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Phytomedicine 2018-Mar

Polygonum aviculare L. extract reduces fatigue by inhibiting neuroinflammation in restraint-stressed mice.

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Sun Haeng Park
Seol Jang
Eunjung Son
Si Woo Lee
Sun Dong Park
Yoon-Young Sung
Ho Kyoung Kim

키워드

요약

BACKGROUND

Chronic fatigue patients experience various neuropsychological symptoms, including fatigue behaviors, chronic pain, and depression. They also display immune system dysregulation. Polygonum aviculare L. extract (PAE) is a traditional herbal medicine used to treat inflammatory diseases by reportedly decreasing pro-inflammatory cytokine production.

UNASSIGNED

We hypothesized that the anti-inflammatory properties of PAE would attenuate fatigue symptoms in a mouse model of restraint stress.

METHODS

We evaluated the effects of PAE on fatigue using three experimental groups: unstressed, vehicle-treated stressed, and PAE-treated stressed mice. This restraint stress paradigm, comprised of restraint for 3 h daily for 15 days, was used to model chronic fatigue.

METHODS

We compared lethargy-like behavior between our experimental groups using forced-swim, sucrose preference, and open-field tests once per week on days 7 and 14 of restraint stress. We also used histology and western blotting to evaluate pro-inflammatory cytokine expression in the brain and serum, and microglial activation in the brain. Finally, we used liquid chromatography/mass spectroscopy (LC/MS) to identify individual components of PAE, and applied cell culture techniques to test the effects of these components on neuronal cells in vitro.

RESULTS

In restraint-stressed mice, PAE treatment decreased lethargy-like behavior relative to vehicle-treated animals. PAE treatment also reduced expression of fatigue-related factors such as corticosterone, serotonin, and catecholamines (adrenaline and noradrenaline) in the brain and serum, and decreased expression of CD68, Ibal-1, and the inflammatory cytokines TNF-α, IL-6, and IL-1β in the brain. Together, these data indicate that PAE reduced fatigue and is anti-inflammatory. Furthermore, histopathological analyses indicated that PAE treatment recovered atrophic volumes and hepatic injuries. Finally, LC/MS analysis of PAE identified four individual chemicals: myricitrin, isoquercitrin, avicularin, and quercitrin. In neuronal cell cultures, treatment with these PAE components inhibited TNF-α production, confirming that PAE treatment reduces neuroinflammation.

CONCLUSIONS

PAE treatment may reduce fatigue by suppressing neuroinflammation and the expression of fatigue-related hormones.

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