| 引用本文:李静1，尚平平1，杨洋2，何姣1，乔博灵1.龙胆苦苷对果糖诱导小鼠高尿酸血症的作用[J].世界中医药,2024,(01):. |
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| 龙胆苦苷对果糖诱导小鼠高尿酸血症的作用 |
| Effect of Gentiopicroside on Fructose-Induced Hyperuricemia in Mice |
| 投稿时间：2022-07-05 |
| DOI：10.3969/j.issn.1673-7202.2024.01.001 |
| 中文关键词: 龙胆苦苷 果糖 高尿酸血症 尿酸 黄嘌呤氧化酶 氧化应激 炎症 肾脏保护 |
| English Keywords:Gentiopicroside Fructose Hyperuricemia Uric acid Xanthine oxidase Oxidative stress Inflammation Kidney protection |
| 基金项目:国家自然科学基金项目（82003928）——基于ERS-UPR跨膜效应蛋白研究秦艽治疗NAFLD的有效物质基础及作用机制；陕西省教育厅专项科研计划项目（2013JK0809）——龙胆苦苷抗高尿酸血症的作用机制研究；陕西省教育厅省级重点实验室科研计划项目（11JS089）——玄参黑度的研究 |
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| 中文摘要: |
| 目的：研究龙胆苦苷对果糖诱导小鼠高尿酸血症的治疗作用。方法：昆明种小鼠连续饮用10%果糖溶液12周以制备高尿酸症小鼠模型，从第9周开始，别嘌呤醇组，龙胆苦苷高、中、低剂量组(80 mg/kg、40 mg/kg、20 mg/kg-)每天灌胃给药1次，共给药4周。末次给药后取血，检测血清谷丙转氨酶（GPT）、谷草转氨酶（GOT）、尿酸（UA）、肌酐（Cr）和血尿素氮（BUN）水平，苏木精-伊红（HE）染色观察肝、肾组织的变化；酶联免疫吸附试验法检测肾组织中超氧化物歧化酶（SOD），丙二醛（MDA），肿瘤坏死因子α（TNF-α）和白细胞介素-6（IL-6）水平，比色法和蛋白质免疫印迹法检测肝组织中黄嘌呤氧化酶（XOD）活性及蛋白表达水平。结果：与模型组比较，龙胆苦苷各给药组小鼠血清GPT、GOT、UA、Cra和BUN水平显著降低（P<0.01），肝、肾病理学变化有所改善；肾脏SOD水平显著升高（P<0.01），MDA、TNF-α和IL-6水平显著降低（P<0.01）；同时肝脏XOD的活性及蛋白表达水平显著下调（P<0.01或P<0.05）。结论：龙胆苦苷通过降低XOD活性和表达，降低尿酸水平，进而减轻肾脏氧化应激和炎症水平，达到肾脏保护作用。 |
| English Summary: |
| To investigate the effect of gentiopicroside on fructose-induced hyperuricemia in mice.Methods:The hyperuricmia KM mice were induced by feeding water containing 10% fructose for consecutive 12 weeks.During the period from 9th week to 12th week，mice from allopurinol group and gentiopicroside groups(80，40，20 mg/kg) received allopurinol and gentiopicroside，respectively by intragastric administration once a day for 4 weeks.The blood was collected after the last administration，to detect glutamic pyruvic transaminase(GPT)，glutamic oxaloacetic transaminase(GOT)，uric acid(UA)，creatinine(Cr) and blood urea nitrogen(BUN) in serum.H&E staining was performed to observe the changes in liver and kidney tissues.Superoxide dismutase(SOD)，malondialdehyde(MDA)，tumor necrosis factor-α(TNF-α) and interleukin 6(IL-6) in kidney tissues were measured by enzyme-linked immunosorbent assay(ELISA)，and the activity and expression of XOD in liver were tested by colorimetry and Western Blotting.Results:Compared with the model group，the mice in gentiopicroside groups showed a decrease in serum GPT，GOT，UA，Cr and BUN(P<0.01)，with improvement in pathological changes of liver and kidney.The SOD in kidney were increased，whereas MDA，TNF-α and IL-6 were lowered(P<0.01).Moreover，gentiopicroside reduced the activity and protein expression of XOD in liver(P<0.01 or P<0.05).Conclusion:Gentiopicroside down-regulates UA in the fructose-induced hyperuricemia mice by modulating the activity and the expression of XOD，thereby alleviating oxidative stress，and inflammation and protecting the kidney. |
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