Pregnancy suppresses neuropathic pain induced by chronic constriction injury in rats through the inhibition of TNF-α.
別タイトル
妊娠はTNF-αの抑制を介して，絞扼性神経損傷モデルラットの神経障害性疼痛を抑制する
著者
小野寺, 美子
(Onodera, Yoshiko)
上位タイトル
Journal of pain research
Vol.10,
(2017.
3)
,p.567-
574
識別番号
ISSN
1178-7090
DOI
10.2147/JPR.S121810
その他
PMID：28331359
博士論文情報
学位授与番号
10107A513
学位授与年月日
2017-06-30
学位名
博士（医学）
学位授与機関
旭川医科大学
抄録
PURPOSE:
Pregnancy-induced analgesia develops during late pregnancy, but it is unclear whether this analgesia is effective against neuropathic pain. The detailed molecular mechanisms underlying pregnancy-induced analgesia have not been investigated. We examined the antinociceptive effect of pregnancy-induced analgesia in a neuropathic pain model and the expression of tumor necrosis factor (TNF)-α, glial fibrillary acidic protein (GFAP), Iba-1, and c-Fos in the spinal dorsal horn just before parturition.
MATERIALS AND METHODS:
Female Sprague Dawley rats (200-250 g) were randomly assigned to one of four groups (pregnant + chronic constriction injury [CCI]; pregnant + sham injury; not pregnant + CCI; and not pregnant + sham injury). Separate groups were used for the behavioral and tissue analyses. CCI of the left sciatic nerve was surgically induced 3 days after confirming pregnancy in the pregnancy group or on day 3 in the not pregnant group. The spinal cord was extracted 18 days after CCI. TNF-α, GFAP, Iba-1, and c-Fos expression levels in the spinal dorsal horn were measured by Western blot analysis. Mechanical threshold was tested using von Frey filaments.
RESULTS:
The lowered mechanical threshold induced by CCI was significantly attenuated within 1 day before parturition and decreased after delivery. TNF-α expression in CCI rats was decreased within 1 day before parturition. Further, GFAP, Iba-1, and c-Fos expression in the spinal dorsal horn was reduced in the pregnant rats. Serum TNF-α in all groups was below measurable limits.
CONCLUSION:
Our findings indicate that pregnancy-induced analgesia suppresses neuropathic pain through reducing spinal levels of TNF-α, GFAP, Iba-1, and c-Fos in a rat model of CCI.
