6-hydroxydopamine induces mechanical hyperalgesia reaction in rats through p38 MAPK signaling pathway / 神经解剖学杂志
Chinese Journal of Neuroanatomy
; (6): 43-49, 2024.
Article
de Zh
| WPRIM
| ID: wpr-1019635
Bibliothèque responsable:
WPRO
ABSTRACT
Objective:
To study the regulatory mechanism of p38 MAPK signaling pathway participate in hyperalge-sia reaction in Parkinson's disease(PD)rats model induced by 6-hydroxy dopamine(6-OHDA).Methods:
Forty male Sprague Dawley(SD)rats were randomly divided into four groupsSham group(Sham),model group(6-OHDA),p38 MAPK inhibitor SB203580 treatment group(6-OHDA+SB203580)and p38 MAPK activator anisomycin(ANS)treatment group(6-OHDA+ANS).PD model was established by intra-striatal injection of 6-OHDA stereotactically.6-OHDA+SB203580 and 6-OHDA+ANS groups was injected with 6-OHDA to establish PD model,and treated with inhibitor SB203580 or activator ANS respectively.The von Frey hairs were applied to measure the mechanical paw with-draw threshold(PWT)of rats.Enzyme linked immunosorbent assay(ELISA)was used to detect the content of IL-6,IL-1β,and TNF-α in rat dorsal root ganglion(DRG).The mRNA levels of genes IL-6,IL-1β,TNF-α,and p38 MAPK in rat DRG was detected by real time RT-PCR.Results:
In the DRG of 6-OHDA included PD rats,the expres-sion levels of IL-6,IL-1β,TNF-α,and p38 MAPK were significantly increased(P<0.05),and the PWT of rats were significantly decreased(P<0.05).The application of activator ANS further increased the expression levels of IL-6,IL-1β,TNF-α,and p38 MAPK,and the PWT of rats were decreased.After application of inhibitor SB203580,the ex-pression levels of IL-6,IL-1β,TNF-α and p38 MAPK were significantly decreased in the DRG of rats(P<0.05),and the PWT were significantly increased in rats(P<0.05).Conclusion:
6-OHDA induces mechanical hyperalgesia reaction in rats,and the molecular mechanism is related to activation of the p38 MAPK signalling pathway.
Texte intégral:
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Base de données:
WPRIM
Langue:
Zh
Journal:
Chinese Journal of Neuroanatomy
Année:
2024
Type de document:
Article