| 魏文静,高 欣,雷 烨,杨薪博,惠瑜瑜.降浊四妙散通过降低血尿酸水平及抑制NLRP3炎症小体对大鼠高尿酸血症及其肾损伤的改善作用研究[J].现代生物医学进展英文版,2023,(8):1436-1441. |
| 降浊四妙散通过降低血尿酸水平及抑制NLRP3炎症小体对大鼠高尿酸血症及其肾损伤的改善作用研究 |
| Protective Effect of Oxymatrine on Myocardial Injury in Septic Shock Rats through TGF-?茁1/Smads Signaling Pathway |
| Received:August 10, 2022 Revised:August 30, 2022 |
| DOI：10.13241/j.cnki.pmb.2023.08.007 |
| 中文关键词: 降浊四妙散 尿酸 NLRP3炎症小体 高尿酸血症 肾损伤 |
| 英文关键词: Jiangzhuo Simiao powder Uric acid NLRP3 inflammasome Hyperuricemia Kidney injury |
| 基金项目:陕西省中医管理局科研项目（LCMS051）；中西医结合治疗糖尿病血管病变创新团队项目（2020XKTD-C01） |
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| 中文摘要: |
| 摘要 目的：探究降浊四妙散通过降低血尿酸水平及抑制NLRP3炎症小体对大鼠高尿酸血症及其肾损伤的改善作用。方法：将28只SD大鼠随机分为对照组、氧酸钾（OA）模型组、OA+SMS组、OA+别嘌醇组，其中，SMS的剂量基于实验动物物质管理标准（每公斤体重成人剂量的10倍）；别嘌醇溶解在OA+别嘌醇组的饮用水中（浓度，150 mg/L）；对照组和OA组给予等量的蒸馏水（胃内容量控制在2 mL/d），持续7周。探讨SMS对肾线粒体活性氧(ROS)和氧化应激(OS)产物、NLRP3-ASC-caspase-1轴的蛋白表达。结果：（1）对照组、OA模型和治疗组的数据存在显著差异（P<0.05）。在第7周结束时，模型组总尿酸排泄量显著高于对照组（P<0.05），SZF组和别嘌醇组显著高于OA组（P<0.05）。（2）与对照组相比，OA组的BUN和Scr水平显著升高（P<0.05），而接受SMS和别嘌醇治疗大鼠的BUN和Scr水平下降（P<0.05）。（3）肾组织结构中，对于OA+SZF和OA+别嘌呤醇组，肾近端肾小管上皮细胞肿胀、空泡变性和炎性细胞浸润减少。（4）OA诱导的高尿酸血症大鼠肾组织中氧化应激指标均升高（P＜0.05）；即超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶之间存在显著的不平衡，而SMS和别嘌醇干预可显著回复以上氧化应激反应指标的动态平衡（P＜0.05）。（5）OA组大鼠肾组织中TXNIP mRNA和蛋白表达显著高于其他组（P<0.05），而SMS和别嘌醇有效抑制TXNIP mRNA 和蛋白表达（P<0.05）；高尿酸血症大鼠NLRP3-ASC-caspase-1 轴中的mRNA和蛋白质表达升高（P<0.05）。SMS干预后组NLRP3-ASC-caspase-1轴的激活显著被抑制（P<0.05）。结论：SMS通过降低高尿酸血症实验大鼠肾脏中血尿酸水平，进而减轻肾损害，同时其可抑制线粒体ROS触发的NLRP3炎性体激活来减轻肾小管损伤和炎症浸润。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the improvement effect of Jiangzhuo Simiao Powder on hyperuricemia and renal injury in rats by reducing serum uric acid level and inhibiting NLRP3 inflammasome. Methods: Twenty-eight SD rats were randomly divided into control group, potassium oxyacid (OA) model group, OA+SMS group, and OA+allopurinol group, among them, the dose of SMS is based on laboratory animal substance management standards (10 times the adult dose per kilogram of body weight); Allopurinol was dissolved in the drinking water of the OA + allopurinol group (concentration, 150 mg/L); The control group and the OA group were given the same amount of distilled water (the intragastric volume was controlled at 2 mL/d) for 7 weeks. To investigate the mediating effect of SMS on renal mitochondrial reactive oxygen species (ROS) and oxidative stress (OS) products, protein expression of NLRP3-ASC-caspase-1 axis. Results: (1) The data of control group, OA model and treatment group were significantly different (P<0.05). At the end of the 7th week, the total uric acid excretion in the model group was significantly higher than that in the control group (P<0.05), and the SZF group and allopurinol group were significantly higher than those in the OA group (P<0.05). (2) Compared with the control group, the levels of BUN and Scr in the OA group were significantly increased (P<0.05), while the levels of BUN and Scr in the rats treated with SMS and allopurinol decreased (P<0.05). (3) In renal tissue structure, for the OA+SZF and OA+allopurinol groups, the epithelial cell swelling, vacuolar degeneration and inflammatory cell infiltration in the proximal renal tubules were reduced. (4) The oxidative stress indexes in renal tissue of OA-induced hyperuricemia rats were all increased (P<0.05); namely, superoxide dismutase (SOD), catalase (CAT) and glutathione There was a significant imbalance between peroxidases, while SMS and allopurinol intervention could significantly restore the dynamic balance of the above oxidative stress response indicators (P<0.05). (5) The expression of TXNIP mRNA and protein in kidney tissue of rats in OA group was significantly higher than that in other groups (P<0.05), while SMS and allopurinol effectively inhibited the expression of TXNIP mRNA and protein (P<0.05); mRNA and protein expression in the murine NLRP3-ASC-caspase-1 axis was elevated (P<0.05). The activation of NLRP3-ASC-caspase-1 axis in the SMS group was significantly inhibited (P<0.05). Conclusion: SMS attenuated tubular damage and inflammatory infiltration by reducing blood uric acid levels in reducing renal damage, while inhibiting the NLRP3 inflammasome activation triggered by mitochondrial ROS. |
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