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大黄素对重症胰腺炎肾损伤模型大鼠血清缺氧诱导因子-1α及糖原合酶激酶-3β水平的影响

发布时间:2018-07-08 11:23

  本文选题:大黄素 + 重症胰腺炎肾损伤 ; 参考:《中国临床药理学杂志》2017年14期


【摘要】:目的研究大黄素对重症胰腺炎肾损伤大鼠血清缺氧诱导因子-1α(HIF-1α)和糖原合酶激酶-3β(GSK-3β)水平影响。方法将60只大鼠随机分为空白组、假手术组、模型组、对照组和实验组,每组12只。模型组和试验组注入牛磺胆酸钠0.1 mL/100 g建立重症胰腺炎肾损伤大鼠模型;假手术组和对照组打开腹腔后仅轻轻翻动十二指肠以及胰腺;空白组大鼠未作任何处理。空白组、假手术组、模型组均予以腹腔注射5μL·g-10.9%Na Cl q6 h;对照组和实验组均按25μg·g-1剂量予以腹腔注射5 g·L~(-1)大黄素q6 h。术后3,6,12h,比较各组大鼠的血清肌酸酐(SCr)、尿素氮(BUN)、HIF-1α和GSK-3β水平。结果空白组、假手术组、对照组和实验组的胰腺组织病理学评分分别为(1.30±0.14),(1.39±0.14),(1.40±0.15)和(2.73±0.30)分,与模型组的胰腺组织病理学评分(9.84±1.05)分相比,差异均有统计学意义(均P0.05),且实验组的胰腺组织病理学评分与空白组、假手术组、对照组比较,差异均有统计学意义(均P0.05)。术后3 h,空白组、假手术组、对照组、模型组和实验组的SCr分别为(60.46±6.78),(61.52±6.78),(60.38±6.74),(120.57±13.43)和(95.35±9.85)μmol·L~(-1),BUN分别为(7.47±0.79),(8.02±0.92),(7.93±0.83),(12.49±1.53)和(8.56±0.89)mmol·L~(-1),HIF-1α分别为(225.46±23.57),(210.57±23.58),(229.67±6.74),(160.46±17.47)和(144.57±14.85)μg·L~(-1),GSK-3β分别为(6.59±0.69),(6.57±0.69),(6.74±0.68),(19.95±2.13)和(10.56±1.39)μg·L~(-1)。术后6 h,空白组、假手术组、对照组、模型组和实验组的SCr分别为(60.57±6.79),(60.55±6.76),(59.50±6.76),(143.57±15.47)和(110.57±12.55)μmol·L~(-1),BUN分别为(7.65±0.84),(8.11±0.93),(8.29±0.92),(15.46±1.64)和(12.35±1.37)mmol·L~(-1),HIF-1α分别为(226.46±24.04),(222.46±23.57),(230.57±24.05),(155.36±15.74)和(127.57±12.84)μg·L~(-1),GSK-3β分别为(6.25±0.67),(6.71±0.69),(6.82±0.71),(25.34±2.64)和(11.56±1.27)μg·L~(-1)。术后12 h,空白组、假手术组、对照组、模型组和实验组的SCr分别为(60.61±6.79),(61.68±6.79),(61.54±6.78),(166.45±17.05)和(131.45±13.46)μmol·L~(-1),BUN分别为(8.03±0.85),(7.98±0.82),(8.79±0.93),(18.66±19.46)和(15.35±1.63)mmol·L~(-1),HIF-1α分别为(219.57±23.63),(226.35±24.04),(220.25±24.04),(148.46±18.94)和(117.46±12.04)μg·L~(-1),GSK-3β分别为(6.77±0.69),(6.70±0.70),(6.86±0.70),(35.02±3.76)和(20.35±2.13)μg·L~(-1)。空白组、假手术组、对照组术后3,6,12 h的SCr、BUN、HIF-1α、GSK-3β与模型组比较,差异均有统计学意义(均P0.05),且实验组与模型组术后3,6,12 h的SCr、BUN、HIF-1α、GSK-3β比较,差异均有统计学意义(均P0.05)。结论大黄素可能通过上调血清HIF-1α和GSK-3β水平,提高肾细胞耐缺氧的能力,从而发挥对重症急性胰腺炎肾损伤的保护作用。
[Abstract]:Objective to study the effects of emodin on the levels of serum hypoxia inducible factor-1 伪 (HIF-1 伪) and glycogen synthase kinase-3 尾 (GSK-3 尾) in rats with renal injury caused by severe pancreatitis. Methods Sixty rats were randomly divided into blank group, sham operation group, model group, control group and experimental group, with 12 rats in each group. The model group and the experimental group were injected with sodium taurocholate 0.1 mL / 100 g to establish the model of renal injury in severe pancreatitis; the sham operation group and the control group only slightly turned the duodenum and pancreas after opening the abdominal cavity; the rats in the blank group did not do any treatment. The blank group, sham operation group and model group were all given intraperitoneal injection of 5 渭 L g-10.9 sodium chloride for 6 h, and the control group and experimental group were given 5 g L ~ (-1) emodin q6 h intraperitoneally at the dose of 25 渭 g ~ (-1). The levels of serum creatinine (SCR), urea nitrogen (bun), HIF-1 伪 and GSK-3 尾 were compared between the three groups. Results the histopathological scores of pancreas in blank group, sham operation group, control group and experimental group were (1.30 卤0.14), (1.39 卤0.14), (, 1.40 卤0.15) and (2.73 卤0.30), respectively, compared with those in model group (9.84 卤1.05). The difference was statistically significant (P0.05), and the pancreatic histopathological score of the experimental group was significantly higher than that of the blank group, sham-operation group and control group (P0.05). 鏈悗3 h,绌虹櫧缁,

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