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目的:通过测定NIV毒素和硒作用下软骨细胞IL-1β、TNF-α含量的变化,从细胞因子角度探讨大骨节病发病机制。方法:在体外单层和立体培养的人胚软骨细胞中加入NIV毒素和硒,构建软骨损伤模型,收集软骨组织、细胞和细胞培养液,用光学显微镜观察体外构建组织的形态;用分光光度法测定软骨细胞DNA含量;用酶联免疫吸附方法(ELISA)检测细胞培养液中IL-1β、TNF-α的水平。结果:形态学观察发现NIV毒素能抑制软骨细胞生长,局部出现点片状坏死;毒素加硒后,上述损伤变化减弱。NIV毒素作用下软骨细胞DNA的合成受到抑制,但培养液中IL-1β、TNF-α含量显著升高,毒素加硒与毒素组变化趋势一致,但数值略下降。结论:NIV毒素能诱导软骨细胞IL-1β与TNF-α的分泌,这可能是造成软骨细胞损伤的原因之一。
OBJECTIVE: To explore the pathogenesis of Kashin-Beck disease from the perspective of cytokines by measuring the changes of IL-1β and TNF-α in chondrocytes under the action of NIV toxin and selenium. Methods: Human embryonic chondrocytes cultured in vitro and monolayer culture were added with NIV toxin and selenium to establish the model of cartilage injury. Cartilage tissue, cells and cell culture fluid were collected. The morphological changes of the constructed tissue were observed by light microscopy. The content of chondrocyte DNA was measured. The levels of IL-1β and TNF-α in cell culture medium were detected by enzyme-linked immunosorbent assay (ELISA). Results: Morphological observation showed that NIV toxin could inhibit the growth of chondrocytes, and local patchy necrosis occurred. After the toxin was added selenium, the change of the damage was weakened. Under the action of NIV toxins, DNA synthesis in chondrocytes was inhibited, but the content of IL-1β and TNF-α in the culture medium was significantly increased. The change trend of toxin plus selenium and toxin group was the same, but the value decreased slightly. Conclusion: NIV toxin can induce the secretion of IL-1β and TNF-α in chondrocytes, which may be one of the causes of chondrocyte injury.