Abstract
BACKGROUND: Moringa oleifera (MO) exhibits hepatoprotective properties and provides an anti-liver fibrosis effect. However, its mechanism related to the anti-liver fibrosis effect was still unclear.
AIM: The objective of this study was to explain the mechanism of liver fibrosis prevention by MO through hepatic stellate cells (HSCs).
MATERIALS AND METHODS: The liver fibrosis model was induced by the intraperitoneal injection of 10% CCl4 twice a week at a one cc/kg BW dose for 12 weeks and followed by a quantity of 2 cc/kg BW for the past 2 weeks. Ethanol extract of MO leaves (150, 300, and 600 mg/kg) was orally administered daily. Double immunofluorescence staining and terminal deoxynucleotidyl transferase dUTP nick end labeling analysis were applied to analyze the markers involved in HSCs activation and a-HSC apoptosis.
RESULTS: The results showed that the administration of MO could reduce transforming growth factor-β and nuclear factor-kappa B (NFκB), increase the expression of tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 and caspase-3, and increase the number of apoptosis a-HSCs.
CONCLUSION: This study showed that the ethanol extract of MO leaves could inhibit liver fibrosis by inhibiting HSCs activation and inducing of a-HSCs apoptosis through the extrinsic pathway.
Publisher
Scientific Foundation SPIROSKI