Wild Bitter Melon Extract Regulates LPS-Induced Hepatic Stellate Cell Activation, Inflammation, Endoplasmic Reticulum Stress, and Ferroptosis

<div>A summary diagram outlines the working mechanisms of WM in LPS-activated HSCs. (a) LPS decreased ER stress and ferroptosis via downregulations of CHOP and GPX4/SLC7A11, respectively. LPS reduced lipid ROS production and cell death, but induced inflammation. On the other hand, LPS promoted liver fibrosis via HSCs activation determined by CTGF, <i>α</i>-SMA, and integrin-<i>β</i>1 upregulation. (b) WM induced ER stress and ferroptosis via upregulations of CHOP and GPX4/SLC7A11, respectively. WM also caused increases in ROS, lipid ROS production, and cell death, but reduced inflammation. Moreover, WM prevented liver fibrosis via HSCs inactivation determined by CTGF, <i>α-</i>SMA, and integrin-<i>β</i>1 downregulation.</div>

Evidence-Based Complementary and Alternative Medicine

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Figure 5

Figure 5: Wild Bitter Melon Extract Regulates LPS-Induced Hepatic Stellate Cell Activation, Inflammation, Endoplasmic Reticulum Stress, and Ferroptosis 

Figure 5 | Wild Bitter Melon Extract Regulates LPS-Induced Hepatic Stellate Cell Activation, Inflammation, Endoplasmic Reticulum Stress, and Ferroptosis 