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Interleukin-4 reversed the Interleukin-1-inhibited proteoglycan synthesis through the inhibition of NO release: a possible involvement of intracellular calcium ion.

机译:白细胞介素4通过抑制NO释放逆转了白细胞介素1抑制的蛋白聚糖合成:可能涉及细胞内钙离子。

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摘要

Interleukin-1 (IL-1) causes cartilage degradation through nitric oxide (NO) synthesis. Although Interleukin-4 (IL-4) antagonizes the IL-1-mediated cartilage degradation, the precise mechanisms are not clear. We examined the effect of IL-4 on NO synthesis in parallel with intracellular Ca levels ([Ca(2+)]i) and proteoglycan (PG) synthesis. IL-4-inhibited IL-1-enhanced NO release in a dose-dependent manner. IL-1-enhanced [Ca(2+)]i in the chondrocytes, and IL-4 attenuated this increase. IL-4 reversed IL-1-inhibited PG synthesis. Accordingly, IL-4 reversed the IL-1-inhibited PG synthesis through the inhibition of NO release. An increase in [Ca(2+)]i with IL-1 is possibly involved in this action.
机译:白介素-1(IL-1)通过一氧化氮(NO)合成引起软骨降解。尽管白介素4(IL-4)拮抗IL-1介导的软骨降解,但其确切机制尚不清楚。我们检查了IL-4对NO合成的影响以及细胞内Ca水平([Ca(2 +)] i)和蛋白聚糖(PG)的合成。 IL-4以剂量依赖性方式抑制IL-1增强NO的释放。 IL-1增强了软骨细胞中的[Ca(2 +)] i,而IL-4减弱了这种增加。 IL-4逆转了IL-1抑制的PG合成。因此,IL-4通过抑制NO释放而逆转了IL-1抑制的PG合成。 IL-1的[Ca(2 +)] i的增加可能与该作用有关。

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