Digestive diseases and sciences · 2026
Effects of Abnormal Lipid Metabolism on Pancreatic Injury and Ferroptosis-Related Indicators in Rats with Severe Acute Pancreatitis.
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Huang Qiyu, Xu Yuxin, Hu Juntao, Tang Zhanhong
Аннотация
OBJECTIVES: Mounting evidence suggests that ferroptosis is closely involved in the development of severe acute pancreatitis (SAP). This study aimed to investigate the association between abnormal lipid metabolism and ferroptosis and elucidate the role of the Keap1/Nrf2/SLC7A11/GPX4 pathway in pancreatic acinar cell injury during SAP.
METHODS: Rats were divided into four experimental groups: sham, hyperlipidemia (HL), SAP, and HL-SAP. Sprague-Dawley rats were adopted to establish HL-SAP model through administering high-fat emulsions via gastric infusion for 14 consecutive days and sodium taurocholic injection. Measure serum amylase, blood lipid, and inflammatory cytokine levels, perform histological analysis, determine the expression levels of proteins in the Keap1/Nrf2/SLC7A11/GPX4 signaling pathway, and evaluate ferroptosis-related changes and oxidative stress.
RESULTS: High-fat emulsion feeding successfully induced hyperlipidemia with elevated blood lipids, while injection of 3.5% sodium taurocholate triggered SAP accompanied by increased serum amylase. The combined intervention effectively established the HL-SAP model. Compared with the SAP rats, the HL-SAP rats exhibited more severe pancreatic damage (72 h mortality: 80 vs. 50%, respectively, plus elevated amylase, inflammation, histopathology scores). Higher amylase levels, intensified inflammation, and increased histopathological scores were also observed in HL-SAP rats. Moreover, HL-SAP rats showed markedly enhanced oxidative stress and ferroptosis-related phenotypes, including increased MDA, ROS and Fe2⁺ levels, as well as decreased GSH and SOD levels. In both SAP and HL-SAP groups, abnormal lipid metabolism was associated with downregulated Nrf2, SLC7A11, and GPX4 expression and upregulated Keap1 expression, and these alterations were more prominent in the HL-SAP group.
CONCLUSION: Abnormal lipid metabolism aggravates oxidative stress, inflammation, and pancreatic acinar cell injury in SAP, and promotes ferroptosis. These effects may be attributed to reduced activity of the Keap1/Nrf2/SLC7A11/GPX4 pathway.
METHODS: Rats were divided into four experimental groups: sham, hyperlipidemia (HL), SAP, and HL-SAP. Sprague-Dawley rats were adopted to establish HL-SAP model through administering high-fat emulsions via gastric infusion for 14 consecutive days and sodium taurocholic injection. Measure serum amylase, blood lipid, and inflammatory cytokine levels, perform histological analysis, determine the expression levels of proteins in the Keap1/Nrf2/SLC7A11/GPX4 signaling pathway, and evaluate ferroptosis-related changes and oxidative stress.
RESULTS: High-fat emulsion feeding successfully induced hyperlipidemia with elevated blood lipids, while injection of 3.5% sodium taurocholate triggered SAP accompanied by increased serum amylase. The combined intervention effectively established the HL-SAP model. Compared with the SAP rats, the HL-SAP rats exhibited more severe pancreatic damage (72 h mortality: 80 vs. 50%, respectively, plus elevated amylase, inflammation, histopathology scores). Higher amylase levels, intensified inflammation, and increased histopathological scores were also observed in HL-SAP rats. Moreover, HL-SAP rats showed markedly enhanced oxidative stress and ferroptosis-related phenotypes, including increased MDA, ROS and Fe2⁺ levels, as well as decreased GSH and SOD levels. In both SAP and HL-SAP groups, abnormal lipid metabolism was associated with downregulated Nrf2, SLC7A11, and GPX4 expression and upregulated Keap1 expression, and these alterations were more prominent in the HL-SAP group.
CONCLUSION: Abnormal lipid metabolism aggravates oxidative stress, inflammation, and pancreatic acinar cell injury in SAP, and promotes ferroptosis. These effects may be attributed to reduced activity of the Keap1/Nrf2/SLC7A11/GPX4 pathway.