目的 探讨阿托伐他汀对血液透析治疗患者心功能及血清可溶性ST2与半乳糖凝集素3(Galectin-3)水平的影响,为透析相关治疗提供参考.方法 前瞻性选取2017年3月至2020年3月合肥市滨湖医院肾内科血液透析中心的维持性血液透析患者60例,采用随机数字表分成治疗组(n=30)与对照组(n=30).对照组患者在血液透析治疗中常规注射重组人促红细胞生成素并控制血压等,治疗组患者则在透析治疗同时予以口服阿托伐他汀(10～20 mg/d)治疗.2组均连续治疗3个月,治疗期均严密监测患者体征变化等.比较2组患者治疗前、治疗3个月后心功能指标[左室射血分数(LVEF)、心排血量(CO)以及室间隔舒张末期厚度(LVST)]、血清可溶性ST2、Galectin G3水平及不良反应发生情况.结果 治疗3个月后,治疗组患者的LVEF、CO水平[(5.00±0.64)L/min、(67.34±7.71)％]较治疗前[(4.10±0.42)L/min、(55.13±7.61)％]显著升高,且治疗组显著高于对照组[(4.20±0.24)L/min、(57.61±7.28)％],差异均有统计学意义(P<0.05);治疗前、治疗3个月后,2组LVST水平比较均无明显变化,差异无统计学意义(P>0.05).治疗3个月后,治疗组患者的血清可溶性ST2、Galectin-3水平[(12.74±7.36)、(6.34±4.20)ng/mL]均较治疗前[(22.09±8.83)、(12.62±6.54)ng/mL]显著下降,且治疗组显著低于对照组[(24.21±9.24)、(14.51±6.47)ng/mL],差异均有统计学意义(P<0.05).2组患者治疗中均无严重的用药不良反应发生,安全性高.结论 在血液透析治疗过程中,阿托伐他汀的应用能够有效降低血清可溶性ST2、Galectin-3水平,显著改善患者的心功能且用药安全性较高,具有一定的应用价值.

目的 分析比较缝线微袋形术与舌下囊肿摘除术治疗舌下腺囊肿的疗效,为临床治疗舌下腺囊肿提供参考.方法 回顾性分析我院2016年2月～2020年2月收治的75例舌下腺囊肿患者临床资料,分为舌下囊肿摘除术组40例、缝线微袋形术组35例.比较两组临床疗效、手术相关指标、并发症、复发情况.结果 舌下囊肿摘除术组临床总有效率97.50％高于缝线微袋形术组88.57％,但比较差异无统计学意义(P＞0.05);缝线微袋形术组术中出血量、手术时间、术后VAS评分均显著低于舌下囊肿摘除术组(P＜0.05);舌下囊肿摘除术组并发症发生率22.50％明显高于缝线微袋形术组5.71％(P＜0.05);缝线微袋形术组复发率14.29％高于舌下囊肿摘除术组的2.50％,但比较差异无统计学意义(P＞0.05).结论 缝线微袋形术治疗舌下腺囊肿临床总有效率不如舌下囊肿摘除术,但疗效仍较好,围术期创伤小、出血量低、疼痛程度低、并发症少,值临床推广使用.

目的 分析腹膜透析(PD)在颅内出血患者肾损伤中的应用价值.方法回顾性分析本院收治的颅内出血急性肾损伤(AKI)患者腹膜透析8例.结果 8例AKI患者中,治愈4例(50.0%),继续腹膜透析2例(25.0%),自动出院1例(12.5%),死亡1例(12.5%).PD后SCr、BUN和血清K+水平均较透析前显著下降(P ＜ 0.05),CO2CP水平较透析前显著升高(P ＜ 0.05).结论 PD对颅内出血AKI具有良好的治疗效果,是AKI治疗的最佳选择.

Objective: To analyze the clinical application of acute physiology and chronic health evaluation(APACHE) scoring in acute renal failure(ARF) patients under sustained low-efficiency dialysis(SLED).Methods: We studied 88 ARF patients under SLED in our hospital in the year from February 2007 to October 2010.We calculated the APACHEIII scores before SLED in 24 hours,and estimated their coefficient of mortality risk also.Results: We collected a total of 88 ARF patients under SLED.Their age ranged(61.1±16.8) years,60 patients were suivial,and 28 patients were died.The death groups used SLED for oliguria,acid-base unbalance,electrolyte disturbance and SIRS,while the survival groups for water load and creatinine increase.The average APACHEIII score was(90.8±28.7),and the coefficient of mortality risk was(0.68±0.31).The APACHEIII score in death and survival groups was(112.3±26.5) and(75.7±15.9) respectively(t=6.75,P0.001).The risk of death was 60.2% when the APACHEIII score was 50,and the fatality was 90.0% when the APACHEIII score was 70.It showed that hyperbilirubinemia(P=0.029),mechanical ventilation(P=0.001) and hypotension(P=0.025)were the risk factors affecting the prognosis of SLED patients by statistical tests.Conclusion: The prognosis of SLED patients is closely correlated to.The APACHEⅢ score between the group of died patients and survival patients under SLED was siginificant differences,APACHEⅢ scoring can be applied to predict mortality of ARF patients under SLED.

Objective:To explore the clinical significance of serum Cys-C measured in the patients with diabetic nephropathy. Method:According to the UAER level,104 patients with diabetic nephropathy were separated into three groups which were A group(45),B group(31) and C group(28),fasting serum Cys-C,2-MG,BUN,Cr levels were measured as well as the normal control group.Result: The Cys-c level of A group was(0.78±0.67)mg/l which was significantly higher than the level of the normal control group which was (0.51±0.12)mg/l(P<0.05).2-MG,BUN and Cr levels of B and C groups were all increased too,but were not apparently higher than normal control group(P>0.05).Along with the aggravation of the disease,Cys-C,2-MG,BUN and Cr levels were increased in B and C groups,and all the difference have statistics significance(P<0.01).Conclusion:Cys-C is an ideal endogenous marker in the reflection of changes of glomerular filtration rate,which plays an important role in the early diagnosis of diabetic nephropathy.

目的探讨LY333531对糖尿病大鼠肾组织转化生长因子β1(TGFβ1)表达的调节作用.方法建立链脲佐菌素(STZ)诱导糖尿病模型,随机分对照组,糖尿病模型组及LY333531给药组(10 mg·kg-1·d-1,灌胃).8周后应用放射活性测定法检测肾组织细胞总蛋白激酶C(PKCt)、细胞浆PKC(PKCc)及细胞膜PKC(PKCm)活性,免疫组化方法检测肾组织TGFβ1表达.结果模型组肾组织PKCt活性、PKCc活性、PKCm活性及PKCm/PKCc明显高于对照组(P＜0.05,P＜0.01);LY333531给药组PKCt活性、PKCc活性、PKCm活性及PKCm/PKCc明显低于模型组(P＜0.05).模型组肾小球TGFβ1表达明显高于对照组(P＜0.01),LY333531对其有明显抑制作用(P＜0.05).结论LY333531对糖尿病肾脏有明显保护作用,机制可能与抑制肾组织TGFβ1过度表达有关.

AIM: To study the effect of breviscapine on the oxidative stress in the liver and kidney in diabetic rats. METHODS: Diabetes was induced by injection of streptozotocin (ST Z). Rats were randomly divided into three groups: control group, model group, mo del group treated with breviscapine. 8 weeks after STZ injection, liver lesion w as evaluated using HE, oil red O staining and kideny lesion using PAS staining. Malondiadehyde (MDA) levels and antioxidant activities in liver and kidney tissu e were determined by spectrophotometric method. RESULTS: Light microscopy in HE staining showed that liver fatty score was significantly lower in the breviscapine group compared with model ani mals (0.55±0.43 vs 1.54±0.65, P0.01). In model group, the presen ce of cytoplasmic lipid deposits was confirmed by oil red O staining, and these changes were significantly lower in the breviscapine group than those in the mod el group (0.75±0.66 vs 2.11±0.82, P0.01). In addition, increased kidney weight (KW), KW/body weight (KW/BW), 24 h albumin excretion rate (AER) a nd glomerular area (A G), glomerular volume (V G) as well as mesangial area (A M) on histological examination of the kidney significantly attenuated by treat ment with breviscapine (P0.05, P0.01). Levels of MDA were higher and sup eroxide diamutase (SOD), catalase (CAT) as well as glutathione peroxidase (GSH-P x) activities were significantly lower in liver and kidney tissue in model rats than those in control group. Breviscapine administration could all remit these c hanges (P0.05). CONCLUSION: The mechanism of protective effect of breviscapine o n liver and kidney may be at least partly correlated with the suppression of inc rease in oxidative stress in diabetic rats.

Objective To investigate the clinical effect of estrogen combined with progestogen replacement therapy on patients with secondary premature ovary failure (POF) induced by Triptergium wifordii (TW). Methods Twenty-one patients who suffered from secondary suspend menses by TW were treated by estrogen combined with progestogen replacement therapy periodically. The serum levels of E2, LH and FSH were examined and changes of menses and clinical manifestations were observed respectively before and 3 months after the ending of treatment.Results All of the patients were confirmed as POF according to the levels of blood sexual hormone and clinical manifestations. The E2 secreted by ovary was higher [ (392.90±77.53 )pmol/L vs. (83.47±8.46)pmol/L, P 0.01 ] and L [ (5.91±2.67)U/L vs.(52.62±15.65)U/L,P 0.01 ],FSH [ (6.70±2.24)U/L vs.( 110.87± 20.34)U/L, P 0.01 ] secreted by pituitary were lower alter treating as compared to those before treating.Their clinical perimenopause symptoms were improved and situations were stable after treatment. The total efficiency for this treatment was 90.47%. Conclusions TW may result in POF. It is an effective method that stopping TW immediately and treating with estrogen combined with progestogen replacement therapy periodically in these patients.

目的探讨霉酚酸酯(MMF)对糖尿病大鼠肾组织结缔组织生长因子(CTGF)表达的影响.方法建立单侧肾切除糖尿病模型,大鼠随机分为对照组、糖尿病组与MMF给药组.8周末检测24小时尿白蛋白排泄率(AER)、肾组织与尿丙二醛(MDA)含量;并行肾组织形态学指标观察;应用免疫组化方法检测肾组织CTGF表达.结果MMF给药组大鼠肾重、肾重/体重、AER与肾小球面积、肾小球容积、系膜区面积明显低于模型组(P＜0.05,P＜0.01);MMF给药组可明显减少糖尿病大鼠肾组织及尿MDA含量(P＜0.05);模型组肾小球CTGF表达明显高于对照组(P＜0.01),MMF给药组这些改变明显减轻(P＜0.01).结论MMF对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织氧化应激、下调CTGF表达有关.

AIM: To investigate the effects and mechanism of enalapril on nephritis of diabetic mice. METHODS: Diabetes was induced by injection of streptozotocin after uninephrectomy. Rats were randomly divided into three groups: control, diabetes, diabetes treated with enalapril (10 mg·kg~-1 ·d~-1 by gavage). 8 weeks after STZ injection, urine albumin excretion rate (AER) were measured, and glomerular morphology were observed by light microscopy. The levels of malonyldialdehyde (MDA) in renal tissue and urine as well as activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) in renal tissue were determined. Immunohistochemistry for ED-1 (macrophage marker), monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) were performed by streptavidin-biotin complex (SABC) technique. RESULTS: Increased kidney weight, ratio of kidney weight to body weight, AER and expansion of mesangial as well as tuft areas on histological examination of the kidney were significantly attenuated by the treatment of enalapril (P0.05, P0.01). Elevated MDA levels in renal tissue and urine as well as decreased SOD, CAT, GSH-PX activities in renal tissue were also remitted by enalapril (P0.05). Increased glomerular macrophage recruitment and expression of MCP-1 was significantly inhibited by enalapril (P0.05). However, elevated ICAM-1 expression was not reduced by enalapril in glomerulus in diabetic rats. CONCLUSION: Possible mechanism of renal protection of enalapril may be at least partly related with suppression of inflammation in kidney of diabetic rats.

目的探讨LY333531对大鼠糖尿病模型肾组织结缔组织生长因子(CTGF)表达的影响.方法建立链脲佐菌素(STZ)诱导糖尿病模型,随机分对照组,糖尿病组及LY333531给药组(10 mg/(kg·d),灌胃.8周后观察各组体重、肾重、肾重/体重、24 h尿白蛋白排泄率(AER)及肾组织蛋白激酶C(PKC)活性的变化,行PAS染色肾小球病理形态学观察及CTGF免疫组化.结果 LY333531给药组大鼠体重明显高于模型组(P<0.05),肾重、肾重/体重、AER及肾小球面积(AG) 、肾小球容量(VG) 及系膜区面积(AM) 明显低于糖尿病组(P<0.05,P<0.01);模型组肾组织PKCt活性、PKCc活性、PKCm活性及PKCm/ PKCc明显高于对照组(P<0.05, P<0.01);LY333531给药组PKCt活性、PKCc活性、PKCm活性及PKCm/ PKCc明显低于模型组(P<0.05).模型组肾小球CTGF表达明显高于对照组(P<0.01),LY333531对其有明显抑制作用(P<0.05).结论 LY333531对糖尿病肾脏有明显保护作用,机制可能与抑制肾组织CTGF过度表达有关.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的探讨灯盏花素对糖尿病大鼠肾组织巨噬细胞浸润的影响。方法建立STZ诱导的单侧肾切除糖尿病模型,随机分:对照组、模型组、灯盏花素给药组与MMF给药组。8wk末检测尿白蛋白排泄率（AER）、肾组织蛋白激酶C（PKC）活性,应用免疫组化方法检测肾组织ED1及单核细胞趋化蛋白1（MCP1）与细胞间黏附因子1（ICAM1）表达。结果灯盏花素或MMF给药组大鼠肾重、肾重/体重、AER明显低于模型组（P&lt;0.05）。模型组肾组织细胞浆、细胞膜及细胞总PKC活性明显高于对照组（P&lt;0.01）,灯盏花素给药组肾组织PKC活性明显低于模型组（P&lt;0.05）,MMF给药组肾组织PKC活性与模型组相比无差异。模型组肾小球ED1阳性细胞数及MCP1、ICAM1表达明显高于对照组（P&lt;0.01）,灯盏花素或MMF给药可明显缓解这些变化（P&lt;0.05）。结论灯盏花素对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织巨噬细胞浸润有关。</span>

To investigate the effect of protein kinase C (PKC) #beta# inhibitor LY333531 on macrophage recruitment in kidney of diabetic rats, diabetes was induced by injection of streptozotocin (STZ) after uninephrectomy. Rats were randomly divided into three groups: control, diabetes diabetes treated with LY333531 (10mg/kg·d by gavage). 8 weeks after STZ injection, 24 hours albumin excretion rate (AER) were measured, and glomerular morphology were observed by light microscopy. The activity of PKC in renal tissue was determined. Immunohistochemistry for ED-1, MCP-1 and ICAM-1 were performed by streptavidin-biotin complex (SABC) technique. It was found that increased kidney weight (KW), ratio of KM to body weight (KW/BW), AER and glomerular area (A_(G)), glomerular volume (V_(G)) as well as mesangial area (A_(M)) on histological examination of the kidney were significantly attenuated by treatment with LY333531 (P<0.05, P<0.01). Elevated PKC activity in renal tissue were also remitted by LY333531 (P<0.05). Compared with control, glomerular macrophage recruitment and expression of MCP-1 and ICAM-1 were significantly increased in diabetic rats (P<0.01), which were all significantly inhibited by LY333531 (P<0.05). It concludes that mechanism of renoprotection of LY333531 may be correlated, at least partly, with suppression on increased macrophage recruitment in diabetic renal tissue.

目的探讨PKC抑制剂LY333531对大鼠糖尿病模型肾组织氧化应激的影响.方法建立单侧肾切除糖尿病模型,30只大鼠随机分成对照组、糖尿病模型组与糖尿病LY333531(10mg·kg-1·d-1,灌胃)给药组,每组10只.8周末观察体重、肾重、肾重/体重及24小时尿白蛋白排泄率(AER)变化,应用PAS染色观察肾组织病理变化,并检测肾组织与尿丙二醛(MDA)含量及肾组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)与谷光甘肽过氧化物酶(GSH-PX)活性.结果LY333531可明显抑制糖尿病大鼠肾重、肾重/体重、AER及肾小球面积(AG)、肾小球容量(VG)及系膜区面积(AM)的增加.与对照组相比,糖尿病模型组肾组织及尿MDA含量明显增加,肾组织SOD、CAT、GSH-PX活性明显下降;与糖尿病模型组比较,LY333531给药组肾组织及尿MDA含量明显降低(P均＜0.05),肾组织SOD、CAT、GSH-PX活性显著增高(P均＜0.05).结论LY333531对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织氧化应激有关.

Objective To investigate renoprotection effect of breviscapine and LY333531 in diabetic rats. Methods Diabetic rats were induced by injection of streptozotocin(STZ) . Rats were randomly divided into four groups: control group, model group, breviscapine(20 mg · kg-1· d-1, by gavage) treatment group and LY333531(10 mg· kg-1· d 1, by gavage ) treatment group. The levels of malondiadehyde(MDA) in renal tissue and urine as well as activities of antioxidant and protein kmase C (PKC) in renal tissue were determined after 8 weeks. Glomerular morphology was observed by light microscopy, and immunohistochemistry was performed. Results The enhancement of kidney weight (KW), KW/body weight (KW/BW), 24-hour urinary albumin excretion rate (AER), glomerular area and glomerular volume as well as mesangial area was found in model group, which was significantly attenuated by treatment with either breviscapine or LY333531 ( P 0. 05) . Meanwhile, elevated MDA levels in renal tissue and urine as well as decreased superoxide diamutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) activities in renal tissue were significantly remitted by breviscapine or LY333531 ( P 0. 05). PKC activities in renal tissue were significantly lower in breviscapine or LY333531 group compared with model group (P 0.05) . Compared with control, glomerular expression of transforming growth factor β1(TGF-(β1) and connective tissue growth factor (CTGF) was significantly increased in model group (P 0.01), which was significantly inhibited by breviscapine or LY333531(P 0.05) . Conclusion Renoprotective mechanism of breviscapine and LY333531 may be, at least partly, correlated with suppression on overexpression of TGF-β1, CTGF in renal tissue of diabetic rats.

Aim To investigate the effect of breviscapine on the expression of transforming growth factor β1 (TGF-β1) and connective tissue growth factor (CTGF)in kidney in diabetic rats. Methods Rats were randomly separated into three groups: control group, diabetic group, diabetic group treated with breviscapine ( 20 mg·kg -1·d -1 by gavage). Body weight(BW), kidney weight (KW), ratio of KW to BW (KW/BW) and 24 hours albumin excretion rate (AER) as well as glomerular area (A G), glomerular volume(V G), mesangial area (A M) were measured at week 8. The levels of MDA in renal tissue and urine as well as activities of superoxide diamutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) in renal tissue were determined. Immunohistochemistry for TGF-β1 and CTGF were performed in glomeruli.Resluts Increased KW, KW/BW, AER and A G, V G, A M were significantly attenuated by treatment with breviscapine (P0.05). Elevated MDA levels as well as decreased SOD, CAT, GSH-PX activities in renal tissue were significantly remitted by breviscapine(P0.05, P0.01, respectively). Compared with those in control group, glomerular expression of TGF-β1 and CTGF were significantly increased in diabetic rats, which were all significantly inhibited by breviscapine(P0.05). Conclusion The mechanism of renoprotection of breviscapine may be at least partly correlated with supression overexpression of TGF-β1 and CTGF in diabetic kidney.

目的探讨霉酚酸酯(MMF)对糖尿病大鼠模型肾组织氧化应激的影响.方法建立单侧肾切除糖尿病模型,大鼠随机分为对照组、糖尿病组与糖尿病MMF 10 mg/(kg*d),灌胃为给药组,每组 10只.8周末观察体重、肾重、肾重/体重及24 h尿白蛋白排泄率 (AER)变化,并检测肾组织与尿丙二醛(MDA)含量及肾组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)与谷光甘肽过氧化物酶(GSH-PX)活性.结果 MMF给药组可明显抑制糖尿病大鼠模型肾重、肾重/体重、AER的增加(P<0.05, P<0.01).与对照组相比,糖尿病模型组肾组织及尿MDA含量明显增加(P<0.01),肾组织SOD、CAT、GSH-PX活性明显下降(P<0.05, P<0.01);MMF给药组可明显降低肾组织及尿MDA含量,提高肾组织SOD、CAT、GSH-PX活性(P<0.05).结论 MMF对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织氧化应激有关.