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Hepatocellular carcinoma (HCC) and hepatoblastoma are common malignant tumor types in China. The aim of the present study was to evaluate the effects of resolvin D1 (RvD1) on inflammatory factor levels and mitogen-activated protein kinase (MAPK) signaling in lipopolysaccharide (LPS)-treated liver cancer cells. First, HepG2 hepatoblastoma and PLC/PRF/5 HCC cells were cultured and treated with LPS with or without various concentrations of RvD1 (0, 0.025, 0.05, 0.1 and 0.2%). Subsequently, ELISA was performed to measure the protein levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in the culture medium. In addition, cell proliferation of the liver cancer cells was assessed by MTT assay. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to detect the expression of TNF-α, IL-1β and IL-6 in the cultured cells. Western blotting was also performed to assess the protein expression of phosphorylated extracellular signal-related kinase (p-ERK), p-c-Jun N-terminal kinase (p-JNK) and p-p38. Compared with the control group, LPS treatment increased the protein levels of TNF-α, IL-1β and IL-6 in the culture medium, and RvD1 inhibited this increase in a concentration-dependent manner. RvD1 also reduced the LPS-induced increase in TNF-α, IL-1β, IL-6, p-ERK, p-JNK and p-p38 expression levels in liver cancer cells. LPS promoted the proliferation of liver cancer cells, while RvD1 attenuated this effect. In summary, the current findings suggest that RvD1 inhibits cell proliferation and the expression of inflammatory cytokines in LPS-treated liver cancer cells by targeting the MAPK pathway.

experimental and therapeutic medicine

Resolvin D1 inhibits the proliferation of lipopolysaccharide‑treated HepG2 hepatoblastoma and PLC/PRF/5 hepatocellular carcinoma cells by targeting the MAPK pathway