Geniposide Alleviates Oxidative Damage in Hepatocytes through Regulating miR-27b-3p/Nrf2 Axis

Geniposide (GEN), a main compound extracted from Gardenia jasminoides fruit, has various biological activities including anti-inflammation, cellular damage alleviation, neuroprotection, and others. However, the effect of GEN on oxidative stress in hepatic cells is yet to be investigated. Our study uncovered that GEN eliminated excess intracellular free radicals by activating the Nrf2/ARE signaling pathway in H2O2 -treated hepatocytes, while the protective effect was blocked by ML385 (an inhibitor of Nrf2). Moreover, H2O2 led to upregulation of miR-27b-3p in L02 cells, which was restrained by GEN. Overexpression of miR-27b-3p greatly weakened the antioxidant capacity of GEN in hepatocytes via directly targeting the Nrf2 gene. Our findings indicated that GEN treatment recovered H2O2-induced oxidative stress via targeting miR-27b-3p and thereby enhanced the antioxidant capacity by stimulating nuclear translocation and accumulation of Nrf2. These findings suggest that inhibition of miR-27b-3p to activate the Nrf2/ARE pathway by GEN is a potential alternative for hepatic oxidative damage alleviation.

Automated summary

Geniposide (GEN) can eliminate excess intracellular free radicals by activating the Nrf2/ARE signaling pathway in hepatic cells, thereby inhibiting oxidative stress and enhancing antioxidant capacity. Additionally, GEN can suppress the upregulation of miR-27b-3p induced by H2O2, leading to improved repair of oxidative damage.