Abstract
Materials and Methods The components with oral bioavailability ≥30% and drug similarity ≥0.18 were screened by the Traditional Chinese Medicine System Pharmacology Database and Analysis Platform (TCMSP), and the effective grouping of Compound-Xueshuantong Capsule was obtained. At the same time, the targets of each drug active component in the Compound-Xueshuantong Capsule were obtained by searching the TCMSP. The effective components and targets of the Compound-Xueshuantong Capsule were annotated by the UniProt database, and the disease treatment targets were searched by the GeneCards database. The disease treatment target is intersected with the drug target and the Wayne diagram is drawn by VennDiagram. The active ingredient targets of the intersection and Compound-Xueshuantong Capsule were inputted into Cytoscape 3.7.2 software to construct the active ingredient-target-disease interaction network. The above targets were inputted into the String database for protein-protein interaction network prediction. Finally, by using the DAVID database, GO and KEGG enrichment analysis was carried out to reveal the potential signal pathway of the Compound-Xueshuantong Capsule in diabetic retinopathy treatment. Results 93 active components of the Compound-Xueshuantong Capsule and 92 targets for treating diabetic retinopathy were screened. The main active components of the Compound-Xueshuantong Capsule in treating diabetic retinopathy were quercetin, luteolin, kaempferol, beta-sitosterol, isorhamnetin, and tanshinone IIa. The effect of the Compound-Xueshuantong Capsule on diabetic retinopathy may be related to IL6, EFGR, CASP3, and VEGFA. In addition, the treatment of diabetic retinopathy mainly involves in the regulation of nuclear receptors and transcription factors in vivo. The target of the Compound-Xueshuantong Capsule in diabetic retinopathy treatment is significantly enriched in the AGE-RAGE signal pathway, TNF signal pathway, HIF-1 signal pathway, and VEGF signal pathway in diabetic complications. Conclusion Compound-Xueshuantong Capsule can treat diabetic retinopathy through multitarget, multipathway, and multipathway regulation of the biomolecular network. The potential biological mechanism of the Compound-Xueshuantong Capsule in diabetic retinopathy treatment may be related to the AGE-RAGE signal pathway, TNF signal pathway, HIF-1 signal pathway, and VEGF signal pathway in diabetic complications, but these findings still need to be confirmed by further clinical research.
Highlights
Diabetes is a disease that affects the organs and the blood glucose metabolism of all organs throughout the body
Collection and Screening of Active Components. e active components of SanQi, HuangQi, DanShen, and XuanSheng in Compound-Xueshuantong Capsule were searched in the TCMSP database. e active components of the Compound-Xueshuantong Capsule were obtained by using oral bioavailability (OB) ≥30% and drug-like (DL) ≥0.18 as screening conditions [9] (OB represents the oral availability of drug components, and DL refers to the similarity between ingredients and known drugs)
Other studies have shown that kaempferol inhibits the activation of the Src-Akt1-ERK1/2 signal pathway by targeting vascular endothelial growth factor (VEGF) and PGF and inhibits the angiogenesis of human retinal endothelial cells [19], which may permit the treatment of neovascularization caused by diabetic retinopathy
Summary
Diabetes is a disease that affects the organs and the blood glucose metabolism of all organs throughout the body. It is mainly divided into type 1 and type 2 diabetes, which can cause microvascular diseases such as brain, kidney, heart, and retina. Hyperglycemia can damage retinal capillaries through a variety of metabolic pathways; on the other hand, it can Evidence-Based Complementary and Alternative Medicine induce apoptosis of retinal pericytes, leading to occlusion, ischemia, and leakage of capillaries [2]. Recent studies have shown that chronic inflammation and neurodegeneration may further aggravate retinal ischemia and hypoxia [3]. Chronic ischemia and hypoxia, which lead to retinal punctured hemorrhage, microaneurysm, and hard exclusion, are the main pathological features of NPDR. The activated renin-angiotensin system (RAS) [2] and vascular endothelial growth factor (VEGF) [3] accelerated the deterioration of NPDR by promoting the proliferation of endothelial cells and new blood vessels, which eventually led to the progression of NPDR to PDR
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