A number of diverse studies have reported the anticancer properties of Cnidium officinale Makino (CO). However, the apoptotic effect of this traditional medicinal herb in human hepatocellular carcinoma cells (HepG2) remains to be elucidated. Therefore, the present study investigated the ability of CO to reduce cell viability through apoptotic pathways. Cell viability was determined using the 2,3‑bis [2-methyloxy-4-nitro-5-sulfophenyl]‑2H‑tetrazolium‑5‑carboxanilide assay. CO extract‑induced apoptosis in HepG2 cells was assessed by Hoechst 33258 staining. The cell cycle was monitored using fluorescence‑activated cell sorting analysis with propidium iodide staining. Furthermore, the present study explored whether various signaling molecules associated with HepG2 cell death were affected by CO treatment, including caspase‑3, B‑cell lymphoma 2 (Bcl-2), tumor protein p53 (p53), cyclin‑dependent kinase 4 (CDK4) and cyclin D. The expression levels of these genes were examined by reverse‑transcription polymerase chain reaction and western blotting. The expression levels of caspase‑3 and p53 were upregulated with CO extract treatment, whereas those of Bcl‑2, CDK4 and cyclin D were significantly downregulated. Cleaved caspase‑3 expression was upregulated following treatment with CO extract in a dose‑dependent manner. Collectively, the data suggest that CO extract has the potential to induce apoptosis of HepG2 cells and may act by suppressing the cell cycle, which leads to caspase‑3 cleavage and p53 signaling.

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