into the following groups: 1 (received 0.7 ml/rat of normal saline, IP), 2 (received 50 mg/kg of TRA, i.p.), 3, 4, 5 (administered TRA as 50 mg/kg simultaneously with MIN at 20, 40, and 60 mg/kg, IP, respectively), and 6 (received MIN alone as 60 mg/kg, IP). The treatment procedure was 21 days. An open field test (OFT) was used to measure motor activity and anxiety-related behavior. Furthermore, oxidative stress; hippocampal inflammation; apoptotic parameters as well as activity of mitochondrial complexes I, II, III, and IV; ATP levels; and mitochondrial membrane potential (MMP) were evaluated. In addition, histomorphological alteration was assessed in two regions of the hippocampus: Cornu Ammonis (CA1) and dentate gyrus (DG).</p><p><strong>Results: </strong>MIN treatment could inhibit TRA-induced anxiety and motor activity disturbances (<i>P</i> < 0.05). In addition, MIN could attenuate reactive oxygen species (ROS), H<sub>2</sub>O<sub>2</sub>, oxidized glutathione (GSSG), and malondialdehyde (MDA) level (<i>P</i> < 0.05), while there was increased reduced glutathione (GSH), total antioxidant capacity (TAC), ATP, MMP, and BCL2 levels (<i>P</i> < 0.05) and also elevation of SOD, GPX, GSR (<i>P</i> < 0.05), and mitochondrial complexes I, II, III, and IV activity (<i>P</i> < 0.05) in TRA-treated rats. In consistence with these findings, MIN could reduce TNF/TNF-α, IL1B/IL1-β, BAX, and CASP3 levels (<i>P</i> < 0.05) in TRA-treated rats. MIN also restored the quantitative (<i>P</i> < 0.05) and qualitative histomorphological sequels of TRA in both CA1 and DG areas of the hippocampus.</p><p><strong>Conclusions: </strong>MIN probably has repositioning capability for inhibition of TRA-induced neurodegeneration via modulation of inflammation, oxidative stress, apoptosis, and mitochondrial disorders.</p>","PeriodicalId":14342,"journal":{"name":"International Journal of Preventive Medicine","volume":"15 ","pages":"47"},"PeriodicalIF":1.7000,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11559692/pdf/","citationCount":"0","resultStr":"{\"title\":\"Minocycline Acts as a Neuroprotective Agent Against Tramadol-Induced Neurodegeneration: Behavioral and Molecular Evidence.\",\"authors\":\"Mina Gholami, Zahra Ghelichkhani, Reza Aghakhani, Daniel J Klionsky, Ozra Motaghinejad, Majid Motaghinejad, Mohammad Kazem Koohi, Jalal Hassan\",\"doi\":\"10.4103/ijpvm.ijpvm_10_24\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Previous evidence indicates that tramadol (TRA) can lead to neurodegenerative events and minocycline (MIN) has neuroprotective properties.</p><p><strong>Aim of the study: </strong>The current research evaluated the neuroprotective effects of MIN for TRA-promoted neurodegeneration.</p><p><strong>Methods: </strong>Sixty adult male rats were placed into the following groups: 1 (received 0.7 ml/rat of normal saline, IP), 2 (received 50 mg/kg of TRA, i.p.), 3, 4, 5 (administered TRA as 50 mg/kg simultaneously with MIN at 20, 40, and 60 mg/kg, IP, respectively), and 6 (received MIN alone as 60 mg/kg, IP). The treatment procedure was 21 days. An open field test (OFT) was used to measure motor activity and anxiety-related behavior. Furthermore, oxidative stress; hippocampal inflammation; apoptotic parameters as well as activity of mitochondrial complexes I, II, III, and IV; ATP levels; and mitochondrial membrane potential (MMP) were evaluated. In addition, histomorphological alteration was assessed in two regions of the hippocampus: Cornu Ammonis (CA1) and dentate gyrus (DG).</p><p><strong>Results: </strong>MIN treatment could inhibit TRA-induced anxiety and motor activity disturbances (<i>P</i> < 0.05). In addition, MIN could attenuate reactive oxygen species (ROS), H<sub>2</sub>O<sub>2</sub>, oxidized glutathione (GSSG), and malondialdehyde (MDA) level (<i>P</i> < 0.05), while there was increased reduced glutathione (GSH), total antioxidant capacity (TAC), ATP, MMP, and BCL2 levels (<i>P</i> < 0.05) and also elevation of SOD, GPX, GSR (<i>P</i> < 0.05), and mitochondrial complexes I, II, III, and IV activity (<i>P</i> < 0.05) in TRA-treated rats. In consistence with these findings, MIN could reduce TNF/TNF-α, IL1B/IL1-β, BAX, and CASP3 levels (<i>P</i> < 0.05) in TRA-treated rats. 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Minocycline Acts as a Neuroprotective Agent Against Tramadol-Induced Neurodegeneration: Behavioral and Molecular Evidence.
Background: Previous evidence indicates that tramadol (TRA) can lead to neurodegenerative events and minocycline (MIN) has neuroprotective properties.
Aim of the study: The current research evaluated the neuroprotective effects of MIN for TRA-promoted neurodegeneration.
Methods: Sixty adult male rats were placed into the following groups: 1 (received 0.7 ml/rat of normal saline, IP), 2 (received 50 mg/kg of TRA, i.p.), 3, 4, 5 (administered TRA as 50 mg/kg simultaneously with MIN at 20, 40, and 60 mg/kg, IP, respectively), and 6 (received MIN alone as 60 mg/kg, IP). The treatment procedure was 21 days. An open field test (OFT) was used to measure motor activity and anxiety-related behavior. Furthermore, oxidative stress; hippocampal inflammation; apoptotic parameters as well as activity of mitochondrial complexes I, II, III, and IV; ATP levels; and mitochondrial membrane potential (MMP) were evaluated. In addition, histomorphological alteration was assessed in two regions of the hippocampus: Cornu Ammonis (CA1) and dentate gyrus (DG).
Results: MIN treatment could inhibit TRA-induced anxiety and motor activity disturbances (P < 0.05). In addition, MIN could attenuate reactive oxygen species (ROS), H2O2, oxidized glutathione (GSSG), and malondialdehyde (MDA) level (P < 0.05), while there was increased reduced glutathione (GSH), total antioxidant capacity (TAC), ATP, MMP, and BCL2 levels (P < 0.05) and also elevation of SOD, GPX, GSR (P < 0.05), and mitochondrial complexes I, II, III, and IV activity (P < 0.05) in TRA-treated rats. In consistence with these findings, MIN could reduce TNF/TNF-α, IL1B/IL1-β, BAX, and CASP3 levels (P < 0.05) in TRA-treated rats. MIN also restored the quantitative (P < 0.05) and qualitative histomorphological sequels of TRA in both CA1 and DG areas of the hippocampus.
Conclusions: MIN probably has repositioning capability for inhibition of TRA-induced neurodegeneration via modulation of inflammation, oxidative stress, apoptosis, and mitochondrial disorders.
期刊介绍：
International Journal of Preventive Medicine, a publication of Isfahan University of Medical Sciences, is a peer-reviewed online journal with Continuous print on demand compilation of issues published. The journal’s full text is available online at http://www.ijpvmjournal.net. The journal allows free access (Open Access) to its contents and permits authors to self-archive final accepted version of the articles on any OAI-compliant institutional / subject-based repository. The journal will cover technical and clinical studies related to health, ethical and social issues in field of Preventive Medicine. Articles with clinical interest and implications will be given preference.
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