柴胡皂苷D对老年膜性肾炎大鼠模型的治疗作用

目的观察柴胡有效成分柴胡皂苷D对老年膜性肾炎大鼠模型的治疗作用。方法通过尾静脉注射兔抗鼠血清建立大鼠被动型Heymann肾炎模型,连续腹腔注射柴胡皂苷D 30 d,观察柴胡皂苷D对实验动物尿蛋白和血清总蛋白、白蛋白、肌酐、尿素氮等生化指标的影响。结果柴胡皂苷D可以降低被动型Heymann肾炎大鼠模型的尿蛋白,并对其生化指标具有改善作用。结论柴胡皂苷D对老年常见肾小球肾炎(膜性肾炎)大鼠模型(被动型Heymann肾炎模型)的肾功能具有改善作用。     

复方康肾片对老年大鼠Heymann肾小球肾炎动物模型的影响

目的 观察复方康肾片对老年大鼠Heymann肾炎动物模型的影响.方法 以肾皮质弗氏完全佐剂混悬液复制老年大鼠Heymann肾炎动物模型,随机分为肾炎动物模型组、复方康肾片高、中、低剂量组,均连续给药28 d.结果 复方康肾片能使大鼠尿量增加(P＜0.05),对血清总蛋白含量变化影响不明显.对血清尿素氮和肌酐水平升高有抑制作用(P＜0.01);对肾炎模型动物血清白蛋白降低趋势有显著的改善作用(P＜0.05).结论 复方康肾片对老年大鼠Heymann肾炎有一定的治疗作用.     

氟砷联合对大鼠子代毒性作用的实验研究

为探讨氟砷联合对大鼠子代的毒性作用,本实验以一批从胚胎期就开始接触氟砷的大鼠子代为研究对象,观察氟砷联合用对大鼠子代体重、脂质过氧化水平及抗氧化能力的影响。结果发现,氟可影响砷在大鼠子代体内的分布;氟砷联合作用对从胚胎期开始染毒大鼠子代体重影响不大,但可引起其体内脂质过氧化水平显著增高、抗氧化能力明显降低;氟砷联合作用对断乳后脱毒的大鼠子代体重、脂质过氧化水平及抗氧化能力均无影响。说明氟砷联合对断     

绞股蓝皂甙对糖尿病大鼠降糖作用的观察

观察绞股蓝皂甙对链脲佐菌素造模的尿病大鼠血糖的影响。结果发现绞股蓝皂甙治疗４周后，糖尿病大鼠空腹血糖、胰岛素、血清甘油三酯，总胆固醇水平、血清过氧化脂质含量均比对照组明显降低，血清超氧化物歧化酶活性明显升高。提示绞股蓝皂甙具有降糖，降脂及可能有抗氧化作用。     

病毒性肝炎患者血清自由基指标变化及百令胶囊疗效观察

采用生物化学方法检测了 4 7例病毒性肝炎患者的血清自由基指标〔超氧化物歧化酶( SOD)、脂质过氧化物 ( L PO)、黄嘌呤氧化酶 ( XOD)〕变化 ,并与用百令胶囊治疗后以上指标变化进行比较。结果治疗前 SOD活性降低 ,LPO和 XOD升高 ;治疗后 SOD升高 ,明显高于对照组。LPO和 XOD下降 ,显著低于对照组。提示自由基及脂质过氧化物升高与病毒性肝炎的发生及发展密切相关 ,百令胶囊治疗后机体抗氧化能力增强     

慢性愤怒应激对衰老大鼠学习记忆能力的影响及其脂质过氧化机制

目的 观察慢性愤怒应激对D-半乳糖(D-gal)引起的衰老大鼠空间学习记忆能力的影响,并从脂质过氧化与抗氧化角度解释其作用机制.方法 采用夹尾间接激怒法诱导被攻击大鼠产生愤怒应激,观察慢性愤怒应激对衰老大鼠空间学习记忆能力和血清SOD活性及心、肝组织MDA、LPF含量的影响,分析心、肝MDA、LPF含量与血清SOD活性的相关性.结果 愤怒D-gal组大鼠较D-gal组寻台时间显著延长(P＜0.05),血清SOD活性显著降低(P＜0.05),心、肝组织MDA、LPF含量显著提高(P＜0.05,P＜0.01),心、肝MDA、LPF含量与血清SOD活性呈负相关.结论 慢性愤怒应激可降低衰老大鼠的学习记忆能力,加速衰老进程.抑制机体抗氧化能力,加重心、肝等重要脏器组织脂质过氧化可能是其机制之一.     

雷公藤甲素对Heymann肾炎模型足细胞病变的影响

目的利用被动型Heymann肾炎模型(passive Heymann nephritis, PHN)研究雷公藤甲素(triptolide)对膜性肾病的疗效及其对足细胞病变的影响. 方法实验动物分为正常对照组、PHN组和雷公藤甲素治疗组.雷公藤甲素(200 μg/kg·d)灌胃治疗,分别在观察7天、14天、21天和28天时宰杀大鼠,留取血清和尿标本,观察尿蛋白、血清白蛋白、肝酶、肌酐和外周血白细胞等指标的变化;留取肾组织标本,行光镜、免疫病理、电镜和免疫电镜检查,并对肾组织IgG、C5b-9沉积以及Nephrin和Podocin的分布进行观察. 结果(1)尿蛋白雷公藤甲素治疗7天即可显著降低PHN大鼠的蛋白尿,至14天、21天和28天时,治疗组大鼠的尿蛋白进一步降低,与Heymann肾炎大鼠之间差异有统计学意义(P＜0.01).在尿蛋白显著降低的同时,血浆白蛋白显著增加.(2)肾小球上皮侧免疫沉积物电镜观察结果显示,雷公藤甲素治疗组上皮侧免疫复合物、钉突以及基膜反应性增殖均较Heymann肾炎组似有所改善,治疗后上皮侧电子致密物减少,基膜反应减轻,但在尿蛋白明显减少的同时,上皮侧电子致密物始终存在.(3)肾小球IgG和C5b-9的沉积经雷公藤甲素治疗后肾小球IgG和C5b-9的沉积与Heymann肾炎大鼠相比,荧光强度有所减少,尤其在治疗后的第7天,减少较为明显.(4)足细胞病变经雷公藤甲素治疗7天、14天、21天和28天后,均可见足细胞的足突损伤比对照组明显减轻,足突融合显著改善,足突宽度显著降低,观察至第28天时,治疗组可见大部分足细胞的足突形态基本恢复正常.(5)足细胞裂孔膜蛋白的变化经雷公藤甲素治疗7天后,足细胞表面Nephrin和Podocin的表达比Heymann肾炎大鼠有明显增加,分布上的异常开始得到纠正,至第21天基本恢复成连续的线样分布.免疫电镜的结果再次显示了治疗后Nephrin的上述修复过程. 结论雷公藤甲素对被动型Heymann肾炎具有显著的治疗作用,能有效地减少蛋白尿,减轻肾组织免疫损伤,促进足细胞病变和裂孔膜蛋白结构的修复.雷公藤甲素疗效机制除了其免疫抑制和抗炎作用外,还与它能显著地改善和修复足细胞病变有关.     

独活香豆素对帕金森病模型大鼠抗氧化功能及谷氨酸含量的影响

目的研究独活香豆素对帕金森病(PD)模型大鼠抗氧化功能及兴奋性氨基酸谷氨酸(Glu)含量的影响。方法采用蛋白酶体抑制剂Lactacystin脑定位注射制备PD大鼠模型,测定模型大鼠血清、脑组织中丙二醛(MDA)、Glu水平、血清中总超氧化物歧化酶(T-SOD)活性。结果独活香豆素能明显降低PD模型大鼠血清、脑组织中MDA、Glu的含量,提高血清中T-SOD的活性。结论抑制血清和脑组织脂质过氧化反应、提高抗氧化酶活性、降低血清和脑组织兴奋性氨基酸Glu含量可能是独活香豆素对抗PD的作用机制之一。     

砷对大鼠肝脏抗氧化作用影响的动态观察

为探讨砷对大鼠肝脏脂质过氧化和抗氧化能力的影响,采用亚慢性动物试验的方法对染砷不同时间大鼠肝脏脂质过氧化和抗氧化水平进行了动态观察。结果表明,在染砷第３０ｄ、第９０ｄ和第１８０ｄ大鼠肝脏丙二醛（ＭＤＡ）含量与对照组无明显差异（Ｐ〉０．０５）。提示砷对肝脏脂质过氧化反应的增强无明显作用;在染砷第３０ｄ、第９０ｄ和第１８０ｄ大鼠肝脏谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均明显低于对照组（Ｐ〈０．０５,     

氧化应激-抗氧化系统与糖尿病肾病

机体存在氧化应激-抗氧化防御系统,正常生理条件下,机体产生的活性氧簇可能被抗氧化系统迅速清除,但糖尿病持续高血糖状态导致的氧化应激产生了过量的活性氧簇,大大超过了机体的清除能力,引起包括糖尿病肾病在内的机体组织的损伤。动物实验研究已证明,抗氧化治疗可以减轻糖尿病肾病的蛋白尿,为糖尿病肾病的临床治疗提供了新的思路。     

低蛋白合并α-酮酸饮食对被动型Heymann肾炎大鼠肾小球足细胞Nephrin表达的影响

目的 观察低蛋白合并α-酮酸饮食对被动型Heymann肾炎大鼠肾小球足细胞Nephrin表达的影响.方法 将40只SD大鼠分为对照组、模型组(PHN组)、低蛋白饮食组(LPD组)和低蛋白合并α-酮酸饮食组(LK组),对照组经尾静脉注射1 mL/100 g生理盐水,其他三组经尾静脉注射1 mL/100 g新西兰大耳兔抗FX1A血清.对照组、PHN组饮食蛋白占饲料质量的10％,LPD组饮食蛋白占饲料质量的5％,LK组饮食蛋白占饲料质量的5％(其中α-酮酸提供1％的蛋白).4周后检测各组24 h尿蛋白定量、血清肌酐、TG、TC及血清白蛋白,激光共聚焦显微镜免疫荧光检查大鼠肾小球足细胞Nephrin表达情况.结果 激光共聚焦显微镜显示,PHN组、LPD组肾小球内Nephrin荧光强度较对照组明显减弱,且部分节段有缺失;LK组肾小球内Nephrin荧光强度较对照组减弱.结论 低蛋白合并α-酮酸饮食对被动型Heymann肾炎大鼠具有肾脏保护作用.     

失代偿期乙型肝炎肝硬化患者尿液视黄醇结合蛋白水平及其临床意义探讨*

目的 探讨检测尿液视黄醇结合蛋白(RBP)水平诊断失代偿期乙型肝炎肝硬化患者并发急性肾损伤(AKI)的价值。方法 2015年5月～2018年5月我院救治的112例失代偿期乙型肝炎肝硬化患者和同期健康体检者35例,采用酶联免疫吸附法检测受试者尿液RBP水平,应用ROC曲线并计算曲线下面积(AUC)分析尿RBP诊断失代偿期肝硬化患者并发AKI的价值。结果 失代偿期肝硬化患者尿液RBP水平为(2.2±1.0)mg/L,显著高于对照组【(0.3±0.1)mg/L,P＜0.05】;28例重度腹水患者尿RBP、尿微量白蛋白(mAlb)和估算的肾小球滤过率(eGFR)水平分别为(3.2±0.6)mg/L、(24.9±7.7)mg/L和(58.3±13.9)mL/min/1.73 m²,其中尿RBP和尿mAlb水平均显著高于31例轻度腹水组或53例中度腹水组,而eGFR水平显著低于轻度腹水和中度腹水患者,差异有统计学意义(P＜0.05);重度腹水患者sCr水平与中度腹水组比较,差异无统计学意义【(92.8±14.0)μmol/L 对(89.8±14.4)μmol/L,P＞0.05】,但显著高于轻度腹水组【(80.4±11.9)μmol/L,P＜0.05】;单因素分析结果显示,43例继发AKI组与69例未继发AKI组在血小板计数和上消化道出血发生率方面比较,差异无统计学意义(P＞0.05),而在mAlb、eGFR、RBP、血钠、TBIL、白细胞计数、PTA、NH^3＋、肝性脑病和自发性腹膜炎方面比较,差异有统计学意义(P＜0.05);尿RBP诊断失代偿期肝硬化患者继发AKI的AUC为0.856(95%CI:0.777～0.915),对应的最佳截断点为2.6 mg/L,其诊断的敏感度和特异度分别为81.4%和84.1%。结论 尿RBP能反映失代偿期肝硬化病情的严重程度,甚至可作为继发AKI的标志物。     

Lipid peroxidation levels in rat cardiac muscle are affected by age and thyroid status

Free radicals, hydroxyperoxides and H(2)O(2) are all known to damage cell components. This study was designed to compare the concentrations of hydroxyperoxide and free radical scavengers in the cardiac muscles of old rats in the hyper- or hypothyroid condition, to determine whether rates of peroxidation would differ with age, thyroid status, or both. Rats were rendered hyper- or hypothyroid by administration of l-thyroxine or methimazole for 4 weeks. Among the old rats, the lipid peroxide (LPO) concentrations, measured as thiobarbituric acid (TBA) reactants, were significantly greater in the hyperthyroid than in the euthyroid state and the LPO concentrations measured as TBA+Fe(3+) reactants, which may be precursors of LPO, were significantly greater in the hyperthyroid state, whereas in young rats, the LPO concentrations measured by TBA or TBA+Fe(3+) methods did not differ significantly in the hyperthyroid state. In the euthyroid state, the concentration of LPO measured as TBA+Fe(3+) reactants was significantly reduced with age. Xanthine oxidase (XOD) activity also was markedly increased with age, being more pronounced in the hyperthyroid than in the euthyroid state. The Mn and Cu/Zn superoxide dismutase activities were greater in the hyperthyroid than in the euthyroid state. Glutathione peroxidase activity decreased with age in the euthyroid and, particularly, in the hyperthyroid state. Catalase activity was not affected in the old rats. Concentrations of alpha-tocopherol in the old rats were high in the hyperthyroid state and low in the hypothyroid state, whereas the levels of beta- and gamma-tocopherols in these rats were unchanged in both conditions as compared with the euthyroid state findings. Data suggest that the site of free radical generation differs in older rats, with additional shifts in the location of intracellular lipid peroxidation being noted during hyperthyroidism. Thus, as rats age, the reduction of the free radical scavenger system and the increase in LPO and XOD activities might induce myocardial dysfunction.     

Enhanced exercise‐induced muscle damage and muscle protein degradation in streptozotocin‐induced type 2 diabetic rats

Aims/Introduction: The effects of 5‐day voluntary exercise on muscle damage and muscle protein degradation were investigated in a streptozotocin‐induced rat model of moderately glycemic, uncontrolled, type 2 diabetes. Materials and Methods: In the preliminary experiment, an oral glucose tolerance (1.0 g/kg) test was carried out to confirm the development of diabetes 3 days after streptozotocin treatment (30 mg/kg). In the genuine experiment, rats were divided into four groups: (i) non‐diabetic rats without exercise (controls); (ii) non‐diabetic rats with exercise; (iii) diabetic rats without exercise; and (iv) diabetic rats with exercise. After 5 days of voluntary wheel running exercise, blood and 24‐h urine were collected, and levels of serum creatine kinase, a marker of muscle damage, and 24‐h urinary excretion of muscle degradation products were determined. Results: Type 2 diabetic rats with insulin deficiency that exercised had higher serum creatine kinase and greater urinary excretions of creatinine, urea nitrogen and 3‐methylhistidine compared with both type 2 diabetic rats with insulin deficiency and non‐diabetic rats that did not exercise. However, there were no differences in serum creatine kinase and urinary excretions of creatinine, urea nitrogen and 3‐methylhistidine between non‐diabetic rats that did and did not exercise. Conclusions: These findings suggest that muscle damage is induced and muscle protein degradation are enhanced by chronic moderate exercise in moderately glycemic uncontrolled type 2 diabetic rats with insulin deficiency at an intensity level of exercise that does not affect muscle damage and muscle protein degradation in non‐diabetic rats. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00130.x, 2011)     

硒锌制剂拮抗慢性氟中毒的实验研究

目的：探讨硒锌制剂对慢性氟中毒的影响及其机理。方法：Wistar大鼠在饮含50mg/L高氟水的同时通过灌胃方式给予不同剂量的硒锌制剂,2个月后,测量大鼠尿液氟浓度和r-GT活性,血液GSH－Px活性及肾组织中LPO水平,GSH含量和SOD活性,结果：发现硒锌制剂通过促进尿氟排泄,增强全血GSH－PX的肾SOD活性,增加肾GSH含量而抑制氟中毒引起的脂质过氧化作用,从面降低尿r-GT活性和肾LPO含量,结论：提示一定剂量的硒锌制剂对慢性氟中 明显的拮抗作用,其机理可能与通过促进尿氟排泄和抗脂质过氧化作用有关。     

Serum, salivary and urinary cortisol level in the evaluation of adrenocortical function in-patients with bronchial asthma

56 patients with bronchial asthma (32 women and 24 men) and 31 healthy volunteers (19 women and 12 men) were investigated. The evaluation of the usefulness of salivary and urinary cortisol levels and urinary cortisol metabolites in 24-hr urine was conducted using the correlation coefficient between the cortisol level in the salivary or urine and that in blood serum. Very high correlation was found between the serum and salivary cortisol level (r=0.817). The correlation coefficient between the serum and urinary cortisol level in basal conditions was 0.759, while that between the saliva and urinary level was 0.723. A moderate degree of correlation (r=0.381) was demonstrated between serum cortisol level and 17-OHCS in urine. From these results it was concluded that salivary and urinary free cortisol level estimations may be a useful and non-invasive screening method of evaluating the glucocorticoid function of the adrenal cortex in asthma patients.     

Xanthine oxidase-derived free radicals directly activate rat pancreatic stellate cells

BACKGROUND AND AIM: Free radicals are reported to be associated with fibrosis in the pancreas. It is generally accepted that pancreatic stellate cells (PSC) play an important role in pancreatic fibrosis. However, the exact role of free radicals in activation of PSC has not been fully elucidated. In the present study, using a superoxide dismutase (SOD) inhibitor, diethyldithiocarbamate (DDC) with cultured PSC, we investigated how free radicals act on the activation of PSC. METHODS: PSC were isolated from male Wister rats. Cultured rat PSC were incubated with DDC for 48 h. Intracellular SOD activity and lipid peroxidation were examined in DDC-treated PSC. Activation of PSC was examined by determining the expression of alpha-smooth muscle actin (alpha-SMA) by immunocytochemistry. The number of PSC using a hemocytometer, type I collagen secretion with ELISA and matrix metalloproteinases (MMP) activities with gelatin zymography were also examined. Secretion of transforming growth factor-beta1 (TGF-beta1) was evaluated by ELISA. The effects of the allopurinol, a xanthine oxidase (XOD) inhibitor, on PSC were also examined. RESULTS: DDC decreased SOD activity and increased lipid peroxidation products in PSC. DDC activated PSC, increasing the number of alpha-SMA positive cells, enhancing secretion of type I collagen and MMP, inhibiting PSC proliferation. Secretion of TGF-beta1, which is known to activate PSC, was increased by DDC treatment. These alterations were prevented by allopurinol. CONCLUSION: These results suggest that free radicals generated by XOD might directly activate PSC.     

血红素氧合酶—1在慢性肾功能不全大鼠肾中的表达及其作用机制

目的 :探讨血红素氧合酶 1(HO 1)在慢性肾功能不全 (CRF)大鼠肾脏中的表达、活性变化以及对肾脏的作用 ,并探讨其作用机制。方法 :2 1只SD大鼠等分为 3组 :假手术组、CRF组和Hemin组。后 2组大鼠在相隔 1周的二次手术中接受肾 5 / 6切除术。第二次术后 8周检测各组血压、尿蛋白及其与尿肌肝比值、血清尿素氮、肌酐 ;观察肾组织病理改变。检测血清及肾组织中HO 1活性及促红细胞生成素 (EPO)含量 ;免疫组化方法检测HO 1在肾脏中的表达、分布。结果 :Hemin组血压、尿蛋白、血肌酐及尿素氮水平明显低于CRF组 (P <0 .0 5 ) ;肾小球系膜增生、间质炎性细胞浸润及纤维化程度明显减轻 (P <0 .0 5 ) ;免疫组化及HO 1活性检测显示 ,HO 1主要分布于肾小管上皮细胞内 ,在CRF大鼠肾脏中 ,HO 1表达及活性降低 ;Hemin组血清及肾组织EPO含量明显高于CRF组。结论 :HO 1通过上调血清及肾组织中EPO含量 ,从而延缓了肾脏病变     

Relationship between pentosidine levels in serum and urine and activity in rheumatoid arthritis

Pentosidine is one of the advanced glycation end-products and is formed by glycosylation and oxidation. The aim of this study is to investigate the relationship between serum and urinary pentosidine levels and the activity of rheumatoid arthritis (RA). Using HPLC with column switching, we measured pentosidine in serum and urine from 77 patients with RA and 62 normal control subjects. The clinical features, blood biochemistry and activity of inflammation were examined in RA patients. Serum and urinary pentosidine in RA were significantly higher than in controls. Pentosidine significantly correlated with age, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor, joint score and Lansbury Index in RA. The levels of pentosidine were higher in patients with active RA than in those with inactive RA. Serum and urine levels of pentosidine correlated with the activity of RA, and serum and urinary pentosidine may be a significant and novel marker for evaluating the disease status and the activity of RA.