1. 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.
- Author
-
陈飞, 林小吉, 杨鲸蓉, 李毅鸣, 赵文龙, and 廖达林
- Subjects
- *
LIPOPROTEIN lipase , *NECROTIZING pancreatitis , *GENE knockout , *KNOCKOUT mice , *LABORATORY mice , *OXIDATIVE stress - 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-αand 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-αand 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. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF