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Octanol alleviates chronic constriction injury of sciatic nerve-induced peripheral neuropathy by regulating AKT/mTOR
Biquan Deng1, Hui Zou1, Keli Hu1
1Department of Orthopedics, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Objective:
Activation of gap junction channels can induce neuropathic pain. Octanol can limit the conductance of gap junctions containing connexin 43 proteins. Thus, this study focused on the roles of octanol in chronic constriction injury (CCI)-induced peripheral neuropathy in mice and its mechanisms of action.
Methods:
Male mice were assigned into control, sham, CCI, CCI + Octanol-20 mg/kg, CCI + Octanol-40 mg/kg and CCI + Octanol-80 mg/kg groups. CCI was performed by applying three loose ligations to mouse sciatic nerve, and the mice with CCI was administered with 20 mg/kg, 40 mg/kg, or 80 mg/kg octanol. The neuropathic pain development was examined by assessing thermal withdrawal latency, paw withdrawal mechanical threshold, and sciatic functional index. Histopathological changes were evaluated by hematoxylin and eosin staining. The phosphorylation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR) was examined by western blotting. The expression of Akt and mTOR was also evaluated by immunofluorescence staining.
Results:
Octanol alleviated the CCI-induced mechanical and thermal hyperalgesia and sciatic functional loss. Additionally, octanol relieved the CCI-induced abnormal histopathological changes. Mechanistically, octanol inactivated the Akt/mTOR pathway in the mice with CCI.
Conclusion:
In conclusion, octanol can alleviate CCI-induced peripheral neuropathic by regulating the Akt/mTOR pathway and might be a novel pharmacological intervention for neuropathic pain.
Insights
Octanol effectively reduces neuropathic pain and nerve damage caused by chronic constriction injury (CCI) in mice. It works by inhibiting the Akt/mTOR pathway, suggesting potential as a new treatment for peripheral neuropathy.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Gap junction channel activation is implicated in neuropathic pain.
- Octanol is known to modulate gap junction conductance, particularly those involving connexin 43.
Purpose of the Study:
- To investigate the therapeutic effects of octanol on chronic constriction injury (CCI)-induced peripheral neuropathy in mice.
- To elucidate the underlying molecular mechanisms of octanol's action in neuropathic pain.
Main Methods:
- Male mice underwent CCI surgery and were treated with varying doses of octanol.
- Neuropathic pain was assessed using thermal hyperalgesia, mechanical allodynia, and sciatic functional index tests.
- Histopathological, western blot, and immunofluorescence analyses were performed to evaluate nerve damage and the Akt/mTOR pathway.
Main Results:
- Octanol administration significantly alleviated mechanical and thermal hyperalgesia and improved sciatic function in CCI mice.
- Histopathological examination revealed that octanol mitigated CCI-induced nerve damage.
- Octanol treatment led to the inactivation of the Akt/mTOR signaling pathway in the affected nerves.
Conclusions:
- Octanol demonstrates significant efficacy in ameliorating CCI-induced peripheral neuropathic pain.
- The therapeutic effect of octanol is mediated through the regulation of the Akt/mTOR pathway.
- Octanol presents a promising novel pharmacological agent for the treatment of neuropathic pain.
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