Antiallodynic and antihyperalgesic effects of decursin associated with correcting mitochondrial dysfunction and oxidative stress in type 1 diabetic mice.

Autor: Ma L; Department of Neurology, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou, Hubei Province, China., Fan YY; Department of Pharmacology and Zhejiang Key Lab of Pathophysiology, Ningbo University, Health Science Center, Ningbo, Zhejiang Province, China., Li BL; School of Mathematics and Statistics, Ningbo University, Ningbo, Zhejiang province, China., Xu F; Central Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang Province, China., Zhao X; Department of Pharmacology and Zhejiang Key Lab of Pathophysiology, Ningbo University, Health Science Center, Ningbo, Zhejiang Province, China. Electronic address: zhaoxin@nbu.edu.cn.
Jazyk: angličtina
Zdroj: Chemico-biological interactions [Chem Biol Interact] 2024 Nov 01; Vol. 403, pp. 111249. Date of Electronic Publication: 2024 Sep 18.
DOI: 10.1016/j.cbi.2024.111249
Abstrakt: A substantial proportion of diabetic patients suffer a debilitating and persistent pain state, known as peripheral painful neuropathy that necessitates improved therapy or antidote. Decursin, a major active ingredient from Angelica gigas Nakai, has been reported to possess antidepressant activity in preclinical studies. As antidepressants have been typically used as standard agents against persistent neuropathic pain, this study aimed to probe the effect of decursin on neuropathic pain associated with streptozotocin-induced type 1 diabetes in male C57BL6J mice. The Hargreaves test and the von Frey test were used to assess pain-like behaviors, shown as heat hyperalgesia and mechanical allodynia respectively. Chronic treatment of diabetic mice with decursin not only ameliorated the established symptoms of heat hyperalgesia and mechanical allodynia, but also arrested the development of these pain states given preemptively at low doses. Although decursin treatment hardly impacted on metabolic disturbance in diabetic mice, it ameliorated exacerbated oxidative stress in pain-associated tissues, improved mitochondrial bioenergetics in dorsal root ganglion neurons, and restored nerve conduction velocity and blood flow in sciatic nerves. Notably, the analgesic actions of decursin were modified by pharmacologically manipulating redox status and mitochondrial bioenergetics. These findings unveil the analgesic activity of decursin, an effect that is causally associated with its bioenergetics-enhancing and antioxidant effects, in mice with type 1 diabetes.
Competing Interests: Declaration of competing interest The authors declare no conflicts of interest in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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