Understanding the molecular mechanism of emodin in inhibiting hepatocellular carcinoma: an in vitro and in vivo approach

Abstract

Emodin, a prominent toxic constituent, is an anthraquinone derivative that known for its various pharmacological properties, including anticancer, antibacterial, anti-angiogenic and anti-inflammatory effects. However, emodin’s toxicity is a significant concern that must be addressed to confirm its safe therapeutic application. In this study, we isolated emodin from Halodule uninervis against hepatocellular carcinoma (HCC) in both in vitro and in vivo. The in vitro anticancer activity of emodin was performed using MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide], AO/EtBr (acridine orange/ethidium bromide), flow cytometry and western blot analysis. The in vivo anticancer activity of emodin was investigated using DEN (Diethylnitrosamine) + CCl₄ (Carbon tetrachloride)-induced HCC in BALB/c mice. Emodin showed an IC₅₀ value of 49.24 μg/mL against HepG2 cells by MTT assay. AO/EtBr, DNA fragmentation, cell cycle analysis using flow cytometry and western blot analysis confirmed the apoptosis induction against HepG2 cells. Emodin reduced the tumor nodules and replaced hepatocyte architecture against DEN + CCl₄-induced HCC in BALB/c mice. These findings concluded that isolated emodin from H. uninervis showed potent anticancer activity against HepG2 cells and DEN + CCl₄-induced HCC in BALB/c mice that could be used for future marine-based anticancer drugs against human hepatocellular carcinoma.