| 陈 飞,林小吉,杨鲸蓉,李毅鸣,赵文龙,廖达林.脂蛋白脂肪酶基因敲除对急性高脂血症性胰腺炎所致肺损伤的影响及其机制研究[J].现代生物医学进展英文版,2022,(15):2841-2845. |
| 脂蛋白脂肪酶基因敲除对急性高脂血症性胰腺炎所致肺损伤的影响及其机制研究 |
| Effects of Lipoprotein Lipase Gene Knockout on Lung Injury Induced by Acute HyperLipidemia Pancreatitis and Its Mechanism |
| Received:January 23, 2022 Revised:February 18, 2022 |
| DOI：10.13241/j.cnki.pmb.2022.15.008 |
| 中文关键词: 脂蛋白脂肪酶 高脂血症 肺损伤 氧化应激 炎症 |
| 英文关键词: Lipoprotein lipase Hyperlipidemia Lung injury Oxidative stress Inflammation |
| 基金项目:福建省自然科学基金项目（2017J01223） |
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| 中文摘要: |
| 摘要 目的：研究脂蛋白脂肪酶（lipoprotein lipase，LPL）基因敲除对雨蛙素诱导的高脂血症急性胰腺炎小鼠肺损伤的影响。方法：将C57BL/6小鼠分为三组，Control组和AP-Model组为野生型C57 BL/6小鼠，LPL ko组为LPL基因敲除C57 BL/6小鼠；Control组小鼠正常饲养，AP-Model和LPL ko组小鼠建立高脂血症性急性胰腺炎模型，比较三组小鼠死亡率、胰腺和肺病理损伤以及血清淀粉酶（amylase, AMY）、丙二醛（malondialdehyde, MDA）、肿瘤坏死因子-α（Tumor necrosis factor-α, TNF-α）和白介素-6（Interleukin-6, IL-6）含量。结果：急性胰腺炎建立48 h后，Control组、AP-Model组和LPL ko组小鼠死亡率分别为0 %、20 %和40 %。与Control组相比，AP-Model组和LPL ko组小鼠急性胰腺炎诱导24和48 h后的胰腺和肺组织湿/干重比值，胰腺和肺组织病理评分，血清AMY、MDA、TNF-α和IL-6含量均显著升高（P<0.05）；与AP-Model组相比，LPL ko组小鼠急性胰腺炎诱导24和48 h后的胰腺和肺组织湿/干重比值，胰腺和肺组织病理评分，血清AMY、MDA、TNF-α和IL-6含量均显著升高（P<0.05）。结论：LPL基因敲除小鼠急性高脂血症性胰腺炎肺损伤更严重，其机制可能与LPL基因敲除引起更强的氧化应激和炎症有关。 |
| 英文摘要: |
| ABSTRACT Objective: To study the effect of lipoprotein lipase (LPL) gene knockout on lung injury in mice with cerulein-induced hyperlipidemia and acute pancreatitis. Methods: C57BL/6 mice were divided into three groups. The Control group and the AP-Model group were wild-type C57 BL/6 mice, and the LPL ko group was the LPL knockout C57 BL/6 mice; the Control group was fed normally, and the AP-Model and A hyperlipidemia acute pancreatitis model was established in the LPL ko group of mice, and the mortality, pancreatic and lung pathological damage, and serum amylase (AMY), malondialdehyde (MDA), tumor necrosis and tumor necrosis levels were compared among the three groups. Factor-α (Tumor necrosis factor-α, TNF-α) and interleukin-6 (Interleukin-6, IL-6) content. Results: 48 hours after the establishment of acute pancreatitis, the mortality rates of mice in the Control group, AP-Model group and LPL ko group were 0%, 20% and 40%, respectively. Compared with the control group, the pancreas and lung tissue wet/dry weight ratios, pancreas and lung histopathological scores, serum AMY, MDA, TNF-α and The content of IL-6 was significantly increased (P<0.05); compared with the AP-Model group, the pancreas and lung tissue wet/dry weight ratio, pancreas and lung tissue pathology of LPL ko group mice 24 and 48 hours after the induction of acute pancreatitis Scores, serum AMY, MDA, TNF-α and IL-6 levels were significantly increased (P<0.05). Conclusion: LPL knockout mice had more severe acute hyperlipidemic pancreatitis lung injury, and the mechanism may be related to the stronger oxidative stress and inflammation induced by LPL knockout. |
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