| 楼恺娴,龚自华,袁耀宗,涂水平,翟祖康,徐家裕.大黄素对急性胰腺炎胰腺组织TGFβ1表达的影响[J].中国中西医结合杂志,2001,(6):433-436 |
| 大黄素对急性胰腺炎胰腺组织TGFβ1表达的影响 |
| Study on Effect of Emodin on TGFβ1 Expression in Pancreatic Tissue of Rats Suffering from Acute Pancreatitis |
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| DOI： |
| 中文关键词: 急性胰腺炎 大黄素 转化生长因子β1 |
| 英文关键词:acute pancreatitis emodin transforming growth factor β 1 |
| 基金项目:国家自然科学基金!资助 (No .39770 935) |
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| 中文摘要: |
| 目的 :通过分析中药大黄素对大鼠急性胰腺炎治疗前后胰腺组织细胞转化因子 β1(TGFβ1)的表达、DNA合成及总蛋白含量的影响 ,从胰腺再生角度探讨大黄素治疗急性胰腺炎的作用机制。方法 :以雨蛙肽 (caerulein)腹腔注射诱导大鼠急性胰腺炎模型 ,并于大黄素治疗前后 6、2 4、4 8、72及 96h处死大鼠。同时应用RT PCR技术检测治疗前后胰腺组织TGFβ1mRNA表达 ,同位素体外掺入法测定胰腺组织DNA合成以及Lowry′s法测定胰腺组织总蛋白含量。 结果 :大黄素治疗后血清淀粉酶显著下降。正常胰腺组织、胰腺炎诱导后 6h未见TGFβ1mRNA表达。TGFβ12 4h后出现表达 ,72h时达高峰。大黄素治疗后 6h即可检测到TGFβ1mRNA表达 ,且 2 4、4 8h时表达均较非治疗组显著增强 ,并于 4 8h时达最大值。同时胰腺炎诱导后 72h ,胰腺组织DNA合成显著下降 ,大黄素治疗后 96hDNA合成明显增加 ,胰腺炎诱导后 4 8h胰腺组织总蛋白含量下降 ,大黄素治疗后 96h显著增加。结论 :大黄素治疗急性胰腺炎的作用机制可能是通过诱导细胞因子TGFβ1基因表达增强 ,调控细胞增殖和分化 ,刺激多种细胞外基质成分合成 ,增加胰组织DNA合成和蛋白含量 ,参与胰腺细胞修复、再塑过程。 |
| 英文摘要: |
| Objective: To investigate the effect and mechanism of emodin on pancreatic repairing and remodeling in treating acute pancreatitis by analyzing the change of cytokine transforming growth factor β 1 (TGFβ 1) gene expression, DNA synthesis and protein content in pancreatic tissue. Methods: Acute pancreatitis was induced in rats by intraperitoneal infusion of caerulein, treated or untreated by emodin. The animals were sacrificed at 6, 24, 48, 72 or 96 hrs after treatment separately. The mRNA expression of TGFβ 1, DNA synthesis and total protein content in pancreatic tissue were tested by reverse transcription polymerase chain reaction (RT PCR), 3?H thymidin method and Lowry′s method respectively. Results: Serum amylase level was decreased significantly after emodin treatment. TGFβ 1 mRNA expression was undetectable in the intact pancreas or in 6 hrs after pancreatitis induction in the non treated group, but revealed at 24 hrs after and reached the peak at 72 hrs later. However, in the emodin treated group, TGFβ 1 mRNA expression was detected at 6 hrs after treatment, with a higher level in 24 hrs and 48 hrs as compared with the non treated group, and reaching the peak at 48 hrs after treatment. Moreover, the DNA synthesis and total protein content in pancreatic tissue decreased significantly at 72 hrs and 48 hrs after induction respectively, but both parameters increased significantly in the emodin treated group 96 hrs after treatment. Conclusion: The mechanism of emodin in treating acute pancreatitis might be by way of enhancing cytokine TGFβ 1 gene expression, regulating cell growth and differentiation, stimulating the formation of extracellular matrix components, increasing DNA synthesis and protein content, and to take part in pancreatic repairing and remodeling. |
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