Eighteen Sprague-Dawley rats were randomly divided into control group (n=5) and model group (n=13). The model group was injected intraperitoneally with streptozotocin(STZ) to establish a diabetic rat model. Eight weeks after STZ injection, successfully modeled diabetic rats were randomly divided into diabetic model group (n=6, with 1 rat dead due to hyperglycemia) and hirudin treatment group (n=5). The hirudin treatment group was administered 5 U hirudin while the control group and diabetic model group were injected subcutaneously with equal volume of phosphate buffered saline once daily for six weeks. During the experiment, the rats' body weight and random blood glucose levels were monitored every two weeks. After 6 weeks of treatment, renal function parameters were measured, and the levels of tumor necrosis factor α (TNF-α), transforming growth factor β1 (TGF-β1), interleukin 6 (IL-6), fibronectin (FN), nephrin, collagen-Ⅳ (COL-Ⅳ), and proteins related to the Janus kinase 2 (JAK2)/signal transduction and transcriptional activator 3 (STAT3) signaling pathway were assessed. Renal histopathological changes were also observed.

Compared with the control group, the diabetic model group showed significantly elevated random blood glucose and renal function parameters during the 6-week treatment (both P < 0.05), along with a significant decrease in body weight(P < 0.05) and renal pathological damage. Compared with the diabetic model group, the renal function parameters of hirudin treatment group were significantly decreased (P < 0.05), the renal pathological damage was ameliorated. Compared with the control group, the expression levels of FN, COL-Ⅳ, TNF-α, TGF-β1, IL-6, p-JAK2, and p-STAT3 in the kidneys of diabetic model group were significantly increased (all P < 0.05), while the expression of nephrin was reduced (P < 0.05). Compared with the diabetic group, the expression level of FN, COL-Ⅳ, TNF-α, TGF-β1, IL-6, p-JAK2, and p-STAT3 in hirudin treatment group were significantly reduced (all P < 0.05), while the nephrin expression increased (P < 0.05).

Hirudin improved renal pathological changes in diabetic rats, and its mechanism may be related to the decrease of fibrosis-related factors and inhibition of the activation of the JAK2/STAT3 pathway.

Eighteen Sprague-Dawley rats were randomly divided into control group (n=5) and model group (n=13). The model group was injected intraperitoneally with streptozotocin(STZ) to establish a diabetic rat model. Eight weeks after STZ injection, successfully modeled diabetic rats were randomly divided into diabetic model group (n=6, with 1 rat dead due to hyperglycemia) and hirudin treatment group (n=5). The hirudin treatment group was administered 5 U hirudin while the control group and diabetic model group were injected subcutaneously with equal volume of phosphate buffered saline once daily for six weeks. During the experiment, the rats' body weight and random blood glucose levels were monitored every two weeks. After 6 weeks of treatment, renal function parameters were measured, and the levels of tumor necrosis factor α (TNF-α), transforming growth factor β1 (TGF-β1), interleukin 6 (IL-6), fibronectin (FN), nephrin, collagen-Ⅳ (COL-Ⅳ), and proteins related to the Janus kinase 2 (JAK2)/signal transduction and transcriptional activator 3 (STAT3) signaling pathway were assessed. Renal histopathological changes were also observed.

Compared with the control group, the diabetic model group showed significantly elevated random blood glucose and renal function parameters during the 6-week treatment (both P < 0.05), along with a significant decrease in body weight(P < 0.05) and renal pathological damage. Compared with the diabetic model group, the renal function parameters of hirudin treatment group were significantly decreased (P < 0.05), the renal pathological damage was ameliorated. Compared with the control group, the expression levels of FN, COL-Ⅳ, TNF-α, TGF-β1, IL-6, p-JAK2, and p-STAT3 in the kidneys of diabetic model group were significantly increased (all P < 0.05), while the expression of nephrin was reduced (P < 0.05). Compared with the diabetic group, the expression level of FN, COL-Ⅳ, TNF-α, TGF-β1, IL-6, p-JAK2, and p-STAT3 in hirudin treatment group were significantly reduced (all P < 0.05), while the nephrin expression increased (P < 0.05).

Hirudin improved renal pathological changes in diabetic rats, and its mechanism may be related to the decrease of fibrosis-related factors and inhibition of the activation of the JAK2/STAT3 pathway.