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Resveratrol attenuates inflammatory pain induced by complete Freund's adjuvant via NF-κB signaling pathway in a mouse model / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 340-345, 2018.
Article in Chinese | WPRIM | ID: wpr-701124
ABSTRACT

AIM:

To investigate the anti-inflammatory action of resveratrol(Res)and its correlation with nu-clear factor-κB(NF-κB)signaling pathway in a mouse model of inflammatory pain.

METHODS:

BALB/c mice(n=60) were randomly divided into 6 groupsnormal control group,inflammatory pain model group, positive control(dexametha-sone,0.5 mg/kg)group and resveratrol(100,50 and 25 mg/kg)groups(10 mice in each group).In order to observe the anti-inflammatory pain effects of reseratrol on mice,the paw withdrawal mechanical threshold,paw withdrawal thermal latency and cold withdrawal times were detected.In order to analyze the mechanism of analgesic effect of resveratrol, the expression levels of NF-κB, inhibitor of NF-κB(IκB)α, inhibitor of NF-κB kinase(IKK)β, tumor necrosis factor (TNF)-αand interleukin(IL)-1βin the spinal cord tissues(L4 ~L6)of the mice were determined by RT-PCR and Western blot.

RESULTS:

The resveratrol at 100 and 50 mg/kg increased the paw withdrawal mechanical threshold,pro-longed the paw withdrawal thermal latency,and decreased the cold withdrawal times in the inflammatory pain mice(P<0.05 or P<0.01).The resveratrol at 100 mg/kg down-regulated the mRNA and protein expression levels of NF-κB, IκBα,IKKβ,TNF-αand IL-1βin the spinal cord tissues(L4~L6)of inflammatory pain mice(P<0.05 or P<0.01).

CONCLUSION:

Resveratrol ameliorates the inflammatory pain of the mice induced by complete Freund's adjuvant.The mechanism is related to the inhibition of NF-κB signaling pathway.

Full text: Available Index: WPRIM (Western Pacific) Type of study: Prognostic study Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2018 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Type of study: Prognostic study Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2018 Type: Article