Effect of autophagy on allodynia, hyperalgesia and astrocyte activation in a rat model of neuropathic pain

International Journal of Molecular Medicine
Hongguang ChenYonghao Yu

Abstract

Primary damage or dysfunction of the nervous system may cause or initiate neuropathic pain. However, it has been difficult to establish an effective treatment for neuropathic pain, as the mechanisms responsible for its pathology remain largely unknown. Autophagy is closely associated with the pathological process of neurodegenerative diseases, neuropathic injury and cancer, among others. The aim of the present study was to examine the changes in the autophagy‑lysosomal pathway and discuss the effects of autophagy on allodynia, hyperalgesia and astrocyte activation in neuropathic pain. A neuropathic pain model was induced by chronic constriction injury (CCI) in rats. Inducers and inhibitors of autophagy and lysosomes were used to assess autophagy, allodynia, hyperalgesia and astrocyte activity. Neuropathic pain was found to induce an increase in the levels of the autophagy‑related proteins, LC3II and Beclin 1 and, and in those of the lysosomal proteins, lysosomal‑associated membrane protein type 2 (LAMP2) and Ras‑related protein Rab‑7a (RAB7), whereas p62 levels were found to decrease from day 1 to 14 following CCI. The autophagy inducer, rapamycin, further increased the LC3II, Beclin 1, lysosomal‑associated membrane protein 2 (...Continue Reading

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Methods Mentioned

BETA
lipidation
antisense oligonucleotide

Software Mentioned

Prism
GraphPad
SPSS

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