瑞舒伐他汀钙对高尿酸血症大鼠炎症因子及动脉损伤的影响及其代谢组学研究

doi:10.12114/j.issn.1007-9572.2026.0114

中国全科医学 ›› 2026, Vol. 29 ›› Issue (36): 5393-5400.DOI: 10.12114/j.issn.1007-9572.2026.0114

• 论著 • 上一篇

瑞舒伐他汀钙对高尿酸血症大鼠炎症因子及动脉损伤的影响及其代谢组学研究

李艳¹, 伊丽米努尔·阿卜杜吾甫尔², 迪丽达尔·希力甫¹^,^*()

1．830000　新疆维吾尔自治区乌鲁木齐市，新疆医科大学第一附属医院心脏重症监护室
2．835000　新疆维吾尔自治区伊犁哈萨克自治州伊宁市，伊犁哈萨克自治州新华医院心血管内一科

收稿日期:2026-04-10 修回日期:2026-09-20 出版日期:2026-12-20 发布日期:2026-10-30
通讯作者: 迪丽达尔·希力甫
作者贡献：
李艳提出主要研究目标，负责研究的构思与设计，研究的实施，撰写论文；伊丽米努尔·阿卜杜吾甫尔进行数据的收集与整理，统计学处理，图、表的绘制与展示；迪丽达尔·希力甫进行论文的修订，文章的质量控制与审查，对文章整体负责，监督管理。
基金资助:
新疆维吾尔自治区卫健委"天山英才"医学骨干项目(TSYC202301B075)

Effects of Rosuvastatin Calcium on Inflammatory Factors and Arterial Injury in Hyperuricemic Rats and Its Metabolomics Analysis

LI Yan¹, YILIMINUER· Abuduwufuer², DILIDAER· Xilifu¹^,^*()

1. Cardiac Care Unit, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830000, China
2. Department of Cardiology (Ward 1), Xinhua Hospital of Ili Kazakh Autonomous Prefecture, Yining 835000, China

Received:2026-04-10 Revised:2026-09-20 Published:2026-12-20 Online:2026-10-30
Contact: DILIDAER· Xilifu

摘要/Abstract

摘要： 背景高尿酸血症是心血管疾病的重要独立危险因素，可通过激活炎症反应、诱导氧化应激等途径导致血管内皮损伤，但其致血管内皮损伤的具体机制及有效的干预策略尚未完全阐明。目的探讨不同剂量瑞舒伐他汀钙对高尿酸血症大鼠肾功能、炎症因子水平及大、小动脉结构的调控作用，为临床防治高尿酸相关血管损伤提供实验依据。方法本研究的实验时间为2021年3月—2024年8月。选取60只8周龄SD大鼠，采用随机数字表法分为空白对照组、模型组、瑞舒伐他汀钙低剂量组（5 mg·kg-1 ·d-1 ）、瑞舒伐他汀钙高剂量组（10 mg·kg-1 ·d-1 ）及阳性对照组（别嘌呤醇，53.57 mg·kg-1 ·d-1 ），共5组，每组12只。除空白对照组外，其余各组通过酵母提取物粉（YEP，21 g·kg-1 ·d-1 ）灌胃联合氧嗪酸钾盐（OA，200 mg·kg-1 ·d-1 ）腹腔注射构建高尿酸血症模型。自造模第1天起，各药物干预组分别给予对应剂量药物灌胃，连续干预4周。检测大鼠血清尿酸、尿素氮、肌酐、C反应蛋白、肿瘤坏死因子α及白介素6水平，采用组织病理学方法观察腹主动脉、尾动脉等大、小动脉的形态学改变；通过相对和绝对定量同位素标记（iTRAQ）技术筛选各组差异蛋白，结合基因本体论（GO）富集分析与京都基因与基因组百科全书（KEGG）代谢通路分析，探究差异蛋白的功能及相关分子机制。结果组别与时间对血清尿酸、尿素氮、肌酐、C反应蛋白、肿瘤坏死因子α、白介素6水平均存在交互作用（P交互<0.05）；组别和时间对上述指标的主效应均显著（P组别<0.05，P时间<0.05）。实验第2周，模型组、瑞舒伐他汀钙低剂量组、瑞舒伐他汀钙高剂量组、阳性对照组尿酸高于空白对照组，模型组肌酐水平高于空白对照组、瑞舒伐他汀钙高剂量组、阳性对照组（P<0.05）。实验第4周，模型组上述3项指标均高于其他组，瑞舒伐他汀钙高剂量组上述3项指标均低于瑞舒伐他汀钙低剂量组（P<0.05）。实验第2、4周，模型组C反应蛋白、肿瘤坏死因子α、白介素6水平均高于对照组（P<0.05）。实验第4周，瑞舒伐他汀钙低剂量组C反应蛋白高于瑞舒伐他汀钙高剂量组、阳性对照组，瑞舒伐他汀钙高剂量组C反应蛋白低于阳性对照组；瑞舒伐他汀钙低剂量组与阳性对照组肿瘤坏死因子α高于瑞舒伐他汀钙高剂量组；瑞舒伐他汀钙低剂量组白介素6高于瑞舒伐他汀钙高剂量组、低于阳性对照组，瑞舒伐他汀钙高剂量组白介素6低于阳性对照组（P<0.05）。组织病理学结果显示，模型组大鼠动脉中膜平滑肌细胞增殖、内皮细胞脱落、管腔狭窄，外膜纤维结缔组织增生；瑞舒伐他汀钙高剂量组动脉损伤修复最为明显，血管结构接近空白对照组。蛋白组学分析表明，高剂量瑞舒伐他汀钙干预后大鼠蛋白表达谱与空白对照组最为接近（12个上调、14个下调），GO富集分析显示差异蛋白主要参与脂蛋白调控、磷脂外流等生物学过程，KEGG通路分析提示差异蛋白主要富集于脂质代谢相关通路。结论瑞舒伐他汀钙可有效降低高尿酸血症大鼠的血尿酸水平及炎症因子表达，对高尿酸介导的血管损伤具有显著修复作用，且该作用呈剂量依赖性；其机制可能与调控脂质代谢相关蛋白及信号通路有关。

关键词: 高尿酸血症, 瑞舒伐他汀钙, 动脉损伤, 炎症因子, 代谢组学

Abstract:

Background

Hyperuricemia is an important independent risk factor for cardiovascular disease. It can induce vascular endothelial injury through pathways such as activating inflammatory responses and triggering oxidative stress. However, the precise mechanisms of hyperuricemia-induced vascular injury and effective intervention strategies for this condition have not been fully elucidated.

Objective

This study aimed to investigate the regulatory effects of different doses of rosuvastatin calcium on renal function, inflammatory factor levels, and the structure of large and small arteries in hyperuricemic rats, so as to provide an experimental basis for the clinical prevention and treatment of hyperuricemia-related vascular injury.

Methods

The experiments were conducted from March 2021 to August 2024. Sixty 8-week-old Sprague-Dawley (SD) rats were selected and randomly divided into five groups using a random number table, with 12 rats in each group: blank control group, model group, low-dose rosuvastatin calcium group (5 mg·kg^-1 ·d^-1 ), high-dose rosuvastatin calcium group (10 mg·kg^-1 ·d^-1 ), and positive control group (allopurinol, 53.57 mg·kg^-1 ·d^-1 ). Except for the blank control group, hyperuricemia models were established in the remaining groups via intragastric administration of yeast extract powder (YEP, 21 g·kg^-1 ·d^-1 ) combined with intraperitoneal injection of potassium oxonate (OA, 200 mg·kg^-1 ·d^-1 ). Starting from the first day of modeling, each drug intervention group received the corresponding dose of drug by gavage daily for 4 consecutive weeks. After intervention, serum levels of uric acid, blood urea nitrogen (BUN), creatinine (Cr), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured. Histopathological examination was performed to observe the morphological changes of large and small arteries, including the abdominal aorta and caudal artery. Isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics was applied to screen differentially expressed proteins between groups. Gene Ontology (GO) enrichment analysis combined with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was then conducted to explore the functions of these differentially expressed proteins and the associated molecular mechanisms.

Results

Significant group-by-time interactions were observed for serum uric acid, BUN, Cr, CRP, TNF-α, and IL-6 (P_interaction<0.05), and both the main effects of group and time on these indicators were statistically significant (P_group<0.05, P_time<0.05). At week 2, serum uric acid levels in the model group, the low-dose rosuvastatin calcium group, the high-dose rosuvastatin calcium group, and the positive control group were significantly higher than those in the blank control group (P<0.05). Serum creatinine level in the model group was significantly higher than those in the blank control group, the high-dose rosuvastatin calcium group, and the positive control group (P<0.05). At the 4th experimental week, the three above-mentioned indicators in the model group were higher than those in both the blank control group and all drug intervention groups, while all three indicators in the high-dose rosuvastatin calcium group were lower than those in the low-dose rosuvastatin calcium group (P<0.05). At both the 2nd and 4th weeks of the experiment, serum levels of CRP, TNF-α, and IL-6 in the model group were higher than positive control group (P<0.05). At the 4th experimental week, serum CRP in the low-dose rosuvastatin calcium group was higher than that in the high-dose rosuvastatin calcium and positive control groups, and lower in the high-dose rosuvastatin calcium group than in the positive control group. TNF-α levels in both the low-dose rosuvastatin calcium and positive control groups were higher than those in the high-dose rosuvastatin calcium group. IL-6 in the low-dose rosuvastatin calcium group was higher than that in the high-dose rosuvastatin calcium group but lower than that in the positive control group, and lower in the high-dose rosuvastatin calcium group than in the positive control group (all P<0.05). Histopathological results showed that rats in the model group exhibited smooth muscle cell proliferation in the arterial tunica media, endothelial cell exfoliation, luminal narrowing, and fibrous connective tissue hyperplasia in the tunica adventitia. The most pronounced repair of arterial injury was observed in the high-dose rosuvastatin calcium group, where the vascular structure closely resembled that of the blank control group. Proteomic analysis showed that, after high-dose intervention, the protein expression profile of the rats most closely resembled that of the blank control group (12 proteins upregulated and 14 downregulated). GO enrichment analysis showed that the differentially expressed proteins were mainly involved in biological processes such as lipoprotein regulation and phospholipid efflux. KEGG pathway analysis indicated that the differentially expressed proteins were mainly enriched in pathways related to lipid metabolism.

Conclusion

Rosuvastatin calcium can effectively reduce serum uric acid levels and inflammatory factor expression in rats with hyperuricemia and exerts a significant reparative effect against hyperuricemia-mediated vascular injury in a dose-dependent manner; its mechanism may be associated with the regulation of lipid metabolism-related proteins and signaling pathways.

Key words: Hyperuricemia, Rosuvastatin calcium, Arterial injury, Inflammatory factors, Metabolomics

中图分类号:

R 589.9

李艳,伊丽米努尔·阿卜杜吾甫尔,迪丽达尔·希力甫. 瑞舒伐他汀钙对高尿酸血症大鼠炎症因子及动脉损伤的影响及其代谢组学研究[J]. 中国全科医学, 2026, 29(36): 5393-5400. DOI: 10.12114/j.issn.1007-9572.2026.0114.
LI Yan,YILIMINUER· Abuduwufuer,DILIDAER· Xilifu. Effects of Rosuvastatin Calcium on Inflammatory Factors and Arterial Injury in Hyperuricemic Rats and Its Metabolomics Analysis[J]. Chinese General Practice, 2026, 29(36): 5393-5400. DOI: 10.12114/j.issn.1007-9572.2026.0114.

图/表 10

参考文献 17

[1]	Mdivnishvili M, Kharebashvili M, Chumburidze V, et al. The impact of hyperuricemia on the progression of atherosclerotic cardiovascular disease[J]. Cureus, 2025, 17(10): e94371. DOI: 10.7759/cureus.94371.
[2]	Du L, Zong Y, Li H R, et al. Hyperuricemia and its related diseases: mechanisms and advances in therapy[J]. Sig Transduct Target Ther, 2024, 9(1): 212. DOI: 10.1038/s41392-024-01916-y.
[3]	Zuo T, Liu X H, Jiang L, et al. Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies[J]. BMC Cardiovasc Disord, 2016, 16(1): 207.
[4]	Piani F, Annesi L, Borghi C. New insights into uric acid metabolism in the pathophysiology of ischaemic heart disease[J]. Eur Cardiol, 2025, 20: e18. DOI: 10.15420/ecr.2024.30.
[5]	Wen m, Yang b, Yu D, et al. Contrastive study of effect of aspirin combined atorvastatin and aspirin alone on hyperuricemia incidence and recurrence rate of stroke in ischemic stroke patients [J]. Chin Gen Pract, 2016, 19(30):3672-3674, 3680.
[6]	Bajaj T, Patel P, Giwa A. Rosuvastatin[M]. Treasure Island: Stat Pearls Publishing, 2025.
[7]	迪丽达尔·希力甫, 赵平, 宋丽娟, 等. 酵母膏联合氧嗪酸钾构建高尿酸血症模型大鼠继发的心血管病变[J]. 中国组织工程研究, 2012, 16(11): 1994-1998.
[8]	Gherghina M E, Peride I, Tiglis M, et al. Uric acid and oxidative stress-relationship with cardiovascular, metabolic, and renal impairment[J]. Int J Mol Sci, 2022, 23(6): 3188.
[9]	Zhang Y, Huang L, Liu R, et al. Dietary 1, 3-diacylglycerol ameliorates hyperuricemiaviadual modulation of urate transporters and inflammasomes in mice[J]. Food Funct, 2025, 16(18): 7253-7265. DOI: 10.1039/d5fo02583d.
[10]	Inkum F, Geng X X, Terkeltaub R, et al. Connecting the dots: gouty arthritis, clonal haematopoiesis and myeloid activation, in a unified inflammation model for atherosclerosis progression[J]. Jt Bone Spine, 2026, 93(3): 105993. DOI: 10.1016/j.jbspin.2025.105993.
[11]	Zhou X F, Liu T X, Xu B Y, et al. Dandelion leaf aqueous extract relieves hyperuricemia and its complications via modulating uric acid metabolism, renal inflammation, and gut microbes[J]. Foods, 2025, 14(22): 3843. DOI: 10.3390/foods14223843.
[12]	迪丽达尔·希力甫, 张向阳. 瑞舒伐他汀钙对高尿酸血症大鼠尿酸及C反应蛋白的影响[J]. 今日健康, 2016, 15(9): 38-39.
[13]	Zhang Z, Wang P, Lei T Y, et al. The role and impact of the IL-6 mediated JAK2-STAT1/3 signaling pathway in the pathogenesis of gout[J]. Front Pharmacol, 2025, 16: 1480844. DOI: 10.3389/fphar.2025.1480844.
[14]	Asiri Y I, Pichaivel M, Parameshwaran S P, et al. Targeting hyperuricemia and NLRP3 inflammasome in gouty arthritis: a preclinical evaluation of allopurinol and disulfiram combination therapy[J]. Pharmaceuticals, 2025, 18(5): 762. DOI: 10.3390/ph18050762.
[15]	Borghi C, Fogacci F, Cicero A F. Crystal clear-part I: the role of uric acid in cardiorenal disease[J]. Eur J Intern Med, 2025, 142: 106432. DOI: 10.1016/j.ejim.2025.07.028.
[16]	Dong X Y, Suo Y, Yu J, et al. Biomimetic nanoparticles simultaneously targeting modulation of lipid metabolism and phenotype of macrophages for programmed atherosclerosis management[J]. ACS Nano, 2025, 19(28): 25628-25644. DOI: 10.1021/acsnano.5c00216.
[17]	Emilsson V, Ilkov M, Lamb J R, et al. Co-regulatory networks of human serum proteins link genetics to disease[J]. Science, 2018, 361(6404): 769-773. DOI: 10.1126/science.aaq1327.

组别	只数	尿酸（μmol/L）			尿素氮（mmol/L）			肌酐（μmol/L）
组别	只数	第0周	第2周	第4周	第0周	第2周	第4周	第0周	第2周	第4周
空白对照组	12	41.08±1.39	46.23±3.11	43.21±2.09	6.71±0.68	6.99±1.11	7.41±0.70	28.50±1.30	26.32±1.13	29.53±2.39
模型组	12	43.41±5.67	219.00±17.54^ad	431.17±4.16^ae	7.58±0.44	7.50±0.33	9.78±0.67^ae	29.28±6.61	37.28±3.90^ad	41.25±1.59^ae
瑞舒伐他汀钙低剂量组	12	45.13±0.37	169.74±7.83^a	89.09±1.21^b	6.33±1.12	6.78±0.74	7.00±0.65^b	22.00±2.60	27.00±3.94	28.00±4.95^b
瑞舒伐他汀钙高剂量组	12	45.37±0.39	128.75±5.16^a	67.00±6.16^bc	7.35±0.41	6.78±0.60	7.80±0.83^bc	24.75±3.11	29.67±1.59^b	27.03±2.55^bc
阳性对照组	12	40.69±5.51	103.75±10.03^a	59.25±2.8^b	6.99±0.37	6.60±0.66	8.15±0.48^b	25.00±3.00	29.50±3.64^b	22.80±3.20^b
F值		F_交互=2 131.90，F_组别=4 578.98，F_时间=4 025.84			F_交互=5.79，F_组别=26.33，F_时间=47.69			F_交互=11.27，F_组别=58.45，F_时间=27.67
P值		P_交互<0.001，P_组别<0.001，P_时间<0.001			P_交互<0.001，P_组别<0.001，P_时间<0.001			P_交互<0.001，P_组别<0.001，P_时间<0.001

组别	只数	尿酸（μmol/L）			尿素氮（mmol/L）			肌酐（μmol/L）
组别	只数	第0周	第2周	第4周	第0周	第2周	第4周	第0周	第2周	第4周
空白对照组	12	41.08±1.39	46.23±3.11	43.21±2.09	6.71±0.68	6.99±1.11	7.41±0.70	28.50±1.30	26.32±1.13	29.53±2.39
模型组	12	43.41±5.67	219.00±17.54^ad	431.17±4.16^ae	7.58±0.44	7.50±0.33	9.78±0.67^ae	29.28±6.61	37.28±3.90^ad	41.25±1.59^ae
瑞舒伐他汀钙低剂量组	12	45.13±0.37	169.74±7.83^a	89.09±1.21^b	6.33±1.12	6.78±0.74	7.00±0.65^b	22.00±2.60	27.00±3.94	28.00±4.95^b
瑞舒伐他汀钙高剂量组	12	45.37±0.39	128.75±5.16^a	67.00±6.16^bc	7.35±0.41	6.78±0.60	7.80±0.83^bc	24.75±3.11	29.67±1.59^b	27.03±2.55^bc
阳性对照组	12	40.69±5.51	103.75±10.03^a	59.25±2.8^b	6.99±0.37	6.60±0.66	8.15±0.48^b	25.00±3.00	29.50±3.64^b	22.80±3.20^b
F值		F_交互=2 131.90，F_组别=4 578.98，F_时间=4 025.84			F_交互=5.79，F_组别=26.33，F_时间=47.69			F_交互=11.27，F_组别=58.45，F_时间=27.67
P值		P_交互<0.001，P_组别<0.001，P_时间<0.001			P_交互<0.001，P_组别<0.001，P_时间<0.001			P_交互<0.001，P_组别<0.001，P_时间<0.001

组别	只数	第0周	第2周	第4周
空白对照组	12	1.23±0.10	1.72±0.14	1.29±0.09
模型组	12	1.29±0.07	3.79±0.16^a	7.68±1.73^a
瑞舒伐他汀钙低剂量组	12	1.46±0.04	2.24±0.09^b	5.01±0.19^ab
瑞舒伐他汀钙高剂量组	12	1.58±0.08	2.03±0.21^b	2.24±0.10^abc
阳性对照组	12	1.57±0.36	2.68±0.59^b	3.54±0.66^abcd
F值		F_交互=86.44，F_组别=106.93，F_时间=563.10
P值		P_交互<0.001，P_组别<0.001，P_时间<0.001

组别	只数	第0周	第2周	第4周
空白对照组	12	1.23±0.10	1.72±0.14	1.29±0.09
模型组	12	1.29±0.07	3.79±0.16^a	7.68±1.73^a
瑞舒伐他汀钙低剂量组	12	1.46±0.04	2.24±0.09^b	5.01±0.19^ab
瑞舒伐他汀钙高剂量组	12	1.58±0.08	2.03±0.21^b	2.24±0.10^abc
阳性对照组	12	1.57±0.36	2.68±0.59^b	3.54±0.66^abcd
F值		F_交互=86.44，F_组别=106.93，F_时间=563.10
P值		P_交互<0.001，P_组别<0.001，P_时间<0.001

组别	只数	第0周	第2周	第4周
空白对照组	12	165.84±0.87	158.18±1.80	151.93±3.42
模型组	12	163.20±3.68	259.61±1.69^a	308.02±1.79^a
瑞舒伐他汀钙低剂量组	12	164.08±3.94	240.00±8.71^a	205.96±3.65^ab
瑞舒伐他汀钙高剂量组	12	160.67±8.35	234.89±9.92^a	157.44±8.48^bc
阳性对照组	12	179.13±21.83	209.10±20.71^a	214.91±24.59^abd
F值		F_交互=223.55，F_组别=127.88，F_时间=902.87
P值		P_交互<0.001，P_组别<0.001，P_时间<0.001

瑞舒伐他汀钙对高尿酸血症大鼠炎症因子及动脉损伤的影响及其代谢组学研究

Effects of Rosuvastatin Calcium on Inflammatory Factors and Arterial Injury in Hyperuricemic Rats and Its Metabolomics Analysis

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组别	只数	第0周	第2周	第4周
空白对照组	12	90.49±1.46	93.99±1.46	85.13±3.79
模型组	12	86.31±1.70	123.85±1.70^a	211.81±4.91^a
瑞舒伐他汀钙低剂量组	12	89.39±2.24	136.18±2.24^a	140.12±3.58^ab
瑞舒伐他汀钙高剂量组	12	84.92±3.26	103.63±3.26^a	103.63±0.92^abc
阳性对照组	12	86.53±7.28	120.45±47.73^a	149.10±9.49^abd
F值		F_交互=60.64，F_组别=61.83，F_时间=392.41
P值		P_交互<0.001，P_组别<0.001，P_时间<0.001

类型	上调蛋白数量	下调蛋白数量	总蛋白数量
空白对照组与模型组差异蛋白	33	8	42
空白对照组与瑞舒伐他汀钙高剂量组差异蛋白	12	14	26
空白对照组与瑞舒伐他汀钙低剂量组差异蛋白	58	24	82
空白对照组与阳性对照组差异蛋白	107	29	136

GO编号	GO术语	蛋白数量（个）	FDR-P值
GO：0010898	脂蛋白正向调控	11	0.005 100
GO：0033700	磷脂外流	8	0.005 100
GO：0034385	富含甘油三酯的血浆脂蛋白	12	0.000 150
GO：0034364	高密度脂蛋白	7	0.000 039
GO：0034358	血浆脂蛋白颗粒	3	0.000 049
GO：0032994	蛋白-脂质复合物	4	0.003 040
GO：0042627	乳糜微粒	5	0.000 074
GO：0034361	极低密度脂蛋白颗粒	3	0.000 150

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