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.