Mesangial proliferative glomerulonephritis (MsPGN) is a common type of glomerular disease characterized by immune complex deposition and inflammation in the kidney, leading to renal dysfunction. Currently, treatment options for MsPGN are limited, and there is a need for effective therapeutic interventions. Hesperidin (HSP), a natural flavonoid glycoside, has shown promising anti-inflammatory and antioxidant properties in various disease models. This study aimed to investigate the therapeutic potential of HSP for MsPGN and explore its possible mechanism of action. A male Wistar rat model of MsPGN was established via tail vein injection of Thy-1 monoclonal antibody, and the rats were divided into four groups: Control, MsPGN, MsPGN + HSP, and MsPGN + Prednisone. After 7 days of intervention, the therapeutic effects of HSP were evaluated through biochemical and histological analyses. Our results demonstrated that HSP treatment significantly reduced the levels of blood urea nitrogen, serum creatinine, total cholesterol, and triglycerides, and improved renal pathology. Additionally, pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, interleukin-2, and monocyte chemoattractant protein-1, were markedly decreased. Immunofluorescence analysis revealed reduced levels of immunoglobulin G and C5b-9, along with decreased immune complex deposition in the kidneys. Furthermore, HSP downregulated the phosphorylation levels of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3), suggesting modulation of the JAK/STAT pathway. In conclusion, HSP might effectively alleviate renal injury, reduce renal inflammatory response, and inhibit renal immune complex deposition, potentially through the suppression of the JAK/STAT pathway.
Keywords: JAK/STAT pathway; hesperidin; immune complex deposition; mesangial proliferative glomerulonephritis; renal injury.
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