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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P<0.05),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P<0.05)。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P<0.05),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P<0.05)。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。
Objective To investigate the effects of emodin on serum levels of hypoxia inducible factor-1α (HIF-1α) and glycogen synthase kinase-3β (GSK-3β) in rats with severe pancreatitis and renal injury. 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. Model group and experimental group were infused with sodium taurocholate 0.1 mL / 100 g to establish a rat model of severe acute pancreatitis and renal injury. The rats in sham-operated group and control group were gently inflected to open duodenum and pancreas, Without any treatment. The rats in the blank group, sham operation group and model group were intraperitoneally injected with 5 μL · g-10.9% NaCl q for 6 h. The control group and experimental group were injected intraperitoneally with 5 g · L -1 rhubarb Prime q6 h. Serum creatinine (SCr), blood urea nitrogen (BUN), HIF-1α and GSK-3β levels were compared between the three groups at 3, 6 and 12 h after operation. Results The histopathological scores of pancreatic tissue in the blank group, the sham operation group, the control group and the experimental group were (1.30 ± 0.14), (1.39 ± 0.14), (1.40 ± 0.15) and (2.73 ± 0.30) There were significant differences between the two groups (all P <0.05), and the difference of pancreatic histopathological score between the experimental group and the blank group, the sham operation group and the control group were statistically significant There was statistical significance (all P <0.05). The SCr of the blank group, the sham operation group, the control group, the model group and the experimental group were (60.46 ± 6.78), (61.52 ± 6.78), (60.38 ± 6.74), (120.57 ± 13.43) and (95.35 ± 9.85) μmol·L -1, BUN were (7.47 ± 0.79), (8.02 ± 0.92), (7.93 ± 0.83), (12.49 ± 1.53) and (8.56 ± 0.89) mmol·L ~ 1 and HIF-1α were (225.46 ± 23.57), (210.57 ± 23.58), (229.67 ± 6.74), (160.46 ± 17.47) and (144.57 ± 14.85) μg · L -1, respectively (6.59 ± 0.69), (6.57 ± 0.69), (6.74 ± 0.68), (19.95 ± 2.13) and (10.56 ± 1.39) μg · L -1, respectively. The SCr of the blank group, the sham operation group, the control group, the model group and the experimental group were (60.57 ± 6.79), (60.55 ± 6.76), (59.50 ± 6.76), (143.57 ± 15.47) and (110.57 ± 12.55) μmol·L -1, BUN were (7.65 ± 0.84), (8.11 ± 0.93), (8.29 ± 0.92), (15.46 ± 1.64) and (12.35 ± 1.37) mmol·L -1 1 and HIF-1α were (226.46 ± 24.04), (222.46 ± 23.57), (230.57 ± 24.05), (155.36 ± 15.74) and (127.57 ± 12.84) μg · L -1, respectively (6.25 ± 0.67), (6.71 ± 0.69), (6.82 ± 0.71), (25.34 ± 2.64) and (11.56 ± 1.27) μg · L -1, respectively. The SCr of the blank group, the sham operation group, the control group, the model group and the experimental group were (60.61 ± 6.79), (61.68 ± 6.79), (61.54 ± 6.78), (166.45 ± 17.05) and (131.45 ± 13.46μmol·L -1 and BUN were respectively (8.03 ± 0.85), (7.98 ± 0.82), (8.79 ± 0.93), (18.66 ± 19.46) and (15.35 ± 1.63) mmol·L ~ (-1) 1 and HIF-1α were (219.57 ± 23.63), (226.35 ± 24.04), (220.25 ± 24.04), (148.46 ± 18.94) and (117.46 ± 12.04) μg · L -1, respectively (6.77 ± 0.69), (6.70 ± 0.70), (6.86 ± 0.70), (35.02 ± 3.76) and (20.35 ± 2.13) μg · L -1, respectively. The levels of SCr, BUN, HIF-1α and GSK-3β in the blank group, the sham operation group and the control group at 3, 6 and 12 h postoperatively were significantly different from those in the model group (all P <0.05) Compared with model group, SCr, BUN, HIF-1α and GSK-3β at 3, 6 and 12 h after operation were significantly different (all P <0.05). Conclusion Emodin may play a protective role in renal injury induced by severe acute pancreatitis by up-regulating the serum levels of HIF-1α and GSK-3β and increasing the hypoxic tolerance of renal cells.