Pancreas · 2026
Emodin Alleviates Microcirculation Disorders in Acute Lung Injury Associated With Severe Acute Pancreatitis by Inhibiting Ferroptosis of Vascular Endothelial Cells.
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Li Jiajia, Wang Yan, Zhang Chunpan, Li Shirong, Qi Wenjie
Аннотация
OBJECTIVE: To investigate the therapeutic effects and mechanisms of Emodin on pulmonary microcirculation disorders in acute lung injury associated with severe acute pancreatitis (SAP-ALI).
MATERIALS AND METHODS: The Sprague-Dawley rats were randomly divided into a control group, SAP-ALI group (SAP; rats were induced through retrograde injection of 5.0% sodium taurocholate into the pancreatic biliary ducts), SAP-ALI+Emodin group (Emodin; administered Emodin throug`h gavage to the rats following the modeling), and SAP-ALI+Fer-1 group (Fer-1; injected Fer-1). Then the pulmonary microcirculation and pathology were observed using a Moor instrument, HE staining, and electron microscopy (EM). The expression of related proteins in serum and lung tissue was determined using enzyme-linked immunosorbent assay (ELISA) and western blotting (WB). In vitro study, human umbilical vein endothelial cells (HUVECs) were exposed to lipopolysaccharide (LPS) and treated with DMSO, Emodin, and Fer-1. The expression of related mRNA and proteins in HUVECs was detected using real-time polymerase chain reaction (RT-PCR), WB, EM, and fluorescence microscopy.
RESULTS: Emodin ameliorate pulmonary microcirculation disorders in SAP-ALI rats and suppresses the inflammatory cytokines, inhibits ferroptosis through upregulated GPX4 and SLC7A11 in lung tissue. In vitro, Emodin suppressed the ferroptosis response by increasing GSH/GSSG level, while decreasing MDA, ROS, and Fe² + levels in HUVECs. Furthermore, Emodin upregulates the expression of GPX4 and SLC7A11 , mitigates mitochondrial damage, and downregulates the expression of NCOA4 in HUVECs.
CONCLUSION: Emodin inhibits ferroptosis in HUVECs by attenuating NCOA4-mediated iron autophagy, thereby ameliorating pulmonary microcirculation disorders in SAP-ALI rats.
MATERIALS AND METHODS: The Sprague-Dawley rats were randomly divided into a control group, SAP-ALI group (SAP; rats were induced through retrograde injection of 5.0% sodium taurocholate into the pancreatic biliary ducts), SAP-ALI+Emodin group (Emodin; administered Emodin throug`h gavage to the rats following the modeling), and SAP-ALI+Fer-1 group (Fer-1; injected Fer-1). Then the pulmonary microcirculation and pathology were observed using a Moor instrument, HE staining, and electron microscopy (EM). The expression of related proteins in serum and lung tissue was determined using enzyme-linked immunosorbent assay (ELISA) and western blotting (WB). In vitro study, human umbilical vein endothelial cells (HUVECs) were exposed to lipopolysaccharide (LPS) and treated with DMSO, Emodin, and Fer-1. The expression of related mRNA and proteins in HUVECs was detected using real-time polymerase chain reaction (RT-PCR), WB, EM, and fluorescence microscopy.
RESULTS: Emodin ameliorate pulmonary microcirculation disorders in SAP-ALI rats and suppresses the inflammatory cytokines, inhibits ferroptosis through upregulated GPX4 and SLC7A11 in lung tissue. In vitro, Emodin suppressed the ferroptosis response by increasing GSH/GSSG level, while decreasing MDA, ROS, and Fe² + levels in HUVECs. Furthermore, Emodin upregulates the expression of GPX4 and SLC7A11 , mitigates mitochondrial damage, and downregulates the expression of NCOA4 in HUVECs.
CONCLUSION: Emodin inhibits ferroptosis in HUVECs by attenuating NCOA4-mediated iron autophagy, thereby ameliorating pulmonary microcirculation disorders in SAP-ALI rats.