Background: Lycium barbarum polysaccharide (LBP) is a promising therapeutic drug in inflammation-related injuries, nevertheless the mechanism of LBP's action is still elusive. The study is to explore the effect of LBP on IL-1β-evoked ATDC5 cell inflammatory injury. Methods: ATDC5 cells were administrated with 10 ng/mL interleukin (IL)-1β to establish an in vitro model of cartilage damage. After management, cell viability was tested through CCK8 assay. The pro-inflammatory cytokines and cyclooxygenase (Cox)-2 were assessed through ELISA, western blot and qRT-PCR. MiR-124 expression in ATDC5 cells was silenced by transfecting with miR-124 inhibitor, and the pro-inflammatory cytokines and Cox-2 were re-assessed. NF-κB and JNK pathways were measured through western blot. Results: IL-1β stimulation accelerated the release of IL-1β, IL-6 and TNF-α, elevated Cox-2 expression. LBP significantly eased IL-1β-induced inflammation. MiR-124 expression was observed to enhance by LBP, and the impacts of LBP on ATDC5 cells were lightened via transfection with miR-124 inhibitor. NF-κB and JNK pathways were activated after IL-1β stimulation, nevertheless were inactivated by LBP administration. Besides, LBP-evoked the repression of NF-κB and JNK pathways were overturned by miR-124 inhibitor. Conclusions: Our study suggests that LBP protects ATDC5 cells from IL-1β-evoked injury through up-regulating miR-124 via blocking NF-κB and JNK pathways.

中文翻译：

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枸杞多糖通过microRNA-124的介导减轻了IL-1β诱发的软骨生成ATDC5细胞的炎症损伤。

背景：枸杞多糖（LBP）是一种与炎症相关的损伤的有前途的治疗药物，尽管如此，LBP的作用机理仍不清楚。该研究旨在探讨LBP对IL-1β引起的ATDC5细胞炎性损伤的作用。方法：对ATDC5细胞给予10 ng / mL白细胞介素（IL）-1β体外建立软骨损伤模型。处理后，通过CCK8测定法测试细胞活力。通过ELISA，蛋白质印迹和qRT-PCR评估促炎细胞因子和环氧合酶（Cox）-2。通过用miR-124抑制剂转染沉默ATDC5细胞中的MiR-124表达，并重新评估促炎细胞因子和Cox-2。通过western blot检测NF-κB和JNK途径。结果：IL-1β刺激促进了IL-1β，IL-6和TNF-α的释放，Cox-2表达升高。LBP显着缓解了IL-1β诱导的炎症。LBP观察到MiR-124表达增强，并且通过miR-124抑制剂的转染减轻了LBP对ATDC5细胞的影响。IL-1β刺激后，NF-κB和JNK通路被激活，但通过LBP给药被灭活。此外，LBP引起的NF-κB抑制和JNK通路被miR-124抑制剂所推翻。结论：我们的研究表明，LBP通过阻止NF-κB和JNK通路上调miR-124来保护ATDC5细胞免受IL-1β诱发的损伤。IL-1β刺激后，NF-κB和JNK通路被激活，但通过LBP给药被灭活。此外，LBP引起的NF-κB抑制和JNK途径被miR-124抑制剂所推翻。结论：我们的研究表明，LBP通过阻止NF-κB和JNK通路上调miR-124来保护ATDC5细胞免受IL-1β诱发的损伤。IL-1β刺激后，NF-κB和JNK通路被激活，但通过LBP给药被灭活。此外，LBP引起的NF-κB抑制和JNK通路被miR-124抑制剂所推翻。结论：我们的研究表明，LBP通过阻止NF-κB和JNK通路上调miR-124来保护ATDC5细胞免受IL-1β诱发的损伤。