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目的 探讨氨基胍 (aminoguanidine,AG)水飞蓟素 (silymarin,Sil)和山莨菪碱 (anisodamine,Ani)对糖基化产物培养下视网膜微血管周细胞 (pericytes,PC)的保护作用。 方法 MTT比色测定结合3 H- Td R掺入和 Fura- 2 AM,观察三种药物对早期糖基化产物 (early glycation products of albumin,EGs)和糖基化终产物 (advanced glycation end products of albumin AGEs)培养的 PC增生、DNA合成和胞浆[Ca2 +]i水平改变的影响。结果 EGs培养下 ,AG组和 Sil组 MTT测定 A值和 3 H- Td R掺入量均较对照组增高 (P<0 .0 1) ,而两组胞浆 [Ca2 +]i水平较对照组减低 (P<0 .0 1和 0 .0 5 ) ,两组比较差异具有显著性的意义 ;AGEs培养下 ,仅 AG组 MTT A值和 3 H- Td R掺入量较对照组增高 (P<0 .0 1) ,胞浆 [Ca2 +]i水平较对照组减低 (P<0 .0 5 )。 结论 AG能有效保护 PC免受 EGs所致的增生和抑制胞浆 [Ca2 +]i水平增高 ,并对 AGEs所致的上述改变亦有一定的保护效应。 Sil仅对 EGs所致的 PC增生抑制和胞浆 [Ca2 +]i水平改变有一定的保护作用 ;Ani对 EGs和 AGEs所致的 PC上述改变均无明显保护作用。
Objective To investigate the protective effect of aminoguanidine (AG) silymarin (Sil) and anisodamine (Ani) on the pericytes (PC) of cultured retinal cells under glycosylation culture. Methods MTT colorimetric assay combined with 3 H-Td R incorporation and Fura-2 AM was used to observe the effects of three drugs on early glycation products of albumin (EGs) and advanced glycation end products of albumin AGEs) cultured in vitro, changes in DNA synthesis and cytoplasmic [Ca2 +] i levels. Results Compared with the control group, the MTT assay A and the amount of 3 H-Td R incorporation in the AGs and Sil groups were significantly increased (P <0.01), while the levels of [Ca2 +] i in the two groups were higher than those in the control (P <0. 01 and 0. 05), the difference between the two groups was significant. Under the culture of AGEs, only MTT A and 3 H-Td R incorporation in AG group were higher than those in control group P <0.01), while the level of [Ca2 +] i in cytoplasm decreased compared with the control group (P <0.05). Conclusion AG can effectively protect PC from EGs-induced hyperplasia and inhibit the increase of cytoplasmic [Ca2 +] i levels, and also have some protective effects on the above changes caused by AGEs. Sil only protects against the proliferation of PC and the change of cytoplasmic [Ca2 +] i induced by EGs. Ani has no protective effect on the changes of PC induced by EGs and AGEs.