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中国精品科技期刊2020
路子佳,高宇,谢瑶,等. 海洋鱼低聚肽复方制剂降尿酸及其修复肾脏损伤的功效[J]. 食品工业科技,2025,46(18):425−434. doi: 10.13386/j.issn1002-0306.2024110060.
引用本文: 路子佳,高宇,谢瑶,等. 海洋鱼低聚肽复方制剂降尿酸及其修复肾脏损伤的功效[J]. 食品工业科技,2025,46(18):425−434. doi: 10.13386/j.issn1002-0306.2024110060.
LU Zijia, GAO Yu, XIE Yao, et al. Effects of Marine Fish Oligopeptide Composite Preparation on Reducing Uric Acid and Repairing Kidney Damage[J]. Science and Technology of Food Industry, 2025, 46(18): 425−434. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024110060.
Citation: LU Zijia, GAO Yu, XIE Yao, et al. Effects of Marine Fish Oligopeptide Composite Preparation on Reducing Uric Acid and Repairing Kidney Damage[J]. Science and Technology of Food Industry, 2025, 46(18): 425−434. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024110060.

海洋鱼低聚肽复方制剂降尿酸及其修复肾脏损伤的功效

Effects of Marine Fish Oligopeptide Composite Preparation on Reducing Uric Acid and Repairing Kidney Damage

  • 摘要: 目的:研究海洋鱼低聚肽复方制剂(Marine Fish Oligopeptide Compound Preparation,MFOCP)降尿酸及其修复肾脏损伤的作用及机制。方法:利用次黄嘌呤和氧嗪酸钾构建高尿酸小鼠模型,造模成功后,采用不同剂量MFOCP干预4周,通过测定高尿酸小鼠血清中的黄嘌呤氧化酶(Xanthine Oxidase,XOD)的活性,尿酸(Uric Acid,UA)、肌酐(Creatinine,Cr)及尿素氮(Blood Urea Nitrogen,BUN)的含量,血清及肾脏组织中炎症因子的含量,肝脏组织中XOD、腺苷脱氨酶(Adenosine Deaminase,ADA)的活性,肾脏组织病理学检测,测定肾脏中尿酸转运和重吸收蛋白的mRNA表达量,评价MFOCP的降尿酸及其修复肾脏损伤的作用。结果:MFOCP低、中、高剂量可显著降低模型小鼠血清中UA含量(P<0.01),XOD的活性(P<0.05)及肾脏组织中炎症因子白细胞介素6(Interleukin-6,IL-6)的含量(P<0.05),可改善模型小鼠肾脏组织病变情况,MFOCP中、高剂量还可显著降低血清中Cr和BUN的含量(P<0.01),显著提高小鼠肾脏组织中有机阴离子转运蛋白2(Organic Anion Transporter 2,OAT2)、三磷酸腺苷结合转运蛋白G(Adenosine Triphosphate Binding Cassette Transporter G2,ABCG2)mRNA的相对表达量(P<0.05)。结论:MFOCP可有效降低高尿酸模型小鼠血清中尿酸水平,修复高尿酸导致的肾脏病理损伤,其作用机制,一方面可通过降低血清中XOD的活性减少尿酸合成;另一方面,可通过调控尿酸转运蛋白OAT2和ABCG2的mRNA表达量促进尿酸的排泄。

     

    Abstract: Objective: To investigate the effects of marine fish oligopeptide composite preparation (MFOCP) on reducing uric acid and repairing kidney damage and the underlying mechanisms. Methods: A high uric acid mouse model was established using hypoxanthine and potassium oxonate. After successful modeling, different doses of MFOCP were used to intervene for 4 weeks. The activity of xanthine oxidase (XOD), levels of uric acid (UA), creatinine (Cr), and blood urea nitrogen (BUN) in the serum of high uric acid mice, levels of inflammatory factors in serum and kidney tissue, activities of XOD and adenosine deaminase in liver tissue, pathological detection of kidney tissue, and mRNA expressions of uric acid transport and reabsorption proteins in the kidney were measured to evaluate the uric acid reducing effect of MFOCP and its role in repairing kidney damage. Results: The low, medium, and high doses of MFOCP significantly reduced serum UA content (P<0.01), XOD activity (P<0.05), and inflammatory cytokine interleukin-6 content in kidney tissue (P<0.05) and ameliorated renal tissue lesions in the model mice. The medium and high doses of MFOCP also significantly reduced serum Cr and BUN contents (P<0.01), and significantly increased the relative expression levels of organic anion transporter 2 (OAT2) mRNA and adenosine triphosphate binding cassette transporter G2 (ABCG2) mRNA in kidney tissue (P<0.05). Conclusion: MFOCP effectively reduced serum uric acid levels in high uric acid model mice and repaired the kidney damage caused by high uric acid, which mechanism of action might be by reducing the activity of XOD in the serum to decrease uric acid synthesis or regulating the mRNA expression levels of uric acid transporters OAT2 and ABCG2 to promote uric acid excretion.

     

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