脂联素抑制人髓核细胞分泌疼痛介质PGE2的初步机制研究

Inhibitory effect of adiponectin on secretion of PGE2 in human nucleus pulposus cells

摘要:

目的验证脂联素在椎间盘源性腰痛患者中可能发挥的抗炎作用，并初步研究其机制。方法首先检测髓核组织内脂联素受体表达水平；随后提取并培养人髓核细胞，检测炎症因子TNF-α对髓核细胞内脂联素受体调控；最后采用慢病毒基因沉默的手段检测脂联素抑制炎症因子诱导髓核细胞产生PGE-2 的作用及机制。结果椎间盘源性腰痛患者髓核组织内脂联素受体Adipo R1/2 表达水平低于正常髓核组织（p <0.05），炎症介质TNF-α能抑制脂联素受体AdipoR1/2 的表达（p <0.05）。当脂联素处理髓核细胞后，TNF-α对PGE-2 分泌的诱导受抑并且呈浓度剂量依赖效应（p <0.05）；髓核细胞过表达Adipo R1/R2 后，均能抑制炎症因子TNF-α诱导髓核细胞产生PGE-2，其中以Adipo R2 为明显（p <0.05）。结论脂联素能够通过两个受体Adipo R1、Adipo R2 抑制抑制髓核细胞合成分泌疼痛介质PGE-2，提示脂联素可能为一个保护性因子在椎间盘源性腰痛环境中发挥抗炎作用。

Abstract:

Objective To investigate the anti-inflammatory effects of adiponectin in patients with discogenic back pain and the potential mechanism. Methods The expression of adiponectin receptor Adipo R1/2 in human nucleus pulposus (NP) tissue was examined. Human NP cells were isolated for further culture. The regulatory effect of TNF -α on adiponectin receptors in NP cells was detected. Moreover, lentiviral gene silencing technology was utilized to investigate the inhibitory effect of adiponectin on TNF -α-induced production of PGE-2 and underlying mechanism. Results The expression of Adipo R1/2 was significantly decreased in NP tissues derived from patients with discogenic back pain compared with normal NP tissues (p< 0.05). TNF-α inhibited the expression of Adipo R1/2, and up-regulated the secretion of PGE2 in NP cells,which was attenuated by adiponectin dose-dependently (p < 0.05). Over-expression of Adipo R1/2 abolished the TNF-α-induced PGE2 production (p < 0.05). Conclusions Adiponectin is potentially a protective mediator in patients with discogenic back pain through AdipoR1/2-dependent inhibition of secretion of PGE2.