Salvianolate Ameliorates Renal Damage Induced by C-BSA in Membranous Nephropathy Rats Through Inhibiting Hypercoagulable State and Alleviating Podocyte Injury

Abstract

Background Membranous nephropathy (MN), one of the primary pathogenic forms of adult nephrotic syndromes, frequently coexists with hypercoagulability and hyperviscosity. MN is prone to thrombosis, embolism, and other complications, leading to the accelerated occurrence of glomerulosclerosis and renal fibrosis. Therefore, it is particularly important to promote blood circulation and remove stasis through anticoagulant therapy. Salvianolate (SAL) is a Chinese patent anticoagulant commonly used in clinical practice to promote blood circulation and remove blood stasis. SAL plays an important role in alleviating urinary protein and renal pathological damage in MN patients. Objectives In the present study, we aimed to investigate the kidney-protective effect of SAL on MN in a rat model. Materials and Methods The rat model of MN was established by tail vein injection of cationic bovine serum albumin (C-BSA). After the treatment, urinary proteins, hypercoagulable state index (fibrinogen (Fib), D dimer (D-D)), hepatic and renal functions, renal pathology, and podocyte marker proteins were analyzed to explore the renal protective effect of SAL on MN rats and its underlying mechanism. Results In the modeled rats, we discovered a significant rise in urinary protein, a hypercoagulable state, and hypoproteinemia. Additionally, the expressions of Wilms’ tumor protein 1 (WT-1), podocalyxin (PCX), and vascular endothelial growth factor (VEGF) in renal tissues were significantly downregulated, indicating remarkable pathological damage to podocytes and renal tissues in MN rats. The expressions of the above-mentioned indices could be greatly reversed by SAL, which could also regulate the hypercoagulable state and suppress podocyte damage and renal pathological harm. Conclusion Our results suggested that the renal protective effect of SAL on C-BSA-induced MN was related to its ability to inhibit hypercoagulable states, upregulate the expressions of WT-1, PCX, and VEGF in the renal tissue, and repair podocyte injury.