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首页> 外文期刊>Drug Design, Development and Therapy >Hirudin Protects Against Kidney Damage in Streptozotocin-Induced Diabetic Nephropathy Rats by Inhibiting Inflammation via P38 MAPK/NF-κB Pathway
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Hirudin Protects Against Kidney Damage in Streptozotocin-Induced Diabetic Nephropathy Rats by Inhibiting Inflammation via P38 MAPK/NF-κB Pathway

机译：血红素通过P38 MAPK / NF-κB途径抑制炎症来防止链脲佐菌素诱导的糖尿病肾病大鼠肾脏损伤

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Background: Inflammation-induced podocyte apoptosis plays an important role in kidney injury during diabetic nephropathy (DN). Hirudin (HIR), a natural compound extracted from leeches, can inhibit inflammation. However, whether HIR can protect the kidneys against inflammation during DN is unknown. In the present study, we aimed to study the effects of HIR on kidney damage in a DN rat model and explore its anti-inflammatory properties. Methods: A streptozotocin-induced DN rat model was generated, and HIR was administered subcutaneously. Immortal podocytes and primary peritoneal macrophages were used for vitro studies. Hematoxylin and eosin staining was used to evaluate renal pathological changes; quantitative polymerase chain reaction and immunoblotting were used to detect gene expression; and TUNEL staining was used to detect apoptotic cells. Results: Our results showed that HIR protected against renal injury, as indicated by kidney weight/body weight, serum creatinine, renal pathological changes, blood urea nitrogen, and detection of urine proteins. Notably, HIR treatment reduced macrophage infiltration, pro-inflammatory cytokine expression, and podocyte apoptosis in the kidney tissues of DN rats. In vitro, high glucose (HG) induced the activation of M1 macrophages, which was accompanied by increased podocyte apoptosis. HIR could decrease HG-induced podocyte apoptosis and suppress pro-inflammatory cytokine expression in podocytes in vitro. This was achieved via inhibition of p38 MAPK/NF-κB activation in renal tissues and podocytes. Conclusion: HIR could inhibit inflammation via the p38 MAPK/NF-κB pathway, prevent podocyte apoptosis, and protect against kidney damage in a DN rat model.
机译：背景：炎症诱导的足细胞凋亡在糖尿病肾病（DN）期间在肾脏损伤中发挥着重要作用。 HIRUDIN（HIR），从水蛭中提取的天然化合物，可以抑制炎症。然而，在DN期间，HIR是否可以保护肾脏免受炎症。在本研究中，我们旨在研究HIR对DN大鼠模型中肾损伤的影响，探讨其抗炎性质。方法：产生了链脲佐菌素诱导的DN大鼠模型，皮疹皮下给药。不朽的大织物和原发性腹膜巨噬细胞用于体外研究。苏木精和曙红染色用于评估肾病病理变化;定量聚合酶链反应和免疫印迹用于检测基因表达;和TUNEL染色用于检测凋亡细胞。结果：我们的研究结果表明，HIR保护肾损伤，如肾脏重量/体重，血清肌酐，肾病理变化，血尿素氮和检测尿蛋白所表明。值得注意的是，HIR治疗降低了DN大鼠肾组织中的巨噬细胞浸润，促炎细胞因子表达和泛骨细胞凋亡。体外，高葡萄糖（Hg）诱导M1巨噬细胞的活化，伴随着凋亡的增加的细胞凋亡。 HIR可以减少HG诱导的泛骨细胞凋亡，体外抑制诱导诱导细胞因子表达。这是通过抑制肾组织和多粒细胞的P38 MAPK / NF-κB活化来实现的。结论：HIR可以通过P38 MAPK / NF-κB途径抑制炎症，预防多细胞凋亡，防止DN大鼠模型中的肾脏损伤。

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