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氨基胍

氨基胍的相关文献在1989年到2022年内共计429篇,主要集中在内科学、药学、外科学 等领域,其中期刊论文334篇、会议论文11篇、专利文献50367篇;相关期刊200种,包括基础医学与临床、中国病理生理杂志、中华危重病急救医学等; 相关会议9种,包括第七届华北长城心脏病学会议、河北省心血管病学2014年会暨第三届经前臂(桡/尺)动脉微创化冠脉介入治疗国际论坛、2014第六届含能材料与钝感弹药技术学术研讨会、中国畜牧兽医学会家畜内科学分会2009年学术研讨会等;氨基胍的相关文献由1142位作者贡献,包括唐兆新、张建新、刘乃丰等。

氨基胍—发文量

期刊论文>

论文:334 占比:0.66%

会议论文>

论文:11 占比:0.02%

专利文献>

论文:50367 占比:99.32%

总计:50712篇

氨基胍—发文趋势图

氨基胍

-研究学者

  • 唐兆新
  • 张建新
  • 刘乃丰
  • 李兰芳
  • 王锐
  • 王友令
  • 刘太平
  • 张会欣
  • 李英
  • 刘长山
  • 期刊论文
  • 会议论文
  • 专利文献

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    • 郑杰洪; 郑映苗; 陈凤梧
    • 摘要: 目的:探究三七总皂苷(PNS)联合氨基胍(AG)治疗对糖尿病肾病大鼠肾功能、血C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、丙二醛(MDA)和超氧化物歧化酶(SOD)水平的影响.方法:取清洁级雄性SD大鼠75只,随机分为正常对照组(15只)和实验组(60只),实验组腹腔注射链脲佐菌素建立糖尿病肾病大鼠模型,平衡喂养3d,将建模成功的实验组大鼠随机分为模型组(13只)、PNS组(13只)、AG组(13只)、联合组(13只),予以对应药物灌胃4周.观察各组大鼠肾脏组织病理形态变化,并比较各组大鼠肾小球容量、血糖、血肌酐、24h尿蛋白、血浆CRP、TNF-α、血清MDA、SOD水平.结果:正常对照组肾小球外观规则完整,系膜细胞稀少,基底膜薄;肾小管形状清晰,基底膜无改变,实验组肾小球明显增大,系膜细胞增加,基底膜增厚,肾小管无明显改变;相比模型组,P NS组、AG组、联合组肾小球病理状态明显改善.模型组、PNS组、AG组、联合组肾小球容量、血糖、血肌酐、24h尿蛋白、血浆CRP、TNF-α水平高于正常对照组,PNS组、AG组、联合组肾小球容量、血糖、血肌酐、24h尿蛋白、血浆CRP、TNF-α水平低于模型组,联合组肾小球容量、血糖、血肌酐、24h尿蛋白、血浆CRP、TNF-α 水平高于PNS组、AG组:差异均有统计学意义(P<0.05).模型组、PNS组、AG组、联合组MDA水平高于正常对照组,SOD水平低于正常对照组;PNS组、AG组、联合组MDA水平低于模型组,SOD水平高于模型组;联合组SOD水平高于AG组:差异均有统计学意义(P<0.05).结论:PNS联合AG治疗对糖尿病肾病可显著改善肾小球病理状态和肾小球功能,降低血浆炎症因子CRP、TNF-α 水平,减轻氧化应激水平.
    • 穆亚敏; 黄希; 宋志勇
    • 摘要: 目的:探讨氨基胍对肺纤维化(PF)大鼠基质金属蛋白酶-13(MMP-13)和组织基质金属蛋白酶抑制物-1(TIMP-1)表达的影响及其对转化生长因子-β1/信号转导分子(TGF-β1/Smads)信号通路的调控机制.方法:SD大鼠随机分为4组:正常组、模型组、实验组、地塞米松组(对照组),每组30只.模型组、实验组、对照组大鼠气管滴注博莱霉素构建PF模型,正常组大鼠滴注等剂量等浓度氯化钠溶液.滴注完毕后,实验组、对照组大鼠每日分别腹腔注射1 ml氨基胍溶液(20 mg/kg)和1 ml地塞米松溶液(20 mg/kg),正常组、模型组分别腹腔注射等剂量生理盐水.处死大鼠,qRT-PCR、免疫组化、Western blot检测各组大鼠肺组织病理学及纤维化改变、TGF-β1、Smad2和Smad7 mRNA表达、MMP-13和TIMP-1表达、TGF-β1、p-Smad2、p-Smad7蛋白表达.结果:与正常组相比,模型组肺组织TGF-β1和Smad2 mRNA表达、TGF-β1、p-Smad2和TIMP-1表达明显升高,Smad7 mRNA和p-Smad7蛋白表达、MMP-13表达明显降低;与模型组相比,实验组和对照组大鼠肺组织TGF-β1和Smad2 mRNA表达、TGF-β1、p-Smad2、TIMP-1表达明显降低,Smad7 mRNA和p-Smad7蛋白表达、MMP-13表达明显升高(P<0.05).结论:氨基胍可保护博来霉素诱导的PF大鼠肺组织,其抗纤维化作用可能通过调控TGF-β1/Smads信号通路实现.
    • 贾贺; 李惠勉
    • 摘要: 目的 研究2型糖尿病大鼠海马区脑血管内皮细胞CD34表达及血管内皮细胞炎症因子肿瘤坏死因子-α、血管内皮生长因子水平变化及氨基胍干预的脑保护作用及机制.方法 将24只SD大鼠按照随机数字表法分为对照组、模型组、治疗组,每组8只,于分组后12周、16周两个时间段观察;对照组给予普通饮食喂养,其余2组按照文献建立糖尿病大鼠模型,模型组及治疗组给予高脂高糖饮食喂养6周,用ONETOUCH血糖仪测定血糖,以随机非空腹血糖>16.7mmol·L-1定为糖尿病模型,造模成功后,治疗组给予氨基胍溶液每天灌胃,对照组及模型组给予等量生理盐水灌胃处理.采用免疫组化方法测定海马区脑血管密度CD34表达变化,采取酶联免疫吸附法测定海马区血管内皮细胞肿瘤坏死因子-α、血管内皮生长因子水平变化.结果 与对照组相比,模型组和治疗组脑血管内皮细胞CD34表达均显著增加(P<0.01),肿瘤坏死因子-α、血管内皮生长因子水平均显著升高(P<0.01);模型组16周CD34表达较12周显著增加(P<0.01),肿瘤坏死因子-α、血管内皮生长因子水平较12周显著升高(P<0.05或0.01);治疗组各时间点CD34表达均显著少于模型组(P<0.01),肿瘤坏死因子-α、血管内皮生长因子水平均显著低于模型组(P<0.01).结论 CD34表达及血管内皮细胞炎症因子肿瘤坏死因子-α、血管内皮生长因子水平变化均参与及影响2型糖尿病大鼠脑血管重塑过程,氨基胍干预对2型糖尿病大鼠脑保护作用是通过抑制肿瘤坏死因子-α、血管内皮生长因子的产生等途径改善糖尿病脑血管重塑,发挥脑保护作用.
    • 贾贺; 李惠勉; 张继佳
    • 摘要: 目的 观察氨基胍对2型糖尿病(T2DM)大鼠行为学改变和树突棘素表达变化的影响.方法 将大鼠随机分为对照组、模型组、氨基胍组.模型组及氨基胍组建立T2DM大鼠模型,造模成功后,氨基胍组给予氨基胍溶液灌胃(剂量为150 mg·kg-1·min-1),模型组给予等量生理盐水灌胃,对照组不予灌胃处理.分别于6、12、16 w应用Morris水迷宫对各组大鼠进行行为学评价;并于12、16 w采用免疫组化法检测各组大鼠海马区树突棘素的表达变化.结果 与对照组相比,12、16 w模型组潜伏期明显延长(P<0.05);树突棘素表达显著减少(P<0.05),并随疾程进展呈递减趋势.与模型组比较,同一时间点氨基胍组大鼠潜伏期明显缩短(P<0.05),树突棘素表达显著增多(P<0.05或P<0.01),并随着治疗进程呈持续增多趋势.结论 氨基胍可促进T2DM大鼠脑树突棘素的表达增加,而发挥脑保护作用,改善T2DM引起的认知功能障碍.
    • 张军; 张琦; 吴艳艳; 邓毅; 曾丽萍
    • 摘要: 目的 探讨黄芩素、氨基胍干预对糖尿病大鼠脑组织中人类表皮样生长因子结构蛋白-7(EGFL-7)表达的影响.方法 选取6~8周龄健康雄性SD大鼠40只,随机分为正常对照(NC)组、糖尿病组、氨基胍组、黄芩素组,每组各10只.NC组予普通饮食喂养;糖尿病组、氨基胍组、黄芩素组建立糖尿病大鼠模型,氨基胍组、黄芩素组分别予氨基胍、黄芩素溶液灌胃.检测各组脑组织EGFL-7表达情况,观察各组脑血管内皮超微结构.结果 与NC组比较,糖尿病组FPG升高,胰岛素降低(P<0.05);与糖尿病组比较,氨基胍组和黄芩素组FPG降低,胰岛素升高(P<0.05).NC组毛细血管腔规则,糖尿病组毛细血管腔不规则,部分狭窄变形,血管周围可见大量水肿液,氨基胍组部分血管形态不规则,黄芩素组血管内皮细胞结构清晰;与NC组比较,糖尿病组EGFL-7表达阳性细胞数、相对灰度值升高[(0.41±0.18)%vs(19.20±2.56)%,(25.32±3.01)%vs(60.10±5.73)%,P<0.05];与糖尿病组比较,氨基胍组和黄芩素组EGFL-7表达阳性细胞数、相对灰度值降低[(19.20±2.56)%vs(14.83±2.31)%、(13.89±3.08)%,(60.10±5.73)%vs(35.90±4.91)%、(34.12±5.04)%,P<0.05].结论 黄芩素、氨基胍可影响糖尿病大鼠脑血管增生和重塑,其作用可能与降低脑组织EGFL-7表达有关.%Objective To investigate the effect of Baicalein and aminoguanidineon on the expression of human epidermal growth factor like domain protein -7 (EGFL-7) in brain tissue of diabetic rats. Methods A total of 40 male SD rats were selected in this study. They were 6 to 8-week-old and randomly divided into four groups :normal control group (NC group ,n = 10 ) ,diabetes group ( n = 10 ) , aminoguanidine group (n=10) ,and Baicalein group (n= 10). NC group was treated with normal diet. Diabetic rat models were established in diabetes group ,aminoguanidine group and Baicalein group. Aminoguanidine group and Baicaleingroup were treated with aminoguanidine and Baicalein solution gavage respectively. The expressions of EGFL-7 in brain tissues were detected and the ultrastructure of cerebral vascular endothelial was observed. Results FPG increased and insulin decreased in diabetes group than in NC group (P<0.05). FPG decreased and insulin increased in aminoguanidine group and Baicalein group than in diabetes group(P<0.05). The capillary lumen was normal in NC group ,but irregular in diabetes group ,showing narrow deformation and a large amount of edema fluid in perivascular area. Part of the capillary lumen was irregular in aminoguanidine group. Vascular endothelial cell structure was clear in Baicalein group. The expression of EGFL-7 positive cell number [(19.20 ± 2.56)% vs (0.41 ± 0.18)% ] , and relative gray value [(60.10 ± 5.73 )% vs (25.32 ± 3.01 )% ] were significantly higher in diabetes group than in NC group (P<0.05). The expression of EGFL-7 positive cell number [(14.83 ± 2.31)% , (13.89 ± 3.08)% vs (19.20 ± 2.56)% ] and relative gray value [(35.90 ± 4.91)% ,(34.12 ± 5.04)% vs (60.10 ± 5.73)% ] were significantly lower in aminoguanidine group and Baicalein group than in diabetes group (P<0.05). Conclusion Baicalein and aminoguanidine can affect the cerebral vascular proliferation and remodeling in diabetic rats ,w hich may due to reduced expression of EGFL-7 in brain tissue.
    • 傅碧玲; 冯朝瑜; 朱赛香; 邹世海; 彭鑫
    • 摘要: 目的 研究氨基胍(AG)对乳酸盐腹膜透析液(L-PDS)致人腹膜间皮细胞(HMrSV5)损伤及血管内皮生长因子(VEGF)表达的影响.方法 采用人腹膜间皮细胞株HMrSV5为体外实验模型,分为无血清DMEM培养液对照组、L-PDS组(2.5%L-PDS)、L-PDS+AG组(2.5%L-PDS+10 mmol/L AG)、单纯AG组(终浓度10 mmol/L).各组以上不同干预因素与HMrSV5细胞共孵育.MTT法检测各组细胞增殖、评估细胞活力,Western blot和逆转录-聚合酶链反应(RT-PCR)检测VEGF蛋白及mRNA的表达.结果 MTT试验表明,L-PDS组OD值为(0.120±0.019),明显低于对照组的(0.298±0.031),差异有统计学意义(P<0.05);L-PDS+AG组OD值为(0.289±0.022),明显高于L-PDS组,差异有统计学意义(P<0.05).Western blot和RT-PCR结果均表明,与对照组比较,L-PDS组细胞中VEGF蛋白和mRNA表达明显增加,与L-PDS组比较,PDS+AG组VEGF蛋白和mRNA的表达明显减低,差异均有统计学意义(P<0.05).结论 AG可拮抗乳酸盐腹膜透析液致人腹膜间皮细胞损伤并下调VEGF的表达.%Objective To investigate the effect of aminoguanidine (AG) on damage in human peritoneal meso-thelial cells (HMrSV5) caused by lactate peritoneal dialysis solution (L-PDS) and expression of vascular endothelial growth factor (VEGF). Methods Depending on the culture of the cell, the cultured HMrSV5 cells were divided to con-trol group (cultured in DMEM), L-PDS group (2.5%L-PDS), L-PDS+AG group (2.5%L-PDS+10 mmol/L AG), and AG group (at a final concentration of 10 mmol/L). MTT assay was used to assess the viability and proliferation of the cells. VEGF protein was determined by western blot, and VEGF mRNA was determined by RT-PCR. Results The optical density (OD) value in L-PDS group was (0.120±0.019), significantly lower than (0.298±0.031) in the control group (P<0.05). The OD value in L-PDS+AG group was (0.289±0.022), which was significantly higher than that in L-PDS group (P<0.05). Expression of VEGF protein and mRNA increased significantly in L-PDS group as compared with those in control group (P<0.05), while the expression decreased significantly in PDS+AG group as compared with those in L-PDS group (P<0.05). Conclusion AG can antagonize the injury of HMrSV5 caused by L-PDS and down-regulate the expression of VEGF.
    • 欧阳宇
    • 摘要: 目的:探讨与分析氨基胍对糖尿病大鼠肾脏非酶糖基化的抑制作用。方法选取90只大鼠作为研究对象,采取随机数字表法分为 A、B、C 三组。A、B 两组均喂养高糖高脂肪饮食及皮下注射小剂量链脲佐菌素建立2型糖尿病大鼠模型,A 组大鼠定期服用含有氨基胍的饮用水,B 组大鼠定期服用等量不含氨基胍的正常饮用水,C 组大鼠定期服用等量不含氨基胍的正常饮用水,设定为对照组。对比三组大鼠治疗后体内高级糖基化产物的变化情况,血肌酐、血尿素氮、内生肌酐清除率、尿蛋白排泄量水平以及肾脏基底膜厚度、肾脏系膜体积变化情况。结果治疗前后,A 组大鼠治疗后高级糖基化产物明显高于治疗前,B 组治疗后明显高于治疗前,C 组大鼠治疗前后无明显变化,但 A 组治疗后糖基化产物的含量明显低于 B 组,组间相比具有显著差异( P <0.05)。治疗后 A 组和 B 组大鼠体内的血肌酐水平、血尿素氮水平、内生肌酐清除率、尿蛋白排泄量均明显升高,C 组无明显变化,但 A 组大鼠的各项指标明显低于 B 组,组间相比具有显著差异( P <0.05)。治疗5周、10周、15周后,A 组和 B 组大鼠肾脏的基底膜厚度和系膜体积均明显增加,C 组无明显变化,但 A 组大鼠肾脏的基底膜厚度和系膜体积明显小于 B 组,组间相比具有显著差异( P <0.05)。结论氨基胍可以通过抑制高级糖基化产物的生成,从而减少其在大鼠肾脏的蓄积,并显著降低尿蛋白的排泄、抑制系膜的增生,在一定程度上防止糖尿病向糖尿病肾病的发展,并且氨基胍的抑制作用与使用时间呈正相关。%Objective To explore and analyze the effect of aminoguanidine on inhibition of non - enzymatic glycation in kidney of diabetic rats. Methods A total of 90 rats were allocated as study subjects,they were randomly divided into A,B and C three groups,rats in groups A and B were fed with high fat and sugar diet and subcutaneously injection of low - dosage of streptozotocin in order to establish type 2 diabetic rat mod-els,rats in group A were administered with drinking water containing regular aminoguanidine,and rats in group B were drinking in same amount of water without aminoguanidine,and rats in group C were not regularly taken the same amount of aminoguanidine in normal drinking water and set as control group. After comparing the changes in three groups of rats treated with advanced glycosylation products,and changes in levels of serum creatinine,blood urea nitrogen,creatinine clearance,urinary protein excretion and thickness of basement membrane and changes in renal mesang-ial volume were compared among these 3 groups. Results After treatment,the advanced glycosylated products in rats of group A and group B were significantly higher than those before treatment,and this product in rats of group C had no significant change before and after treatment,but content of glycosylated product in rats of group A after treatment was significantly lower than that of rats in group B,and the difference was signifi-cant( P < 0. 05)between these two groups. After treatment,blood levels of creatinine and urea nitrogen,creatinine clearance and urinary protein excretion in rats of group A and group B were significantly increased,rats in group C had no significant change,but these indicators in rats of group A were significantly lower than those of rats in group B,and the difference was significant( P < 0. 05)between these two groups. After treatment for five weeks,10 weeks and 15 weeks,the thickness of basement membrane and volume of renal mesangium in rats of group A and group B were significantly increased,and the change in rats of group C was not significant,but the thickness of basement membrane and volume of renal mesan-gium in rats of group A were significantly less than those of rats in group B,and the difference was significant( P < 0. 05). Conclusion Amin-oguanidine can inhibit the formation of advanced glycation products,thereby reducing their accumulation in kidney of rats and the decreased urina-ry protein excretion can significantly inhibit the proliferation of mesangium to a certain extent,hence it may prevent the development of diabetes and diabetic nephropathy,hence the inhibition of aminoguanidine is positively correlated with the duration for utilization.
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