Emodin alleviates chronic constriction injury-induced neuropathic pain and inflammation via modulating PPAR-gamma pathway.

Autor: Badshah I; Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan., Qazi NG; Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan., Ali F; Department of Pharmacy, Kohat University of Science and Technology, Kohat, Pakistan., Minhas AM; Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan., Alvi AM; Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan., Kandeel M; Department of Biomedical sciences, College of Veterinary Medicine, King Faisal University, Al-hofuf, Al-Ahsa, Saudia Arabia., Imran M; Department of Biomedical Science, Pak-Austria Fachhochule: Institute of Applied Science and Technology, Mang Haripur, KPK, Pakistan., Hassan SSU; Shanghai Key Laboratory for Molecular Engineering of Chiral Drugs, School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.; Department of Natural Product Chemistry, School of Pharmacy, Shanghai Jiao Ton University, Shanghai, China., Bungau S; Department of Pharmacy, Faculty of Medicine and Pharmacy, University of Oradea, Oradea, Romania.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2023 Jul 13; Vol. 18 (7), pp. e0287517. Date of Electronic Publication: 2023 Jul 13 (Print Publication: 2023).
DOI: 10.1371/journal.pone.0287517
Abstrakt: 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.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2023 Badshah et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje