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吴跃跃, 陈灶萍, 盛励, 等. 脂联素受体介导小檗碱减轻糖尿病肾病肾脏脂毒性[J]. 中国临床医学, 2024, 31(3): 433-439. DOI: 10.12025/j.issn.1008-6358.2024.20231508
引用本文: 吴跃跃, 陈灶萍, 盛励, 等. 脂联素受体介导小檗碱减轻糖尿病肾病肾脏脂毒性[J]. 中国临床医学, 2024, 31(3): 433-439. DOI: 10.12025/j.issn.1008-6358.2024.20231508
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WU Y Y, CHEN Z P, SHENG L, et al. Adiponectin receptor mediated berberine to alleviate renal lipid toxicity in mice with diabetic kidney disease[J]. Chin J Clin Med, 2024, 31(3): 433-439. DOI: 10.12025/j.issn.1008-6358.2024.20231508
Citation: WU Y Y, CHEN Z P, SHENG L, et al. Adiponectin receptor mediated berberine to alleviate renal lipid toxicity in mice with diabetic kidney disease[J]. Chin J Clin Med, 2024, 31(3): 433-439. DOI: 10.12025/j.issn.1008-6358.2024.20231508
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脂联素受体介导小檗碱减轻糖尿病肾病肾脏脂毒性

Adiponectin receptor mediated berberine to alleviate renal lipid toxicity in mice with diabetic kidney disease

    摘要
  • 摘要:
    目的 探讨脂联素受体1/2(adiponectin receptor 1/2, AdipoR1/R2)介导小檗碱减轻糖尿病肾病肾脏脂毒性的作用。
    方法 选择C57BLKS/J db/db小鼠，以db/m小鼠为对照，分为4组，每组8只，分别给予小檗碱(150 mg·kg﹣1·d﹣1)或安慰剂灌胃，连续12周。干预结束后测定血糖、血脂、尿微量白蛋白/肌酐比值、尿白蛋白排泄率；取肾脏组织进行病理形态学检查，通过油红O染色、免疫组化、ELISA和Western印迹测定肾脏脂质沉积、AdipoR1/R2表达、转化生长因子β1(TGF-β1)及Ⅳ型胶原(Col-Ⅳ)表达等。用人肾小球内皮细胞系(HGEC)验证AdipoR1/R2介导小檗碱减轻肾脏脂毒性的作用。
    结果 小檗碱干预后，db/db小鼠体质量减轻，血糖、血脂、蛋白尿减少(P＜0.05)，肾脏脂质沉积、病理改变减轻；db/db小鼠肾脏组织AdipoR1/R2表达上调，TGF-β1、Col-Ⅳ表达下调，PPAR-α、p-AMPK表达上调(P＜0.05)。db/db小鼠血清干预后，高脂培养的HGEC细胞中TGF-β1、Col-Ⅳ表达下调，PPAR-α、p-AMPK表达上调(P＜0.05)；沉默HGEC细胞上的AdipoR1/R2后，TGF-β1、Col-Ⅳ表达上调，PPAR-α及p-AMPK表达下调(P＜0.05)。
    结论 小檗碱可以减轻糖尿病肾病小鼠模型的肾脏脂毒性，该作用可能由脂联素受体介导。

     

    Abstract:
    Objective To explore whether adiponectin receptor 1/2 (AdipoR1/R2) mediates berberine to alleviate renal lipid toxicity in mice with diabetic kidney disease.
    Methods C57BLKS/J db/db mice and db/m mice were selected and divided into 4 groups, with 8 in each group. db/db mice and db/m mice were given berberine (150 mg·kg﹣1·d﹣1) or placebo by gavage for 12 weeks, respectively. After intervention, blood glucose, blood lipids, urinary microalbumin/creatinine ratio and urinary albumin excretion rate were determined. Kidney tissues were taken for pathological examination, and oil red O staining, immunohistochemistry, ELISA and Western blotting were used to examine lipid deposition, AdipoR1/R2 expression and fibrosis markers expressions, etc., respectively. The human glomerular endothelial cell line (HGEC) was used to verify the role of AdipoR1/R2 in berberine alleviating renal lipid toxicity.
    Results After berberine intervention, the body weight, blood glucose, lipids, proteinuria, renal lipid deposition, and renal pathological changes decreased in db/db mice (P < 0.05); the expressions of AdipoR1 and AdipoR2 increased, expressions of TGF-β1 and Col-Ⅳ decreased, and the expressions of PPAR-α and p-AMPK increased in kidney tissue of db/db mice (P < 0.05). In high-fat cultured HGEC cells treated with berberine-treated db/db mouse serum, the expressions of TGF-β1 and Col-Ⅳ decreased, while the expressions of PPAR-α and p-AMPK increased (P < 0.05); after AdipoR1/R2 on HGEC cells were silenced, the expressions of TGF-β1 and Col-Ⅳ increased, while the expressions of PPAR-α and p-AMPK decreased (P < 0.05).
    Conclusions Berberine can reduce renal lipid toxicity in diabetic nephropathy mice, and adiponectin receptor may mediate this effect of berberine.

     

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