胰岛β细胞参与急性胰腺炎后胰腺再生过程的研究 |
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引用本文: | 胡国勇,赵严,沈杰,杨丽娟,熊杰,万荣,郭传勇,王兴鹏.胰岛β细胞参与急性胰腺炎后胰腺再生过程的研究[J].中华胰腺病杂志,2011,11(5). |
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作者姓名: | 胡国勇 赵严 沈杰 杨丽娟 熊杰 万荣 郭传勇 王兴鹏 |
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作者单位: | 同济大学附属第十人民医院上海市第十人民医院消化内科,上海,200072 |
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基金项目: | 教育部高等学校博士学科点专项科研基金,上海市科技创新行动计划重点项目 |
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摘 要: | 目的 探讨胰岛β细胞在实验性急性胰腺炎(AP)后胰腺再生过程中的作用.方法 SD大鼠87只,按数字表法随机分为对照组(15只)、糖尿病组(24只)、AP组(24只)和糖尿病+AP组(24只).采用腹腔注射链脲佐菌素(STZ,60 mg/kg体重)或左旋精氨酸(L-Arg,2.5 g/kg体重,2次)方法分别建立糖尿病和AP模型.术后1、3、5、7d分批处死大鼠.检测血淀粉酶和血糖水平;计算胰腺湿重比;胰腺组织常规病理学检查,计算胰腺坏死面积百分比和组织转化区域百分比;免疫荧光检测胰岛β细胞的再生基因( Reg4)和胰岛素的表达.结果 注射STZ后,大鼠血糖明显升高,注射L-Arg后大鼠胰腺组织水肿、坏死、炎细胞浸润,血淀粉酶明显升高,表明制模成功.制模后第3天糖尿病+ AP组的胰腺坏死面积为(71.6±6.0)%,显著大于AP组的(42.3±4.0)%;第7天的组织转化面积为(45.6±5.4)%,显著小于AP组的(78.5±6.4)%.糖尿病+AP组胰岛β细胞的Reg4和胰岛素表达均较AP组明显减少.结论 STZ破坏了胰岛β细胞,加重精氨酸诱导的AP的损伤,并抑制胰腺的再生过程.
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关 键 词: | 急性胰腺炎 胰岛β细胞 胰腺再生 再生基因4 |
Involvement of pancreatic beta cell in pancreatic regeneration following experimental acute pancreatitis |
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Authors: | HU Guo-yong ZHAO Yan SHEN Jie YANG Li-juan XIONG Jie WAN Rong GUO Chuan-yong WANG Xing-peng |
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Abstract: | Objective To investigate the role of pancreatic β cell on pancreatic regeneration following experimental acute pancreatitis.Methods Eighty-seven SD male rats were randomly divided into four groups:control group ( n =15 ),STZ group ( n =24),L-Arg group ( n =24 ),STZ + Arg group ( n =24).60 mg/kg of STZ was administrated by intraperitoneal injection to induce the diabetes model.2.5 g/kg body weight of LArg was administrated by intraperitoneal injection to induce the acute pancreatitis model.The rats were sacrificed 1,3,5,7 d later and the serum levels of amylase and glucose were measured.Relative pancreatic weight (pancreatic weight/body weight) were measured.Pancreatic tissue underwent routine pathologic examination,and the percentage of area of necrosis and tissue transformation was calculated.The expression of Reg4 and insulin was performed by immunofluorescence.Results Serum level of glucose significantly increased after STZ injection.After L-Arg injection,serum level of amylase significantly increased,and there was pancreatic tissue edema,necrosis,infiltration of inflammatory cells,which suggested the successful model induction.The percentage of area of necrosis in STZ + L-Arg group was (71.6 ± 6.0) % at the 3rd day,which were significantly higher than (42.3 ± 4.0 ) % in L-Arg group; the percentage of area of transformation was (45.6 ± 5.4) %,which were significantly lower than (78.5 ± 6.4) % in L-Arg group.Expression of Reg4 in pancreatic islets of STZ + L-Arg group was significantly lower than those in L-Arg group.Conclusions STZ impairs pancreatic β cells,aggravates pancreatic damage following L-arginine induced pancreatitis and inhibits pancreatic regeneration. |
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Keywords: | Acute pancreatitis Pancreatic beta Cells Pancreatic regeneration Reg4 |
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