复方二黄制剂对肾大部切除大鼠肾脏保护作用的疗效观察

目的观察复方二黄制剂对5／6肾切除大鼠慢性肾衰竭的防治作用。方法采用5／6肾切除模型,分为假手术组、肾大部切除组、尿毒清组、复方二黄制剂高剂量组、复方二黄制剂低剂量组,分别灌胃给药共8周。在灌胃前、灌胃后第4周和第8周时将每组大鼠称重,第8周留取24h尿液后处死大鼠,取血,离心取上清,留取肾组织。分别测定尿量、肾重,检测24h尿蛋白、血肌酐（SCr）、尿素氮（BUN）,进行统计学分析。结果肾大部切除后,大鼠逐渐出现肾衰竭,复方二黄制剂能使肾衰竭大鼠的体重、肾重／体重比、24h尿蛋白、SCr、BUN有不同程度的改善。结论复方二黄制剂对肾大部切除大鼠的慢性肾衰竭有一定的防治作用。     

泽兰防治慢性肾衰竭的实验研究

目的：观察泽兰对大鼠腺嘌呤慢性肾衰竭的影响;探讨泽兰防治慢性肾衰竭的药效学作用和机制。方法：建立大鼠腺嘌呤肾衰竭模型,用泽兰低（05g·100g-1·d-1）、中（1g·100g-1·d-1）、高（2g·100g-1·d-1）三组剂量连续灌胃共24d。观察大鼠一般状态的改变。第24天,结束灌胃,检测大鼠红细胞（RBC）、血红蛋白（Hb）、红细胞容积（HCT）和钙（Ca）、磷（P）、尿素氮（BUN）、肌肝（Scr）及肿瘤坏死因子（TNF-α）。观察肾病理组织学改变。结果：模型组体重进行性下降,给药组则升高。泽兰低中剂量在防治慢性肾衰竭是有效的;泽兰低中剂量升高RBC、Hb、HCT（P〈0.01）,纠正钙磷代谢紊乱（P〈0.05,P〈0.01）,降低BUN、Scr值（P〈0.01）,降低TNF-α含量（P〈0.01）,与尿毒清组比较无统计学意义（P〉0.05）。高剂量组则作用不明显（P〉0.05）。结论：适宜剂量的泽兰对大鼠慢性肾衰竭有改善作用。其机制与泽兰纠正肾衰竭时的贫血、低钙高磷现象、氮质血症,减少TNF-α对肾脏的纤维化损害有关。     

降浊颗粒对慢性肾衰竭模型微炎症状态的影响

目的：采用5/6肾切除方法建立大鼠慢性肾衰竭动物模型。以中药复方制剂＂降浊颗粒＂进行治疗,观察并评价治疗效果,探讨降浊颗粒对慢性肾衰竭模型微炎症状态的影响。方法：将大鼠随机分为正常组、模型组、对照组和治疗组。治疗组、对照组手术4周后给予＂降浊颗粒＂3.35g.kg-1.d-1灌胃,对照组给予＂尿毒清＂300mg·kg-1.d-1灌胃,模型组同时给予等量生理盐水灌胃;疗程8周。分别于给药前、第8周检测肌酐、尿素氮、24h尿蛋白定量,于第8周检测血C-反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）水平。结果：治疗组大鼠一般情况优于对照组,治疗组给药前BUN、Scr、24h尿蛋白定量与对照组比较差异无统计学意义（P〉0.05）,第8周BUN、Scr、24h尿蛋白定量、CRP、TNF-α明显低于模型组（P〈0.01）,BUN、Scr、CRP、TNF-α的改变优于对照组（P〈0.05）。结论：＂降浊颗粒＂对慢性肾衰竭大鼠有较好的治疗效果,可延缓慢性肾衰竭进展。其机制可能与减轻慢性肾衰竭微炎症反应有关。     

腺嘌呤灌胃联合高磷饮食诱导慢性肾衰竭血管钙化大鼠模型的探讨

目的:观察腺嘌呤灌胃联合高磷饮食方法诱导的慢性肾衰竭血管钙化大鼠模型。方法:30只SD大鼠随机分为正常对照组及模型组,每组15只。实验第1~4周,模型组大鼠按250 mg/kg剂量给予腺嘌呤混悬液灌胃及含1.8%高磷饲料喂养,第5~6周腺嘌呤改为隔日灌胃。正常对照组灌胃等体积生理盐水。共给药6周。6周后杀检取材,苏木精-伊红(HE)染色法观察两组大鼠肾脏病理及主动脉钙化结节形成情况;检测主动脉血管壁钙含量及碱性磷酸酶(ALP)水平;全自动生化仪测定血钙(Ca2+)、血磷(P3-)、血肌酐(Scr)、血尿素氮(BUN)、血清全段甲状旁腺激素(i PTH)水平。结果:与正常对照组比较,模型组肾小球结构紊乱,肾小管扩张积水,腔内有炎性细胞的浸润,肾小管内棕褐色结晶沉积,肾脏间质纤维化,肾脏血管明显减少;模型组主动脉出现广泛的呈连续线性分布的钙化结节;模型组大鼠主动脉钙含量及ALP水平均明显升高,差异有统计学意义(P0.01);与正常对照组比较,模型组大鼠血P3-、Scr、BUN、i PTH水平均明显升高,差异有统计学意义(P0.01),血Ca2+水平明显下降,差异有统计学意义(P0.01)。结论:腺嘌呤灌胃联合高磷饮食是制备慢性肾衰竭血管钙化大鼠模型较为快速、可行、准确的方法,值得进一步推广。     

复方鳖甲软肝片对慢性肾衰竭大鼠肾组织TGF-β1表达的影响

目的:探讨复方鳖甲软肝片对慢性肾衰竭(CRF)大鼠肾组织转化生长因子β1(TGF-β1)表达的影响.方法:采用5/6肾切除法制作大鼠CRF实验动物模型.将大鼠随机分为7组:正常组、假手术组、模型组、蒙诺组和复方鳖甲软肝片低、中、高剂量组.术后2个月处死大鼠,用肾小球硬化指数(GSI)和肾小管-间质损伤评分来评价各组大鼠肾组织病理改变,并应用免疫组化法检测肾组织TGF-β1的表达.结果:模型组与正常组和假手术组相比,GSI和肾小管-间质损伤评分明显升高(P＜0.05),肾组织TGF-β1表达显著增加(P＜0.05);复方鳖甲软肝片低、中、高剂量组和蒙诺组与模型组相比,GSI和肾小管-间质损伤评分明显降低(P＜0.05),肾组织TGF-β1表达明显减少(P＜0.05);复方鳖甲软肝片低、中、高剂量组、蒙诺组四组间在GSI、肾小管-间质损伤评分和TGF-β1表达方面比较均无统计学差异(P＞0.05).结论:复方鳖甲软肝片能下调CRF大鼠肾组织TGF-β1的过度表达,减轻肾脏病理组织学损伤,这一下调作用可能是该药治疗CRF和抗肾纤维化的机制之一.     

肾血康对肾性贫血大鼠外周血象与红细胞脆性及EPO含量的影响

目的:探讨肾血康治疗肾性贫血大鼠的药理、药效.方法:将SD大鼠随机分为空白组、模型组及中药组,以中药肾血康对腺嘌呤所致慢性肾衰竭大鼠进行治疗,并比较大鼠治疗前后的外周血象、EPO含量、红细胞脆性等各项指标.结果:肾血康能降低肾衰竭大鼠血中Scr及BUN,降低红细胞脆性,而升高其血中Hb、RBC、HCT、EPO水平.结论:肾血康能有效改善腺嘌呤所致慢性肾衰竭大鼠的贫血症状,防止肾小球硬化,延缓肾功能的进一步恶化.     

益肾汤经结肠透析对慢性肾衰竭大鼠肠上皮细胞IRE1α、GRP78表达的影响

目的:观察益肾汤经结肠透析对慢性肾衰竭(CRF)大鼠肠上皮细胞IRE-1α、GRP78表达的影响。方法:随机在60只健康雄性SD大鼠中抽取45只，腺嘌呤灌胃诱导建立CRF大鼠模型，其余15只为正常组。将造模成功大鼠随机分为CRF组、尿毒清结肠透析组和益肾汤结肠透析组，尿毒清结肠透析组予尿毒清结肠透析，益肾汤结肠透析组予益肾汤结肠透析，实验周期为4周。实验过程中记录大鼠一般状况、体重、血肌酐(Scr)、血尿素氮(BUN)的变化，4周末取肾组织、结肠组织行HE染色观察组织学改变，免疫组化检测各组结肠组织IRE1α、GRP78的表达及分布情况，实时荧光定量PCR法测定IRE1α、GRP78 mRNA表达情况。结果:(1) CRF组大鼠一般情况较正常组差，体重增长减慢(P <0.05)，而尿毒清结肠透析组及益肾汤结肠透析组与CRF组相比有所改善，体重增加(P <0.05);(2)与正常组比较，CRF组Scr、BUN值升高(P <0.05)，免疫组化示肠上皮细胞IRE1α、GRP78表达均明显上调(P <0.05),PCR结果显示GRP78、IRE1α mRNA相对表达量...     

肾毒宁冲剂对慢性肾衰竭大鼠肾组织TGF-β1和CTGF的影响

目的：观察肾毒宁冲剂对5/6肾切除慢性肾衰竭（CRF）大鼠肾组织转化生长因子-β1（TGF-β1）、结缔组织生长因子（CTGF）的影响。方法：取雄性SD大鼠,通过Platt法5/6肾切除制作CRF模型,术后2周行大鼠断尾采血,测定血清肌酐（Scr）、尿素氮（BUN）值,根据Scr随机分为模型组、尿毒清组及肾毒宁组,并设正常组和假手术组。饲养或治疗8周后处死大鼠,测定血Scr、BUN、Hb、RBC,用Real-time PCR法测定肾组织内TGF-β1及CTGF的表达。结果：肾毒宁组血Scr、BUN、Hb、RBC与模型组相比有统计学差异（P〈0.01）。肾毒宁冲剂对肾组织内TGF-β1、CTGF表达有较强的抑制作用（P〈0.05和P〈0.01）,尿毒清冲剂作用次之,肾毒宁组与尿毒清组间无统计学差异。结论：肾毒宁冲剂通过抑制肾组织TGF-β1、CTGF的表达,降低血清Scr、BUN含量,从而起到延缓CRF肾功能的恶化,改善肾脏纤维化的作用。     

复方鳖甲软肝片对单侧输尿管结扎大鼠肾组织NF-κB 表达的影响

目的:探讨核转录因子-κB(NF-κB)在肾间质纤维化中的表达情况及其复方鳖甲软肝片的干预作用.方法:采用单侧输尿管结扎(UUO)肾间质纤维化模型.将大鼠随机分为7组,即:正常组、假手术组、模型组、苯那普利组和复方鳖甲软肝片低、中、高剂量组.术后4周处死大鼠,观察肾组织病理改变,并应用免疫组织化学方法检测肾组织NF-κB的表达.结果:模型组肾组织表现为纤维化病理改变,正常组及假手术组肾小管上皮细胞、肾间质细胞胞浆有较弱的NF-κB表达;模型组肾小管上皮细胞、肾间质细胞激活的NF-κB在胞核强阳性表达;复方鳖甲软肝片组病理改变较模型组纤维化程度减轻,NF-κB的表达较模型组显著减少,有统计学差异(P<0.05),与苯那普利组比无统计学差异但也有所减少.结论:复方鳖甲软肝片通过抑制NF-κB的过度表达而减缓肾纤维化病程进展.     

复方萆薢汤对尿酸性肾病大鼠尿NGAL和KIM-1的影响

目的：观察复方萆薢汤对尿酸性肾病大鼠尿中性粒细胞明胶酶相关脂质运载蛋白（NGAL）和肾损伤因子-1（KIM-1）的影响.方法：将72只SD雄性大鼠随机分为6组,正常对照组、模型组、别嘌呤醇组、低（BX1）、中（BX2）、高剂量（BX3）复方萆薢汤组,采用氧嗪酸钾制作尿酸性肾病大鼠模型,造模后分组给药,分别给予生理盐水、别嘌呤醇、低、中、高剂量复方萆薢汤[10g· kg-1·d-1、20 g· kg-1·d-1、40 g·kg-1·d-1]灌胃,于给药后每隔1周,检测各组大鼠血清尿酸（UA）、尿素氮（BUN）、肌酐（Scr）水平;并于每次取血前1天留取24h尿液,检测尿NGAL和KIM-1的含量.结果：（1）自治疗第2周起,模型组与正常对照组比较,血清UA、BUN、Scr升高,差异有统计学意义（P＜0.05）,低、中、高剂量复方萆薢汤组,大鼠血清UA、BUN、Scr较模型组均明显降低（P＜0.05）,呈剂量依赖性,但均高于正常对照组（P＜0.05）;低剂量复方萆薢汤组与别嘌呤醇组效果相当（P＞0.05）;（2）与模型组比较,自治疗第1周起,低、中、高剂量复方萆薢汤组尿NGAL和KIM-1的含量明显降低（P＜0.05）,并随剂量的增加降低明显,但低剂量复方萆薢汤组与别嘌呤醇组之间NGAL和KIM-1的含量差异无统计学意义（P＞0.05）.结论：复方萆薢汤能降低尿酸性肾病大鼠血清UA、BUN、Scr的水平,降低NGAL和KIM-1在尿酸性肾病大鼠尿中的表达,具有保护肾功能的作用.     

尿毒清颗粒对糖尿病大鼠肾脏炎症损伤的影响

目的探讨尿毒清颗粒对糖尿病大鼠肾脏炎症损伤的保护作用。方法选用链脲佐菌素（STZ）诱导的糖尿病大鼠模型。实验分3组：正常对照组（N组）、糖尿病未干预组（D组）、尿毒清颗粒治疗组（Q组,2．6g·kg-1·d-1灌胃）,于第4、8周末检测血肌酐（SCr）、尿肌酐（Ucr）,计算肌酐清除率（Ccr）,检测血清超敏C反应蛋白（hs—CRP）、肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）,光镜观察肾组织病理改变,免疫组织化学检测肾组织核因子xB（NF-kB）、单核细胞趋化蛋白1（MCP-1）表达,检测肾皮质MCP-1mRNA表达。结果尿毒清颗粒可以提高糖尿病大鼠Ccr（P〈0．01）,改善肾脏病理损伤,减少血清hs-CRP、肾组织NF-kB、MCP-1表达（P〈0．1）5,P〈0．01）,对血清TNF-α、IL-6影响不显著。结论炎症反应参与糖尿病大鼠肾脏损伤,尿毒清颗粒能降低血清及肾脏炎症介质表达,对糖尿病大鼠肾脏炎症损伤起保护作用。     

脊髓损伤对大鼠骨转换及骨密度的影响

目的：探讨脊髓损伤（spinal cord injury,SCI）对大鼠骨转换及骨密度的影响。方法：60只3月龄SD大鼠均分为SCI组与对照组。SCI组于T10处完全横断脊髓;对照组仅行椎板切除术。术后1、3、6周时处死动物测血清钙（Ca）、磷（P）、碱性磷酸酶（ALP）、尿钙、磷、肌酊（Cr）以及股骨、股骨骨密度（bone mineral density,BMD）。:桂花 血钙、尿钙、尿钙／肌酝在伤后不同时间段均升高;血ALP在伤后1周时显著下降,3、6周时恢复正常。胫骨近端,股骨远、近端的BMD在6周时较对照组下降且差异显著。结论：SCI大鼠可见明显的骨转换增高以及破骨活性增强,其生化、骨密度的改变与人体有较好的相关性。SD大鼠可用于评价SCI后骨代谢改变,具可以作为SCI后骨质疏松的模型。     

Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. I. Renal function and biochemical changes.

BACKGROUND: Both dietary phosphorus restriction and the ingestion of ammonium chloride (NH(4)Cl) given to rats on a high-phosphorus diet have been shown to preserve renal function in the azotaemic rat. Parathyroidectomy also has been reported to preserve renal function and, in addition, to prevent kidney hypertrophy in the remnant kidney model. Our goals were (i) to evaluate in azotaemic rats the effect of dietary phosphorus on renal function in a shorter time frame than previously studied and (ii) to determine whether NH(4)Cl administration (a) enhances the renoprotective effect of dietary phosphorus restriction and (b) improves renal function in the absence of parathyroid hormone (PTH). METHODS: High (H; 1.2%), normal (N; 0.6%) and low (L; <0.05%) phosphorus diets (PD) were given for 30 days to 5/6 nephrectomized rats. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups were HPD + NH(4)Cl, HPD, NPD + NH(4)Cl, NPD, LPD + NH(4)Cl and LPD. The effect of NH(4)Cl administration was also evaluated in 5/6 nephrectomized, parathyroidectomized (PTX) rats on NPD. RESULTS: In each of the three dietary phosphorus groups, creatinine and urea clearances were greater (P<0.01) in rats receiving NH(4)Cl. Neither creatinine nor urea clearance was reduced by high dietary phosphorus. Urine calcium excretion was greatest in the LPD group and was increased (P < or = 0.001) in all three groups by NH(4)Cl ingestion. An inverse correlation was present between plasma calcium and phosphorus in the parathyroid intact (r = -0.79, P<0.001) and PTX groups (r = -0.46, P = 0.02). In PTX rats, NH(4)Cl ingestion increased (P < or = 0.01) creatinine and urea clearances and both an increasing plasma calcium concentration (r = 0.67, P<0.001) and urine calcium excretion (r = 0.73, P<0.001) increased urine phosphorus excretion. CONCLUSIONS: At 30 days of renal failure (i) NH(4)Cl ingestion increased creatinine and urea clearances, irrespective of dietary phosphorus; (ii) high urine calcium excretion, induced by dietary phosphorus restriction and NH(4)Cl ingestion, did not adversely affect renal function; (iii) high dietary phosphorus did not decrease renal function; (iv) the absence of PTH did not preserve renal function or prevent NH(4)Cl from improving renal function; and (v) both an increasing plasma calcium concentration and urine calcium excretion resulted in an increase in urine phosphorus excretion in PTX rats.     

尿毒清颗粒对糖尿病大鼠足细胞损伤的保护作用研究

目的：探讨尿毒清颗粒对糖尿病大鼠足细胞损伤的保护作用。方法：将SD大鼠制备成STZ糖尿病模型,实验分3组：正常对照组、糖尿病未干预组、尿毒清颗粒治疗组（2.6g·kg-1·d-1灌胃）,于实验第4周、8周末检测血糖、血肌酐、尿肌酐及尿白蛋白排泄率,光镜、电镜下观察肾组织病理改变并计数足突宽度,免疫组化观察足细胞相关蛋白分子nepherin、podocin的表达,Real time-PCR检测肾皮质nepherin、podocin mRNA表达。结果：尿毒清颗粒可以改善糖尿病大鼠肌酐清除率,降低尿白蛋白排泄,改善肾脏病理,减轻足突融合,维持足细胞相关蛋白分子的分布与表达。结论：初步证实尿毒清颗粒能通过上调足细胞相关蛋白分子水平减轻足细胞损伤,对糖尿病大鼠足细胞损伤具有保护作用。     

Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. Part II--Kidney hypertrophy and calcium deposition.

BACKGROUND: Kidney hypertrophy is stimulated by both partial nephrectomy and NH(4)Cl administration. Also, parathyroidectomy (PTX) has been reported to prevent kidney hypertrophy induced by a high protein diet. Our goal was to determine in the azotaemic rat: (i) the combined effects of NH(4)Cl administration and dietary phosphorus on the development of kidney hypertrophy and calcium deposition in the kidney and (ii) whether the absence of parathyroid hormone (PTH) affected the development of kidney hypertrophy and calcium deposition. METHODS: High (HPD, 1.2%), normal (NPD, 0.6%) or low (LPD, <0.05%) phosphorus diets were given to 5/6 nephrectomized rats for 30 days. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups of rats were: (i) HPD + NH(4)Cl; (ii) HPD; (iii) NPD + NH(4)Cl; (iv) NPD; (v) LPD + NH(4)Cl and (vi) LPD. In a separate study, PTX was performed to determine whether PTH affected renal hypertrophy in 5/6 nephrectomized rats given NH(4)Cl. RESULTS: Both with and without NH(4)Cl (+/-NH(4)Cl), kidney weight was greatest (P<0.05) in the HPD groups. In each dietary phosphorus group, kidney weight was greater (P<0.05) in the NH(4)Cl group. In both the +/-NH(4)Cl groups, kidney calcium content was greatest (P<0.05) in the HPD group, but was less (P<0.05) in the NPD and HPD groups given NH(4)Cl. An inverse correlation was present between creatinine clearance and kidney calcium content (r = -0.51, P<0.001). When factored for kidney weight, creatinine clearance was less (P<0.05) in the HPD group in both the +/-NH(4)Cl groups, but was greater in the HPD + NH(4)Cl than in the HPD group. In PTX rats, kidney weight was greater (P<0.05) and kidney calcium deposition was less (P<0.05) in rats given NH(4)Cl. CONCLUSIONS: In azotaemic rats studied for 30 days, NH(4)Cl administration induced kidney hypertrophy. A HPD also induced kidney hypertrophy. The effects on kidney calcium deposition were divergent for which NH(4)Cl administration decreased and a HPD increased calcium deposition. The inverse correlation between kidney calcium content and creatinine clearance suggests that kidney calcium deposition is harmful to renal function. When factored for kidney weight, the lower creatinine clearance in the high phosphorus group suggests that kidney hypertrophy does not completely compensate for the harmful effects of a HPD. This result also suggests that a longer study would probably result in more rapid deterioration in the high phosphorus group. In PTX rats, the absence of PTH did not prevent NH(4)Cl from inducing kidney hypertrophy and reducing kidney calcium deposition. In conclusion, NH(4)Cl and dietary phosphorus each independently affect kidney growth and calcium deposition in the growing rat with renal failure.     

蛇床子素对绝经后骨质疏松症大鼠骨代谢的调节作用及机制

目的 探究蛇床子素对绝经后骨质疏松症(postmenopausal osteoporosis,PMO)模型大鼠骨代谢生化指标及磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/AKT)通路的影响.方法 选取90只雌性大鼠,采用随机数字表法将大鼠分为:健康对照组、模型组、雌二醇组和蛇床子素低、中、高剂量组,每组15只.除健康对照...     

杜仲黄酮类3种药物成分治疗大鼠骨质疏松的比较研究

目的研究杜仲黄酮类3种药物成分治疗大鼠骨质疏松的疗效。方法将51只SD大鼠随机分为假手术组、模型组、雌激素组、槲皮素组、山奈酚组和芦丁组。假手术组与模型组给予羧甲基纤维素钠,雌激素组与3个药物组分别给予雌激素及对应药物。12 w后测定大鼠体重及子宫重量,并测定骨形成及代谢相关血液学、尿液指标,Micro-CT分析骨相关参数及骨小梁形态。结果相同药物浓度下,山奈酚、芦丁、槲皮素3种药物成分均可降低尿液中钙、磷的丢失,同时增强碱性磷酸酶的活性,其中山奈酚的作用优于芦丁和槲皮素。山奈酚、芦丁和槲皮素均可改善绝经后骨质疏松的骨微结构,增加骨密度,尤其是山奈酚,但均不能使骨小梁结构完全恢复。结论杜仲黄酮类3种药物成分中,山奈酚治疗大鼠骨质疏松的疗效最佳,芦丁次之,槲皮素最弱。     

How dietary phosphate, renal failure and calcitriol administration affect the serum calcium-phosphate relationship in the rat.

BACKGROUND: The effect of hyperphosphataemia on serum calcium regulation in renal failure has not been well studied in a setting in which hypercalcaemia is not parathyroid hormone (PTH) mediated. In azotemic rats with a normal serum calcium concentration, an increased dietary phosphate burden affects serum calcium regulation because of its effects on skeletal resistance to PTH, calcitriol production, and possibly intestinal calcium absorption. Our goal was to determine how hyperphosphataemia affected the development of hypercalcaemia during calcitriol-induced hypercalcaemia and PTH suppression in azotemic rats with established hyperparathyroidism. METHODS: Rats underwent a two-stage 5/6 nephrectomy or corresponding sham operations. After surgery, rats were given a high phosphate diet (P 1.2%) for 4 weeks to exacerbate hyperparathyroidism and were then changed to a normal diet (P 0.6%) for 2 weeks to normalize serum calcium values in the azotemic rats. At week 7, rats were divided into five groups and sacrificed after receiving three intraperitoneal doses of calcitriol (CTR, 500 pmol/100 g) or vehicle at 24 h intervals. The five groups and dietary phosphate content were: group 1, normal renal function (NRF)+0.6% P+vehicle; group 2, NRF+0.6% P+CTR; group 3, renal failure (RF)+0.6% P+vehicle; group 4, RF+1.2% P+CTR; and group 5, RF+0.6% P+CTR. Both the 0.6% and 1.2% phosphate diets contained 0.6% calcium. RESULTS: Serum creatinine values were increased (P<0.05) in 5/6 nephrectomized rats (groups 3, 4 and 5), as were serum calcium values (P<0.05) in CTR-treated rats (groups 2, 4 and 5) and serum phosphate values (P<0.05) in CTR-treated azotemic rats (groups 4 and 5). Serum PTH values were suppressed (P<0.05) in CTR-treated hypercalcemic rats (groups 2, 4 and 5) and increased (P<0.05) in azotemic rats not given CTR (group 3). In the azotemic groups (groups 3, 4 and 5), an inverse correlation was present between serum calcium and phosphate in each group, despite a wide variation in serum calcium values. The slope of the inverse relationship between serum calcium and phosphate was steeper in CTR-treated azotemic rats on a 1.2% phosphate (group 4) diet than on a 0.6% phosphate (group 5) diet (P=0.02). Thus, for a similar increase in the serum phosphate concentration, serum calcium values decreased more in group 4 than in group 5. The independent effect of dietary phosphate on serum calcium values was also confirmed by analysis of covariance. Finally, the serum calcium concentration was shown to be greater for any given serum phosphate value in CTR-treated rats than in those not on CTR. CONCLUSIONS: In azotemic rats with calcitriol-induced hypercalcaemia, the magnitude of hypercalcaemia is affected by: (i) the serum phosphate concentration; and (ii) differences in dietary phosphate content. Calcitriol administration also acts to shift upwards the relationship between serum calcium and phosphate so that a higher serum calcium concentration can be maintained for any given serum phosphate value.     

脊髓损伤大鼠股骨松质骨超微结构的变化

目的　探讨脊髓损伤 (SCI)对大鼠骨组织超微结构的影响及其在SCI后骨代谢变化中的意义。方法　 40只 3个月龄SD大鼠均分为SCI组与对照组。SCI组于T1 0 处完全横断脊髓 ;对照组仅行椎板切除术。术后 1、3周时处死动物后用透射电镜对股骨髁部进行超微结构观察并检测血清钙(Ca)、碱性磷酸酶 (ALP)、尿钙、尿钙 /肌酐 (Ca/Cr)的变化。结果　SCI组大鼠 1周时可见显著的成骨细胞凋亡的发生 ;3周时可见凋亡的骨细胞 ,而成骨细胞多处于正常状态。截瘫鼠血钙、尿钙、尿钙 /肌酐酶在伤后不同时间段均升高 ;血ALP在伤后 1周时显著下降 ,3周时恢复正常。结论　SCI后早期成骨代谢受抑制可能与成骨细胞凋亡有关 ;骨细胞凋亡可能在破骨 -成骨脱偶联中起中介作用     

Role of Oxalobacter formigenes in preventing calcium oxalate kidney stones

Objective To screen Oxalobacter formigenes (OxF) from fresh feces of healthy adults, and study its effect on the the prevention of calcium oxalate kidney stones. Methods OxF was screened and cultured from fresh feces of healthy adults. The rat model of calcium oxalate stone was established by esophageal gavage of 0.8% of ethylene glycol. Rats were divided into a control group and four groups of rats with ethylene glycol-induced calcium oxalate kidney stones according to random number table. Three groups were treated with 106 CFU, 107 CFU, 108 CFU viable OxF every day, respectively, for 4 weeks. The blood and 24-hour urine samples were collected to detect the serum creatinine, urea nitrogen, serum and urine calcium, phosphorus, magnesium and urine oxalate every week. At the end of the 4th week, the rats were sacrificed and the kidney tissues were stained with HE and Yasue. The deposition and content of calcium oxalate crystals were observed under a light microscope. Results The bacteria strain isolated from fresh feces of healthy adults was 100% as same as the known ATCC35274 bacteria strain, which means the strain screened is OxF. Among the 5 groups, there were no significant differences in body weight, Scr, BUN, serum calcium, blood magnesium, blood phosphorus, urinary magnesium and urinary phosphorus. The 24-hour urinary calcium excretion in the model group was significantly lower than that of the control group (P＜0.05). After intervention with OxF solution, the 24-hour urinary calcium excretion in the 108 CFU OxF group was significantly higher than that in the model group (P＜0.05), while there was no significant difference between the other intervention groups and the model. The oxalic acid excretion of 106 CFU OxF group and 107 CFU OxF group was lower than that of the model, but the difference did not reach statistical significance (P＞0.05). The 24 h oxalic acid excretion in the 108 CFU OxF group was significantly lower than that of the model at the end of first week (P＜0.05), and continued to decrease for the next 3 weeks. After 4 weeks of intervention, no crystal formation was observed in the control group under the deflection microscope, but a large amount of calcium oxalate crystals were formed in the renal cortex and renal medulla. The crystals were piled up and connected to each other. Yasue staining coincided with the calcium oxalate crystal in the same part of the kidneys. Compared with the model, there was no significant change in the score of calcium oxalate crystal in the kidneys of 106 CFU OxF group and 107 CFU OxF group, while the score of calcium oxalate crystal in the kidneys of 108 CFU OxF group was significantly lower (P＜0.05). Conclusions OxF are successively screened from healthy adults. Daily administration of 108 CFU OxF can safely and effectively reduce the urinary oxalic acid excretion, prevent the formation of calcium oxalate crystals and inhibit the formation of stones in kidneys of rats.