| 章露尹,陆贝.3-甲基腺嘌呤对急性胰腺炎大鼠PI3K-Akt信号通路调节和肝细胞保护作用的研究[J].浙江中西医结合杂志,2024,34(12): |
| 3-甲基腺嘌呤对急性胰腺炎大鼠PI3K-Akt信号通路调节和肝细胞保护作用的研究 |
| Protection and mechanism of 3-methyladenine on liver cells in rats with acute pancreatitis through the PI3K-Akt signaling pathway |
| 投稿时间：2024-04-22 修订日期：2024-09-05 |
| DOI： |
| 中文关键词: 急性胰腺炎 3-甲基腺嘌呤 自噬 PI3K/AKT 信号通路 |
| 英文关键词:Acute pancreatitis 3-methyladenine Autophagy Phosphatidylinositol 3-kinase-Protein kinase Signal pathway |
| 基金项目:[基金项目] 浙江省医药卫生科技计划项目面上项目计划(2023KY921) |
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| 中文摘要: |
| 【摘要】目的 为了研究3-甲基腺嘌呤（3-MA）对急性胰腺炎Sprague-Dawley大鼠肝细胞的保护作用和调控机制。方法 健康雄性清洁级SD大鼠45只，随机数字表法分为AP模型组（n=15，L-精氨酸二次腹腔注射法制模）、3-甲基腺嘌呤组(n=15，AP模型制备后静脉注射3-MA）、假手术组(n=15，仅注射生理盐水对照）。模型制备后12h、24h、48h处死大鼠取材，每批5只。观察各组大鼠死亡率、HE染色肝组织病理改变，肝组织PI3K、AKT蛋白，NF-κB蛋白，肝功能指标ALT、AST，血清炎症因子IL-1、IL-6等表达变化。 结果 与假手术组相比，AP模型组各时间点肝组织病理学改变、血清炎性因子、肝功能指标相应升高(P< 0.05)，肝组织中NF-κB、PI3K、AKT蛋白表达明显上升(P<0.05)，呈时间依赖性。3-MA组各项指标均较AP组有改善，结果有统计学差异(P<0.05)。 结论 3-甲基腺嘌呤能改善SAP大鼠肝细胞损伤，抑制自噬相关蛋白的表达，可能通过PI3K/AKT通路调控自噬发挥作用。 |
| 英文摘要: |
| 【Abstract】Objective To investigate the effect and regulatory mechanism of 3-methyladenine (3-MA) on hepatocytes of Sprague Dawley (SD) rats with severe acute pancreatitis (SAP). Method Forty five healthy male clean grade SD rats were randomly divided into an AP model group (n=15, AP rat model prepared by secondary intraperitoneal injection of L-arginine), a 3-methyladenine group (n=15, AP model prepared by intravenous injection of 3-MA), and a sham surgery group (n=15, only injected with saline solution). After model preparation, SD rats were euthanized at 12h, 24h, and 48h for sampling, with 5 rats in each batch. Observe the mortality rate of rats in each group, HE staining of liver tissue pathological changes, PI3K, AKT protein, NF in liver tissue- κ Changes in the expression of B protein, liver function indicators ALT and AST, and serum inflammatory factors IL-1 and IL-6. Result Compared with the SO group, the AP group showed a significant increase in liver tissue pathological injury, serum inflammatory factors, liver function indicators in serum and NF- κ B in liver cells at various time points (P<0.05). The expression of PI3K and AKT proteins significantly increased (P<0.05) and showed a time-dependent relationship (P<0.05). All indicators in the 3-MA group improved compared to the AP group, with statistical differences (P<0.05). Conclusion 3-methyladenine can improve liver cell damage in SAP rats, inhibit the expression of autophagy related proteins, and may regulate autophagy through the PI3K/AKT pathway. |
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