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目的:探讨中药单体姜黄素(Cur)对人晶状体上皮细胞系(HLE-B3)增殖及细胞内Ⅰ型和Ⅲ型胶原蛋白合成的影响。方法:20mg/L的Cur作用于HLE-B3 24h后MTT法检测吸光度值(OD值),苏木精-伊红染色观察细胞形态,流式细胞术检测细胞周期变化,ELISA法检测Ⅰ型和Ⅲ型胶原蛋白表达。结果:rhbFGF组OD值较正常组升高,Cur组OD值较rhbFGF组降低,抑制率达53.70%;Cur组细胞数目明显减少,胞浆减少,轮廓不清,交织的网状结构减少,甚至有的细胞变圆,细胞核凝集,见核固缩现象,胞浆嗜酸性染色;G1期的细胞Cur组较rhbFGF组明显增加,S期的细胞Cur组较rhbFGF组明显减少,G2期的细胞Cur组较rhbFGF组无明显变化;Ⅰ型胶原蛋白浓度为Cur组较rhbFGF组明显下降,Ⅲ型胶原蛋白浓度Cur组较rhbFGF组也明显下降。结论:Cur抑制rhbFGF诱导的HLE-B3增殖的同时也能抑制HLE-B3内Ⅰ、Ⅲ型胶原蛋白合成,干扰HLE-B3纤维化,可望成为防治后囊膜混浊的理想药物。
Objective: To investigate the effect of curcumin (Cur), a Chinese traditional medicine, on the proliferation of human lens epithelial cell line (HLE-B3) and the synthesis of intracellular type I and type III collagen. Methods: The absorbance (OD value) was measured by MTT assay after 24h treatment of 20mg/L CurE with HLE-B3. Hematoxylin-eosin staining was used to observe the cell morphology. Flow cytometry was used to detect cell cycle changes. ELISA was used to detect type I and Type III collagen expression. Results: The OD value of rhbFGF group was higher than that of normal group. The OD value of Cur group was lower than that of rhbFGF group, and the inhibition rate was 53.70%. The number of cells in Cur group was significantly reduced, the cytoplasm was reduced, the outline was unclear, and the interwoven network structure was reduced. Some cells became round, the cell nuclei agglutinated, the phenomenon of nuclear condensation was observed, and the cytoplasm was eosinophilic; the Cur group of G1 phase was significantly increased compared with the rhbFGF group, and the Cur group of S phase was significantly decreased compared with the rhbFGF group; the cells of G2 phase were Cur There was no significant change in the group compared with the rhbFGF group; the concentration of type I collagen in the Cur group was significantly lower than that in the rhbFGF group, and the type III collagen concentration in the Cur group was significantly lower than that in the rhbFGF group. Conclusion: Cur inhibits the proliferation of HLE-B3 induced by rhbFGF and inhibits the synthesis of type I and type III collagen in HLE-B3. It interferes with the fibrosis of HLE-B3 and is expected to be an ideal drug for prevention of posterior capsule opacification.