本文選題：大黃素 + 重癥胰腺炎腎損傷��； 參考：《中國臨床藥理學(xué)雜志》2017年14期

【摘要】：目的研究大黃素對重癥胰腺炎腎損傷大鼠血清缺氧誘導(dǎo)因子-1α(HIF-1α)和糖原合酶激酶-3β(GSK-3β)水平影響。方法將60只大鼠隨機分為空白組、假手術(shù)組、模型組、對照組和實驗組,每組12只。模型組和試驗組注入�；悄懰徕c0.1 mL/100 g建立重癥胰腺炎腎損傷大鼠模型;假手術(shù)組和對照組打開腹腔后僅輕輕翻動十二指腸以及胰腺;空白組大鼠未作任何處理�？瞻捉M、假手術(shù)組、模型組均予以腹腔注射5μL·g-10.9%Na Cl q6 h;對照組和實驗組均按25μg·g-1劑量予以腹腔注射5 g·L~(-1)大黃素q6 h。術(shù)后3,6,12h,比較各組大鼠的血清肌酸酐(SCr)、尿素氮(BUN)、HIF-1α和GSK-3β水平。結(jié)果空白組、假手術(shù)組、對照組和實驗組的胰腺組織病理學(xué)評分分別為(1.30±0.14),(1.39±0.14),(1.40±0.15)和(2.73±0.30)分,與模型組的胰腺組織病理學(xué)評分(9.84±1.05)分相比,差異均有統(tǒng)計學(xué)意義(均P0.05),且實驗組的胰腺組織病理學(xué)評分與空白組、假手術(shù)組、對照組比較,差異均有統(tǒng)計學(xué)意義(均P0.05)。術(shù)后3 h,空白組、假手術(shù)組、對照組、模型組和實驗組的SCr分別為(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分別為(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分別為(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分別為(6.59±0.69),(6.57±0.69),(6.74±0.68),(19.95±2.13)和(10.56±1.39)μg·L~(-1)。術(shù)后6 h,空白組、假手術(shù)組、對照組、模型組和實驗組的SCr分別為(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分別為(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分別為(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分別為(6.25±0.67),(6.71±0.69),(6.82±0.71),(25.34±2.64)和(11.56±1.27)μg·L~(-1)。術(shù)后12 h,空白組、假手術(shù)組、對照組、模型組和實驗組的SCr分別為(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分別為(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分別為(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分別為(6.77±0.69),(6.70±0.70),(6.86±0.70),(35.02±3.76)和(20.35±2.13)μg·L~(-1)�？瞻捉M、假手術(shù)組、對照組術(shù)后3,6,12 h的SCr、BUN、HIF-1α、GSK-3β與模型組比較,差異均有統(tǒng)計學(xué)意義(均P0.05),且實驗組與模型組術(shù)后3,6,12 h的SCr、BUN、HIF-1α、GSK-3β比較,差異均有統(tǒng)計學(xué)意義(均P0.05)。結(jié)論大黃素可能通過上調(diào)血清HIF-1α和GSK-3β水平,提高腎細胞耐缺氧的能力,從而發(fā)揮對重癥急性胰腺炎腎損傷的保護作用。
[Abstract]:Objective to study the effects of emodin on the levels of serum hypoxia inducible factor-1 偽 (HIF-1 偽) 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 偽 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 鹵0.14), (1.39 鹵0.14), (, 1.40 鹵0.15) and (2.73 鹵0.30), respectively, compared with those in model group (9.84 鹵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,絀虹櫧緇，

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