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目的 :体外用TNF -α、IL - 1β、LPS刺激心肌细胞后 ,观察心肌细胞的变化。 方法 :体外培养心肌细胞 ,用不同浓度的TNF -α、IL - 1β、LPS等刺激心肌细胞后 ,分别于 8h、2 4h、4 8h观察心肌细胞有无发生肥大反应 ,于2 4h、4 8h、72h观察心肌细胞有无凋亡。结果 :在予TNF -α、IL - 1β、LPS刺激心肌细胞后 ,与对照组相比 ,10 μg/L、15μg/L的TNF -α、2 0 μg/L、10 0 μg/L的IL - 1β和 10mg/L、15mg/L、2 0mg/L的LPS均能明显促进心肌细胞肥大 ,以刺激后 2 4h明显。同时 2 0 μg/L的TNF -α、10 0 μg/L的IL - 1β和 3× 10 4g/L的LPS可引起心肌细胞凋亡 ,以 72h为明显。结论 :TNF -α、IL - 1β、LPS可以引起心肌细胞的肥大和凋亡 ,炎症反应增高可能是心血管疾病的主要原因。
OBJECTIVE: To observe the changes of cardiomyocytes after stimulating cardiomyocytes with TNF-α, IL-1β and LPS in vitro. Methods: Cardiomyocytes were cultured in vitro and the cardiomyocytes were stimulated with different concentrations of TNF - α, IL - 1β, LPS and so on. After 8h, 24h, 48h respectively, the hypertrophy of cardiomyocytes was observed. At 24 h, 48 h 72h observation of myocardial cell apoptosis. Results: After stimulated with TNF - α, IL - 1β, and LPS, TNF - α of 10 μg / L, 15 μg / L, 20 μg / L and 100 μg / L of IL - 1β and 10mg / L, 15mg / L, 20mg / L of LPS can significantly promote myocardial hypertrophy, 24h after stimulation obvious. At the same time, 20 μg / L of TNF-α, 100 μg / L of IL - 1β and 3 × 10 4 g / L of LPS induced cardiomyocyte apoptosis, which was obvious at 72h. Conclusion: TNF - α, IL - 1β, LPS can induce hypertrophy and apoptosis of cardiomyocytes, and the increase of inflammatory reaction may be the main reason of cardiovascular diseases.