The Effect of MSCs with/without Silymarin Against Liver Fibrosis in HepG2 Cell Line with Focused on Caspase3, NFKβ, Apoptosis, Proliferation, Necrosis, and Collagen

Background: Liver fibrosis is characterized by irreversible damage to the liver parenchyma. The mechanism of fibrosis is based on the activation of collagen, nuclear factor kappa (NF-kβ) activation, and inhibition of ne-crosis, apoptosis, caspase-3 and proliferation. The HepG2 cell line is an evolved human liver cancer cell that exhibits a human hormone response. Hepatocyte stem cells have antifibrotic, anti-inflammatory, and im-munomodulatory properties, can suppress apoptosis and necrosis, and promote proliferation. Methods: This is an experimental in vitro study using pre-test and post-test. Hepatocyte stem cells were obtained from the neonatal umbilical cord. The cell lines were divided into four groups. Analysis was performed on below variable including caspase-3, NF-kβ, necrosis, apoptosis, proliferation and cytopathological capacity. Results: Cytopathological studies of the hepG2 cell line showed fibroblast growth. Mesenchymal stem cells reduced NF-kβ activity, but not caspase 3 activity. Mesenchymal stem cells also significantly reduced apoptosis and necrotic activity, but silymarin was not significantly affected. Mesenchymal stem cells also significantly increased proliferation (p <0.001), but silymarin was not significantly affected. Conclusion: Mesenchymal stem cells significantly inhibited NF-kβ, necrosis, apoptosis, and proliferation ac-tivation, but caspase-3 inhibition was not significantly affected.