Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway.
Neuropathic pain has been characterized as chronic pain resulting from pathological damage to the sensorimotor system. Because of its complex nature, it remains refractory to most of the therapeutic interventions, and surgical intervention and physiotherapy alongside steroidal treatments remain the...
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Public Library of Science (PLoS)
2023-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0287517&type=printable |
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| author | Ismail Badshah Neelum Gul Qazi Fawad Ali Amber Mahmood Minhas Arooj Mohsin Alvi Mahmoud Kandeel Muhammad Imran Syed Shams Ul Hassan Simona Bungau |
| author_facet | Ismail Badshah Neelum Gul Qazi Fawad Ali Amber Mahmood Minhas Arooj Mohsin Alvi Mahmoud Kandeel Muhammad Imran Syed Shams Ul Hassan Simona Bungau |
| author_sort | Ismail Badshah |
| collection | DOAJ |
| description | Neuropathic pain has been characterized as chronic pain resulting from pathological damage to the sensorimotor system. Because of its complex nature, it remains refractory to most of the therapeutic interventions, and surgical intervention and physiotherapy alongside steroidal treatments remain the only treatment protocols with limited success, hence solidifying the need to find efficacious therapeutic alternatives. Emodin was used as a post-treatment for its potential to be neuroprotective in the treatment of chronic constriction injury-induced NP. The first day following surgery, Emodin treatment began, and it lasted until the 21st day. On days 3, 7, 14 and 21, all behavioral investigations were conducted. The sciatic nerve and spinal cord were extracted for further molecular examination. Emodin elevated response latency, was able to delay the onset of mechanical hyperalgesia in rats on days 7, 14, and 21 and reduced the CCI-induced paw deformation. Emodin treatment significantly reduced lipid peroxidation and NO levels while restoring the GST, GSH and catalase. It significantly improved the disorientation of the sciatic nerve and spinal cord confirmed by H & E staining and reduced inflammatory markers as observed by the quantification of COX-2, TNF-α, p-NFκb and up-regulated PPAR-γ levels by ELISA and PCR. According to the findings, Emodin has antinociceptive and anti-hyperalgesic properties, which reduced pain perception and inflammation. We also suggested the involvement of PPAR-γ pathway in the therapeutic potential of emodin in chronic nerve injury. |
| format | Article |
| id | doaj-art-e1166be0b9f848588624b9d9c1e1e2a7 |
| institution | Kabale University |
| issn | 1932-6203 |
| language | English |
| publishDate | 2023-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-e1166be0b9f848588624b9d9c1e1e2a72025-08-20T03:51:09ZengPublic Library of Science (PLoS)PLoS ONE1932-62032023-01-01187e028751710.1371/journal.pone.0287517Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway.Ismail BadshahNeelum Gul QaziFawad AliAmber Mahmood MinhasArooj Mohsin AlviMahmoud KandeelMuhammad ImranSyed Shams Ul HassanSimona BungauNeuropathic pain has been characterized as chronic pain resulting from pathological damage to the sensorimotor system. Because of its complex nature, it remains refractory to most of the therapeutic interventions, and surgical intervention and physiotherapy alongside steroidal treatments remain the only treatment protocols with limited success, hence solidifying the need to find efficacious therapeutic alternatives. Emodin was used as a post-treatment for its potential to be neuroprotective in the treatment of chronic constriction injury-induced NP. The first day following surgery, Emodin treatment began, and it lasted until the 21st day. On days 3, 7, 14 and 21, all behavioral investigations were conducted. The sciatic nerve and spinal cord were extracted for further molecular examination. Emodin elevated response latency, was able to delay the onset of mechanical hyperalgesia in rats on days 7, 14, and 21 and reduced the CCI-induced paw deformation. Emodin treatment significantly reduced lipid peroxidation and NO levels while restoring the GST, GSH and catalase. It significantly improved the disorientation of the sciatic nerve and spinal cord confirmed by H & E staining and reduced inflammatory markers as observed by the quantification of COX-2, TNF-α, p-NFκb and up-regulated PPAR-γ levels by ELISA and PCR. According to the findings, Emodin has antinociceptive and anti-hyperalgesic properties, which reduced pain perception and inflammation. We also suggested the involvement of PPAR-γ pathway in the therapeutic potential of emodin in chronic nerve injury.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0287517&type=printable |
| spellingShingle | Ismail Badshah Neelum Gul Qazi Fawad Ali Amber Mahmood Minhas Arooj Mohsin Alvi Mahmoud Kandeel Muhammad Imran Syed Shams Ul Hassan Simona Bungau Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway. PLoS ONE |
| title | Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway. |
| title_full | Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway. |
| title_fullStr | Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway. |
| title_full_unstemmed | Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway. |
| title_short | Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway. |
| title_sort | emodin alleviates chronic constriction injury induced neuropathic pain and inflammation via modulating ppar gamma pathway |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0287517&type=printable |
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