短穗兔耳草提取物对高尿酸血症小鼠肾脏保护作用研究

目的 研究短穗兔耳草提取物对高尿酸血症小鼠肾脏有无保护作用。方法 以氧嗪酸钾盐诱导小鼠高尿酸血症模型为实验系统,通过检测血清尿酸和黄嘌呤氧化酶含量和肾脏病理病变等指标,评价短穗兔耳草提取物对高尿酸血症小鼠肾脏的保护作用。结果 短穗兔耳草可显著降低模型大鼠血清、尿酸和黄嘌呤氧化酶含量, 改善了小鼠肾脏结构的变化。结论 短穗兔耳草具有降尿酸活性及肾脏保护作用。     

氟伐他汀对SD大鼠糖尿病肾病的保护作用

目的观察氟伐他汀对SD大鼠糖尿病肾病的保护作用并探讨其作用机制。方法以STZ诱导大鼠糖尿病,氟伐他汀治疗6周后,检测24h尿蛋白含量以及血清尿酸、肌酐和尿素氮含量,并测定肾脏组织中甘油三酯和总胆固醇含量。结果糖尿病大鼠24h尿蛋白和血清尿酸、肌酐和尿素氮含量均明显高于正常组大鼠,氟伐他汀具有明显的逆转作用。氟伐他汀还减少了糖尿病大鼠肾脏中甘油三酯和总胆固醇含量。结论氟伐他汀可减轻糖尿病肾病,具有肾保护作用,其机制可能与减少肾脏中脂类堆积有关。     

痛风颗粒各部位对高尿酸血症大鼠尿酸和黄嘌呤氧化酶活性的影响

目的 通过观察痛风颗粒各部位对高尿酸血症大鼠血尿酸、尿尿酸、血黄嘌呤氧化酶活性和肝脏黄嘌呤氧化酶活性的影响,探讨其治疗痛风的物质基础和机制.方法 以腺嘌呤合乙胺丁醇法诱导大鼠高尿酸血症模型,分别用磷钨酸法和酶比色法检测尿酸和黄嘌呤氧化酶的含量.结果 黄酮类成分在降尿酸和抑制黄嘌呤氧化酶活性上均起主要作用;生物碱类成分对尿中尿酸的排泄和血清黄嘌呤氧化酶活性的抑制起较重要作用,有机酸类成分均未表现出明显作用;全方和有效部位组合有明显的降尿酸和抑制黄嘌呤氧化酶活性的作用.结论 黄酮类、生物碱和有机酸类有效部位组合后的药效与处方药一致,是该处方的有效部位群,对高尿酸血症模型大鼠表现出的降尿酸和抑制黄嘌呤氧化酶活性的作用最为显著.     

yy大黄酸对糖尿病大鼠肾脏还原型辅酶Ⅱ基因表达的影响

目的 观察大黄酸对糖尿病大鼠肾脏氧化应激的影响.方法链脲佐菌素(STZ)诱导的糖尿病肾病大鼠模型随机分为模型组与治疗组,治疗6周后,比较各组大鼠肾组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,同时检测各组大鼠血糖、血肌酐、尿素氮、24 h尿蛋白定量等.采用逆转录-聚合酶链反应(RT-PCR)方法检测p22phox及p47phox的表达.结果治疗组较模型组明显改善尿清蛋白、尿素氮水平和肾脏肥大指数.肾脏MDA含量明显下降(P<0.05),SOD活性显著上升(P<0.05).与对照组比较,模型组p47phox和p22phox mRNA表达明显增多,大黄酸干预使其表达明显降低.结论大黄酸对2型糖尿病肾脏病变有一定的保护作用,其机制可能是通过抑制氧化应激反应,下调糖尿病大鼠p22phox及p47phox的表达对2型糖尿病模型大鼠肾脏产生保护作用.     

蜂蜜对大鼠血尿酸水平及肾损伤研究

目的：观察氧嗪酸钾模型大鼠饮用洋槐蜂蜜（AH）水溶液后，对大鼠血尿酸水平及肾功能的影响。方法：雄性SD大鼠60只，随机分为空白对照组（CON组）、氧嗪酸钾模型组（OA模型组）、10%果糖组（10%F组）以及不同浓度蜂蜜组（25%、12.5%及6.25%AH组）。所有大鼠正常饲料喂养，CON对照组每日皮下注射5%羧甲基纤维素钠（CMC-Na）溶液同时饮用无菌水，其余各组大鼠每日皮下注射100 mg/kg OA CMC-Na混悬溶液，同时饮用无菌水、果糖或不同浓度AH水溶液。本实验为期4周。实验前及实验期间大鼠每周称重并取血一次，实验结束后取血、尿、粪便及肾脏组织，测定血、尿、粪便中尿酸含量、血清肌酐（Cre）及尿素氮（BUN）水平及肾脏组织炎症因子，并进行肾脏组织病理切片观察。结果：与空白对照组相比，蜂蜜可显著降低大鼠体质量（P<0.05），增加大鼠肾脏脏器系数，升高大鼠血尿酸、尿尿酸（UUA）、血清肌酐及尿素氮水平，降低大鼠粪尿酸（FUA）水平；蜂蜜可下调大鼠肾脏组织肿瘤坏死因子-α(TNF-α)水平（P<0.05）、上调单核细胞趋化蛋白1(MCP-1)及转化生长因子β1(...     

大黄和泽泻提取物对二甘醇致小鼠肾脏损伤的保护作用研究

目的:研究大黄和泽泻提取物对二甘醇(DEG)致小鼠肾脏损伤的保护作用及其机制。方法:采用ig给予DEG方法建立小鼠肾脏损伤模型,ig给予大黄和泽泻提取物后测定血清中肌酐(Cr)和尿素氮(BUN)浓度,测定超氧化物歧化酶(SOD)和谷胱甘肽过氧化酶(GSH-PX)活性及丙二醛(MDA)含量变化。结果:小鼠ig给予DEG后有明显中毒表现,肾脏体质量比增加,血清中Cr和BUN水平升高,肾组织SOD和GSH-PX活性降低、MDA含量增加;给予大黄和泽泻提取物后小鼠中毒表现明显减轻,肾脏体质量比减少,血清中Cr和BUN水平明显降低,肾组织SOD和GSH-PX活性升高、MDA含量降低。结论:大黄和泽泻提取物对DEG所致小鼠肾脏损伤具有明显的保护作用,该作用与其改善肾脏抗氧化酶活性及抑制脂质过氧化反应有关。     

中医辨证治疗痛风效果的临床观察

<正>痛风是由于嘌呤代谢紊乱及尿酸排泄减少引起的疾病。日常餐饮不当,存在不科学的饮食结构,嗜食富含嘌呤、蛋白质、热能高而且长期嗜酒饮食习惯而发病。常伴有高血压、糖尿病、高脂血症、肥胖、动脉硬化、冠心病。尿酸是机体含氮的代谢产物,与尿素氮、肌酐一起从肾脏排出体外,当肾功能损害造成肾小管排泄尿酸盐障碍,产生高尿酸血症导致反复发作,最终引发形成痛风性急性关节炎、痛风石沉积,甚则累及关节导致畸形、累及肾脏而形成慢性间质性肾     

大黄酸分散体的制备及其对糖尿病肾病大鼠肾功能的影响

目的以聚乙烯吡咯烷酮(PVP)为载体,将大黄酸制成固体分散体。观察大黄酸固体分散体对糖尿病大鼠肾功能的影响。方法采用溶剂法制备大黄酸固体分散体;对制备的固体分散体进行差热分析和红外光谱分析。采用链脲佐菌素(STZ)诱导大鼠糖尿病模型,观察大黄酸固体分散体对糖尿病肾病大鼠肾功能的影响。结果 12周后,糖尿病大鼠血中尿素氮(BUN)、内生肌酐清除率(Ccr)、24 h尿蛋白排泄量(UPE)明显升高(P<0.01)。肾组织ET含量、24 h尿ET排泄量(UET)显著升高(P<0.01)。给予糖尿病肾病大鼠大黄酸固体分散体干预后,糖尿病大鼠的BUN、Ccr、UPE减少,UET和肾组织中ET含量降低。结论大黄酸固体分散体能改善糖尿病大鼠的肾脏功能。     

虎参痛风胶囊对高尿酸血症及尿酸性肾病大鼠的影响

目的　探讨虎参痛风胶囊 (Hus)对大鼠高尿酸血症模型血尿酸、肾功能等的影响 ,了解其对痛风的治疗作用。方法　应用灌胃给予腺嘌呤和喂饲含 10 g·kg- 1酵母的饲料制备大鼠慢性高尿酸血症、尿酸性肾病模型 ,同时应用药物治疗。 18d后采血 ,全自动生化分析仪测定血清总蛋白、白蛋白、白球比、Cr、BUN、TG、HDL、胆固醇的含量 ,取肾脏做电镜切片和尿酸特殊染色 (Gomori尿酸特殊染色法 ,1951年 )。结果　Hus和别嘌呤醇 (All)一样均能降低痛风小鼠和大鼠的血尿酸、肌酐、尿素氮含量 (与模型组比 ,P <0 0 5,n =7) ,大剂量Hus甚至可降低到正常水平 ,优于All(P <0 0 5,n =7)。All组 ,Hus组肾脏特殊染色显示髓质及肾乳头黑褐色尿酸盐结晶沉积较模型组明显减少 ,以All组、50 0mg·kg- 1Hus组减少特别明显。同时 2 50mg·kg- 1Hus组血白蛋白、白球比甚至高于空白组 ,50 0mg·kg- 1Hus组血胆固醇比空白组还低。结论　Hus具有良好的抗痛风作用 ,良好的肾脏保护和降低血胆固醇、提高机体免疫力、对疾病的耐受力的作用 ,并随着剂量的增加 ,用药时间延长效果越好     

抗痛风药Febuxostat

高尿酸血症是由于尿酸产生增多和／或肾尿酸分泌减少所致，它是诱发痛风的最危险的因素。使用药物降低血内尿酸浓度是预防痛风发生的常用方法之一，这类药物包括可以阻断肾小管腔膜对尿酸吸收的促尿酸尿药和黄嘌呤氧化酶／黄嘌呤脱氢酶抑制剂。但是，促尿酸尿药禁用于肾功能障碍病人，而具正常肾功能的病人用此类药物则会导致尿碱化；别嘌醇则是目前唯一上市的黄嘌呤氧化酶／黄嘌呤脱氢酶抑制剂，     

Astilbin attenuates hyperuricemia and ameliorates nephropathy in fructose-induced hyperuricemic rats

Astilbin is a flavonoid compound isolated from the rhizome of Smilax china L. The effects and possible mechanisms of astilbin on hyperuricemia and nephropathy rats were elucidated in this study. Different dosages of astilbin (1.25, 2.5, and 5.0 mg/kg) were administered to 10?% fructose-induced hyperuricemic rats. The results demonstrated that astilbin significantly decreased the serum uric acid (Sur) level by increasing the urinary uric acid (Uur) level and fractional excretion of urate (FEUA) but not inhibiting the xanthine oxidase (XOD) activity. In addition, kidney function parameters such as serum creatinine (Scr) and blood urea nitrogen (BUN) were recovered in astilbin-treated hyperuricemic rats. Further investigation indicated that astilbin prevented the renal damage against the expression of transforming growth factor- β1 (TGF-β1) and connective tissue growth factor (CTGF) and also exerted a renal protective role by inhibiting formation of monosodium urate (MSU) and production of prostaglandin E? (PGE?) and interleukin-1 (IL-1). These findings provide potent evidence for astilbin as a safe and promising lead compound in the development of a disease-modifying drug to prevent hyperuricemia and nephropathy.     

高胆固醇与心血管危险因素相关性研究

目的探讨高胆固醇血症患者与血压、ALT、AST、血糖、血尿酸、尿素氮、肌酐水平,体重及体重指数、脂肪肝发生率的关系。方法收集海南医学院附属医院高胆固醇血症患者430例以及胆固醇正常者100例,抽血检测其血脂代谢水平（TG、TC、LDL、HDL）以及ALT、AST、血糖、血尿酸、尿素氮、肌酐水平和B超检出脂肪肝的水平,同时测量体重及体重指数,并测量血压。结果与胆固醇正常的体检者相比,高胆固醇血症患者的AST、血尿酸、肌酐水平及脂肪肝患病率、体重及体重指数、血压明显高于正常者,在统计学上有显著性差异。结论高胆固醇与体重指数、血压、脂肪肝、ALT、血尿酸、血尿素氮呈正相关。     

桑抹茶对高尿酸血症模型大鼠血尿酸水平及肠道菌群的影响

目的 观察桑抹茶对高尿酸血症模型大鼠血清尿酸及肠道菌群的调节作用。方法 采用高嘌呤饲料喂养复制高尿酸血症大鼠模型,同时给予桑抹茶干预,于实验期末,用全自动生化仪检测血清尿酸、肌酐、尿素氮水平,ELISA法检测血清及肝组织黄嘌呤氧化酶活性和细菌内毒素水平;收集粪便,提取肠道菌群DNA,进行16S rRNA生物信息学分析。结果 桑抹茶干预能显著降低模型大鼠血清尿酸、肌酐、尿素氮水平及血清、肝组织黄嘌呤氧化酶活性;增加肠道乳杆菌比例,降低血清内毒素水平。RAD结果显示,肠道菌群分类水平与血尿酸、黄嘌呤氧化酶活性相关。结论 桑抹茶具有降尿酸作用,该作用可能与调节肠道菌群,降低血清内毒素水平,抑制黄嘌呤氧化酶活性有关。     

Administration of procyanidins from grape seeds reduces serum uric acid levels and decreases hepatic xanthine dehydrogenase/oxidase activities in oxonate-treated mice

In this study we have investigated the effects of administration of procyanidins from grape seeds on serum uric acid levels in a model of hyperuricaemia in mice pretreated with oxonate, as well as the xanthine dehydrogenase and xanthine oxidase activities in mouse liver in vivo. The procyanidins, when orally administered to the oxonate-pretreated hyperuricaemic mice, were able to elicit a dose-dependent hypouricaemic effect. At a dose of 400 mg/kg for 3 days, the serum urate levels of the oxonate-pretreated mice were not different from the normal mice. In addition, the hepatic activities of xanthine dehydrogenase and xanthine oxidase in the procyanidins-treated mice were found to decrease significantly. However, the hypouricaemic effects observed in the experimental animals did not seem to parallel the changes in xanthine dehydrogenase and xanthine oxidase activities, implying that the procyanidins might be acting via other mechanisms apart from simple inhibition of enzyme activities. Furthermore, the procyanidin-treated animals exhibited normal growth while the allopurinol-treated animals exhibited some retarded growth. These results demonstrated for the first time that the procyanidins from grape seeds possess in vivo urate-lowering activities. The potential application of these natural compounds in the treatment of hyperuricaemia is discussed.     

Moderate hyperuricaemia ameliorated kidney damage in a low-renin model of experimental renal insufficiency

Uric acid has promoted renal fibrosis and inflammation in experimental studies, but some studies have shown nephroprotective effects due to alleviated oxidative stress. We studied the influence of experimental hyperuricaemia in surgically 5/6 nephrectomized rats. Three weeks after subtotal nephrectomy or sham operation, the rats were allocated to control diet or 2.0% oxonic acid (uricase inhibitor) diet for 9 weeks. Then blood, urine and tissue samples were taken, and renal morphology and oxidative stress were examined. Inflammation and fibrosis were evaluated using immunohistochemistry and real-time PCR (RT-PCR). Remnant kidney rats ingesting normal or oxonic acid diet presented with ~60% reduction of creatinine clearance and suppressed plasma renin activity. Oxonic acid diet increased plasma uric acid levels by >80 μmol/L. In remnant kidney rats, moderate hyperuricaemia decreased glomerulosclerosis, tubulointerstitial damage and kidney mast cell count, without influencing the fibrosis marker collagen I messenger RNA (mRNA) content. In both sham-operated and 5/6 nephrectomized rats, the mast cell product 11-epi-prostaglandin-F_2α excretion to the urine and kidney tissue cyclooxygenase-2 (COX-2) levels were decreased. To conclude, hyperuricaemic remnant kidney rats displayed improved kidney morphology and reduced markers of oxidative stress and inflammation. Thus, moderately elevated plasma uric acid had beneficial effects on the kidney in this low-renin model of experimental renal insufficiency.     

Effect of metal exposure in rats: amelioration by diallylsulphide

The effect of diallylsuphide (DAS) was investigated on mercuric chloride (HgCl₂)-induced renal damage in rats. Oral administration of DAS (200?mg/kg) effectively inhibited the levels of antioxidant enzymes as compared to HgCl₂-treated group. Exposure to HgCl₂ also resulted in an increase in the uric acid, creatinine and blood urea nitrogen levels. A significant decrease in the uric acid, creatinine and blood urea nitrogen was also observed in DAS-pre-treated HgCl₂ group. The results suggest that DAS possesses significant potential as nephroprotective agent.     

微小剂量阿司匹林对高尿酸血症模型小鼠血尿酸的影响考察

目的:考察微小剂量阿司匹林对高尿酸血症模型小鼠血尿酸水平等的影响。方法:75只小鼠随机分为5组,包括正常对照组、高尿酸对照组和阿司匹林低、中、高实验组。对照组给予0.5%羧甲基纤维素钠溶液,实验组分别给予3种剂量(12.5、25、50mg·kg-1)阿司匹林溶液,每天1次,持续1周后,除正常对照组外,其余4组腹腔注射尿酸溶液,建立高尿酸血症模型,并于建模后1h取血样测定尿酸、肌酐和尿素氮水平。结果:与高尿酸对照组比较,各剂量阿司匹林对肌酐、尿素氮影响不明显,但可显著升高血尿酸水平(P<0.0001),但随剂量增加,血尿酸水平逐渐降低。结论:微小剂量阿司匹林可导致高尿酸血症模型小鼠血尿酸水平升高,推测其作用机制可能与抑制尿酸排泄有关。