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| 保护素D1对痛风性肾病小鼠的保护作用及机制研究 |
| Protective effect and mechanism of protectin D1 in gouty nephropathy mice |
| 投稿时间：2026-01-28 修订日期：2026-08-14 |
| DOI： |
| 中文关键词: 保护素D1 痛风性肾病 巨噬细胞 炎症 |
英文关键词: protectin D1 gouty nephropathy Macrophage Inflammation
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| 基金项目:湖北省卫生健康委员会中医药科研项目(ZY2021M054)；中部战区总医院育英计划项目(ZZYFH202120) |
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| 中文摘要: |
| 目的 探讨保护素D1(PD1)对痛风性肾病小鼠的保护作用及机制研究。方法 选择SPF级C57BL/6雄性小鼠45只,随机分成为3组:对照组、模型组和PD1组,通过连续14天灌胃腺嘌呤(100mg/kg/d)和乙胺丁醇(250mg/kg/d)构建痛风性肾病小鼠模型,PD1组每天腹腔注射0.5mg/kg PD1,对照组和模型组给予等量生理盐水。检测小鼠尿酸(UA)、肌酐(Cr)和尿素氮(BUN)水平。苏木素-伊红(HE)染色观察各组小鼠肾脏病理情况,流式细胞术检测肾脏组织巨噬细胞细胞表达,酶联免疫吸附法(ELUSA)法检测各组小鼠肾脏组织白介素(IL)-1、IL-10和肿瘤坏死因子(TNF)-α含量。结果 与对照组比较,模型组血清UA、Cr和BUN水平明显升高(P<0.05)；与模型组相比,PD1组血清UA、Cr和BUN水平明显降低(P<0.05)。HE染色显示,模型组小鼠肾小球萎缩,肾小管水肿、坏死,胞浆出现针形结晶,而PD1组小鼠肾脏组织病变较模型组明显改善。相较于对照组,模型组小鼠肾脏组织M1型巨噬细胞比例明显增加,M2型巨噬细胞比例明显降低(P<0.05)；相较于模型组,PD1组小鼠肾脏M1型巨噬细胞比例显著减少,M2型巨噬细胞比例增加(P<0.05)。与对照组相比,模型组小鼠肾脏IL-1和TNF-α表达升高,IL-10表达降低(P<0.05)；而与模型组相比,PD1组小鼠肾脏IL-1和TNF-α表达降低,IL-10表达升高(P<0.05)。结论 PD1可降低血UA水平,同时通过促进巨噬细胞向M2型极化,降低肾脏组织炎症,发挥保护作用。 |
| 英文摘要: |
| Objective To investigate the protective effect and mechanism of protectin D1 (PD1) in gouty nephropathy mice. Methods Forty-five male C57BL/6 mice were randomly divided into three groups: control group, model group, and PD1 group. A gouty nephropathy mouse model was established by continuous gavage administration of adenine (100 mg/kg/d) and ethambutol (250 mg/kg/d) for 14 days. The PD1 group received daily intraperitoneal injections of PD1 (0.5 mg/kg), while the control and model groups received an equivalent volume of saline. Serum levels of uric acid (UA), creatinine (Cr), and blood urea nitrogen (BUN) were measured. Renal pathology was observed using hematoxylin-eosin (HE) staining. Flow cytometry was employed to detect macrophage subsets in renal tissue. The levels of interleukin (IL)-1β, IL-10, and tumor necrosis factor (TNF)-α in renal tissue were quantified by enzyme-linked immunosorbent assay (ELISA). Results?Compared with the control group, serum levels of UA, Cr, and BUN were significantly elevated in the model group (P < 0.05). Compared with the model group, these levels (UA, Cr, BUN) were significantly reduced in the PD1 group (P < 0.05). HE staining revealed glomerular atrophy, renal tubular edema, necrosis, and needle-shaped crystals in the cytoplasm of renal tubular cells in the model group. In contrast, renal tissue lesions were markedly improved in the PD1 group compared to the model group. Flow cytometry demonstrated that compared to the control group, the expression of M1 macrophages was significantly increased, while M2 macrophage expression was significantly decreased in the renal tissue of the model group (P < 0.05). Compared to the model group, the PD1 group exhibited significantly reduced M1 macrophage expression and increased M2 macrophage expression in the kidney (P < 0.05). ELISA results showed that compared to the control group, renal expression of IL-1β and TNF-α was increased, and IL-10 expression was decreased in the model group (P < 0.05). Conversely, compared to the model group, the PD1 group exhibited decreased expression of IL-1β and TNF-α, and increased expression of IL-10 in renal tissue (P < 0.05). Conclusion PD1 exerts a protective effect against gouty nephropathy by promoting macrophage polarization towards the M2 phenotype. |
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