PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
ECN from Tussilago Farfara Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model
Version 1
: Received: 14 August 2020 / Approved: 18 August 2020 / Online: 18 August 2020 (12:00:15 CEST)
How to cite:
Khan, A.; Khalid, S.; Khan, A.; Shal, B.; Kang, E.; Lee, H.; Seo, E.K.; Khan, S. ECN from Tussilago Farfara Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model. Preprints2020, 2020080389. https://doi.org/10.20944/preprints202008.0389.v1
Khan, A.; Khalid, S.; Khan, A.; Shal, B.; Kang, E.; Lee, H.; Seo, E.K.; Khan, S. ECN from Tussilago Farfara Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model. Preprints 2020, 2020080389. https://doi.org/10.20944/preprints202008.0389.v1
Khan, A.; Khalid, S.; Khan, A.; Shal, B.; Kang, E.; Lee, H.; Seo, E.K.; Khan, S. ECN from Tussilago Farfara Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model. Preprints2020, 2020080389. https://doi.org/10.20944/preprints202008.0389.v1
APA Style
Khan, A., Khalid, S., Khan, A., Shal, B., Kang, E., Lee, H., Seo, E.K., & Khan, S. (2020). ECN from <em>Tussilago Farfara</em> Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model. Preprints. https://doi.org/10.20944/preprints202008.0389.v1
Chicago/Turabian Style
Khan, A., Eun Kyoung Seo and Salman Khan. 2020 "ECN from <em>Tussilago Farfara</em> Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model" Preprints. https://doi.org/10.20944/preprints202008.0389.v1
Abstract
7β-(3-ethyl-cis-crotonoyloxy)-1α-(2-methylbutyryloxy)-3,14-dehydro-Z-notonipetranone (ECN), a sesquiterpenoid obtained from a natural origin (Tussilago farfara)has proved to be effective in minimizing various side effects associated with opioids and nonsteroidal anti-inflammatory drugs. The current study focused on investigating the effects of ECN on neuropathic pain induced by partial sciatic nerve ligation (PSNL) by mainly focusing on oxidative stress, inflammatory and apoptotic proteins expression in mice. Neuropathic pain was induced in mice by PSNL surgery performed on day 1 and ECN (1 and 10 mg/kg, i.p.), was administered once daily for 11 days, starting from the third day after surgery. ECN post-treatment was found to reduce hyperalgesia and allodynia in a dose dependent manner. ECN significantly reversed the severity of neuropathic pain by improving distress symptoms and survival rate. ECN remarkably reversed the histopathological abnormalities associated with oxidative stress, apoptosis and inflammation. Furthermore, ECN prevented the suppression of antioxidants (glutathione, glutathione-S-transferase, catalase, superoxide dismutase, NF-E2-related factor-2 (Nrf2), hemeoxygenase-1 and NAD(P)H: quinone oxidoreductase) by PSNL. Moreover, pro-inflammatory cytokines (tumor necrotic factor alpha, interleukin 1 beta, interleukin 6, cyclooxygenase-2 and inducible nitric oxide synthase) expression was reduced by ECN administration. Treatment with ECN was successful in reducing caspase-3 level consistent with the observed modulation of pro-apoptotic proteins. Additionally, ECN showed protective effect on the lipid content of myelin sheath as evident from FTIR spectroscopy which showed the shift of lipid component bands to higher values. Thus, anti-neuropathic potential of ECN might be due to inhibition of oxidative stress, inflammatory mediators and pro-apoptotic proteins.
Medicine and Pharmacology, Pharmacology and Toxicology
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
