Abstract

αB-crystallin (CRYAB) is a small heat shock protein that is able to inhibit neuroinflammatory responses under various pathological conditions. Some studies have proven that neuroinflammatory mechanisms play important roles in bone cancer pain (BCP). However, whether CRYAB participates in the maintenance of BCP has not yet been examined. Walker256 tumour cells were inoculated into the tibia to induce a rat model of BCP. Von Frey hairs were used to measure mechanical allodynia. Immunohistochemistry and western blotting were used to examine the expression level of CRYAB in the spinal dorsal horn. The gradual development of mechanical allodynia was induced by the injection of Walker256 cells into the tibia. The downregulation of spinal CRYAB expression was found in BCP rats. The intrathecal administration of CRYAB (from days 9 to 15 post-inoculation) dose-dependently alleviated mechanical allodynia in BCP rats. Additionally, there were concomitant increases in spinal CRYAB expression and decreases in TNF-α expression. Spinal CRYAB may participate in the maintenance of BCP in rats. The findings will help to identify new drugs for the management of BCP.

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