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[摘要]
目的:探究白皮杉醇对糖尿病视网膜病变模型大鼠的治疗效果及作用机制。
方法:建立糖尿病视网膜病变模型,随机分为模型组、常规用药组、低剂量和高剂量白皮杉醇组各10只。模型组使用100mg/kg的生理盐水灌胃,常规用药组使用100mg/kg的依帕司他灌胃,低剂量、高剂量白皮杉醇组分别使用100、200mg/kg白皮杉醇灌胃。使用光学显微镜观察五组大鼠视网膜组织,Western blot检测五组大鼠视网膜组织中Bax、Bcl-2蛋白的表达,酶联免疫吸附试验法检测五组大鼠视网膜组织VEGF、HIF-1α、ANGⅡ、Ang-1、Ang-2、Tie-2水平。
结果:高剂量白皮杉醇组大鼠视网膜组织中Bax、Ang-1/Ang-2比值(1.76±0.05、3.16±0.09)高于低剂量白皮杉醇组(1.01±0.21、2.98±0.02)(P<0.05)。高剂量白皮杉醇组大鼠视网膜组织中Bcl-2、VEGF、HIF-1α、ANGⅡ、Ang-1、Ang-2、Tie-2水平(0.37±0.06ng/mL、121.89±5.45ng/mL、0.38±0.01pg/mL、7.58±0.10ng/mL、8.56±0.04μg/L、3.24±0.25μg/L、3.00±0.04μg/L)低于低剂量白皮杉醇组(0.96±0.21ng/mL、140.25±8.10ng/mL、0.42±0.02pg/mL、8.12±0.09ng/mL、9.10±0.46μg/L、4.12±0.23μg/L、3.46±0.15μg/L)(P<0.05)。
结论:白皮杉醇通过作用于Ang/Tie受体信号通路,抑制氧化应激损伤、新生血管的生成,有效保护糖尿病视网膜病变大鼠的视网膜组织,且呈剂量依赖,为临床上治疗糖尿病视网膜病变的治疗提供了理论依据。
[Key word]
[Abstract]
AIM: To explore the effect and mechanism of paclitaxel on diabetic retinopathy model rats.
METHODS: The diabetic retinopathy model was established and randomly divided into model group, routine drug group, low dose and high dose picetaxel group with 10 rats each. In the model group, 100mg/kg normal saline was used for gavage, while in the conventional group, 100mg/kg epalrestat was used for gavage. The low dose and high dose picetaxel groups were given 100 and 200mg/kg picetaxel respectively. The retina tissue of five groups of rats was observed by optical microscope, Western blot was used to detect the expression of Bax and Bcl-2 protein, and enzyme-linked immunosorbent assay was used to detect the levels of VEGF, HIF-1 α, ANG Ⅱ, Ang-1, Ang-2 and Tie-2.
RESULTS: The ratio of Bax and Ang-1/Ang-2 in the retina of the high dose group was(1.76±0.05, 3.16±0.09)higher than that of the low dose group(1.01±0.21, 2.98±0.02)(P<0.05). The levels of Bcl-2, VEGF, HIF-1 α, ANG Ⅱ, Ang-1, Ang-2, and Tie-2 in high dose picetaxel group were(0.37±0.06, 121.89±5.45ng/mL, 0.38±0.01pg/mL, 7.58±0.10ng/mL, 8.56±0.04μg/L, 3.24±0.25μg/L, 3.00±0.04μg/L)respectively lower than the lower levels(0.96ng/mL, 0.42±0.02pg/mL, 8.12±0.09ng/mL, 9.10±0.46μg/L, 4.12±0.23μg/L, 3.46±0.15μg/L)(P<0.05).
CONCLUSION: Paclitaxel can inhibit oxidative stress injury and angiogenesis by acting on Ang/Tie receptor signaling pathway, effectively protect retinal tissue of diabetic retinopathy rats in a dose-dependent manner, which provides a theoretical basis for clinical treatment of diabetic retinopathy.
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