|
|
Background: Endothelial dysfunction represents a critical pathological feature of acute pancreatitis (AP). Shenfu injection (SFI) has been demonstrated to protect both endothelial cells and pancreatic tissues affected by AP; however, the precise mechanisms underlying its protective effects remain incompletely understood. The study investigated the protective role of SFI in oxidative-stressed endothelial cells and in acute pancreatitis through the regulation of CLDN4.
Methods: Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to create an oxidative stress environment, followed by SFI treatment to assess cell viability, apoptosis, and reactive oxygen species (ROS) levels. Additionally, shRNA technology was employed to knock down CLDN4 expression in order to evaluate its role in SFI-mediated protection. Finally, an AP rat model was established to investigate the effects of SFI on AP-induced pancreatic damage and the role of CLDN4.
Results: SFI significantly enhances cell viability, reduces apoptosis, and lowers ROS levels in HUVECs under oxidative stress. At the molecular level, SFI upregulates CLDN4 expression, and depletion of CLDN4 attenuates the protective effects of SFI against oxidative stress. In the AP rat model, SFI administration alleviated pancreatic tissue damage and reduced inflammation, while CLDN4 knockdown diminished these protective effects.
Conclusions: These findings identify CLDN4 as a key mediator of SFI’s protective effects on both oxidative-stressed endothelial cells and inflamed pancreatic tissues, underscoring its potential as a therapeutic target in AP.
DOI: 10.7754/Clin.Lab.2025.250673
|
