Abstract
Danhong injection (DHI) restrains diabetic retinopathy and nephropathy (DR and DN) advancement in diabetic mice. However, the downstream mechanism of its modulation is not fully studied. Diabetic model mice (db/db mice) were intravenously injected with DHI and corresponding virus particles. MiR-30d-5p and JAK1 were detected. The body weight and fasting blood glucose mice were measured every 4 weeks. The renal tissues and serum of mice were collected, and the contents of creatinine and blood urea nitrogen were biochemically analyzed. IL-6, IFN-γ and TNF-α were detected by ELISA, with the pathological conditions of renal tissues in mice by He staining, and the adjustment conditions by TUNEL. Human retinal pigment epithelium (ARPE-19) cells were selected to induce DR model in vitro by high glucose, and exposed to DHI for treatment. The corresponding plasmids were transfected, and miR-30d-5p and JAK1 were detected, with the proliferation ability by plate cloning, apoptosis by flow cytometry, and cell migration ability by Transwell. The angiogenesis ability of cells was assessed by tube formation assay. The targeting relationship between miR-30d-5p and JAK1 was detected. The results manifested that miR-30d-5p was declined in DR and DN, while JAK1 expression was elevated. DHI was able to improve DR and renal injury. DHI could regulate the miR-30d-5p-JAK1 axis in vivo, and miR-30d-5p targeted and regulated JAK1. Upregulation of miR-30d-5p or inhibition of JAK1 could improve DR and renal injury. The results implies that DHI can repress the development of DR and DN by elevating miR-30d-5p and targeting JAK1.