H-D Lou1, S-Y Wang, T Guo, Y Yang. 1. Department of Ophthalmology, Weifang Eye Hospital, Weifang, China. 94117782@qq.com.
Abstract
OBJECTIVE: To explore the effects of miR-21 on the rats with proliferative diabetic retinopathy by regulating the transforming growth factor-beta (TGF-β) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into the normal group (n=12), model group (n=12), and inhibitor group (TGF-β signaling inhibitor) (n=12). No treatment was performed in the normal group, the diabetic retinopathy model was established in the model group, and the model was established in the inhibitor group after the intraperitoneal injection of the inhibitor. Then, the materials were sampled for detection. In each group, the retinal morphology was observed via hematoxylin-eosin (HE) staining, the expressions of TGF-β1 and Smad3 were detected via immunohistochemistry, the relative protein expression levels of phosphorylated Smad3 (p-Smad3) and TGF-β were determined via Western blotting, the expression of miR-21 was detected via quantitative Polymerase Chain Reaction (qPCR), and the hemodynamic indicators of the ocular tissues were detected using the color Doppler ultrasonography. RESULTS: The HE staining results revealed that the rats in the model group had evident retinal damage, which could be effectively improved using the inhibitor. According to the immunohistochemistry detection results, the positive expression level of TGF-β1 was substantially raised in both model group and inhibitor group compared with that in the normal group (p<0.05), and it was notably lower in the inhibitor group than that in the model group (p<0.05). Moreover, the three groups did not differ in the positive expression level of Smad3 (p>0.05). The Western blotting results showed that the model and inhibitor groups had remarkably higher relative protein expression levels of p-Smad3 and TGF-β1 than the normal group (p<0.05), and they were markedly lowered in the inhibitor group compared with those in the model group (p<0.05). According to the qPCR results, the expression level of miR-21 was notably elevated in both model group and inhibitor group compared with that in the normal group (p<0.05), and there was no difference in the expression level of miR-21 between the former two groups (p>0.05). Finally, based on the color Doppler ultrasonography findings, the levels of the hemodynamic indicators substantially declined in both model group and inhibitor group compared with those in the normal group (p<0.05), and they were notably higher in the inhibitor group than those in the model group. CONCLUSIONS: We found that miR-21 regulates the TGF-β signaling pathway to affect the hemodynamics in the rats with proliferative diabetic retinopathy.
OBJECTIVE: To explore the effects of miR-21 on the rats with proliferative diabetic retinopathy by regulating the transforming growth factor-beta (TGF-β) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into the normal group (n=12), model group (n=12), and inhibitor group (TGF-β signaling inhibitor) (n=12). No treatment was performed in the normal group, the diabetic retinopathy model was established in the model group, and the model was established in the inhibitor group after the intraperitoneal injection of the inhibitor. Then, the materials were sampled for detection. In each group, the retinal morphology was observed via hematoxylin-eosin (HE) staining, the expressions of TGF-β1 and Smad3 were detected via immunohistochemistry, the relative protein expression levels of phosphorylated Smad3 (p-Smad3) and TGF-β were determined via Western blotting, the expression of miR-21 was detected via quantitative Polymerase Chain Reaction (qPCR), and the hemodynamic indicators of the ocular tissues were detected using the color Doppler ultrasonography. RESULTS: The HE staining results revealed that the rats in the model group had evident retinal damage, which could be effectively improved using the inhibitor. According to the immunohistochemistry detection results, the positive expression level of TGF-β1 was substantially raised in both model group and inhibitor group compared with that in the normal group (p<0.05), and it was notably lower in the inhibitor group than that in the model group (p<0.05). Moreover, the three groups did not differ in the positive expression level of Smad3 (p>0.05). The Western blotting results showed that the model and inhibitor groups had remarkably higher relative protein expression levels of p-Smad3 and TGF-β1 than the normal group (p<0.05), and they were markedly lowered in the inhibitor group compared with those in the model group (p<0.05). According to the qPCR results, the expression level of miR-21 was notably elevated in both model group and inhibitor group compared with that in the normal group (p<0.05), and there was no difference in the expression level of miR-21 between the former two groups (p>0.05). Finally, based on the color Doppler ultrasonography findings, the levels of the hemodynamic indicators substantially declined in both model group and inhibitor group compared with those in the normal group (p<0.05), and they were notably higher in the inhibitor group than those in the model group. CONCLUSIONS: We found that miR-21 regulates the TGF-β signaling pathway to affect the hemodynamics in the rats with proliferative diabetic retinopathy.