8-Gingerol

8-Gingerol can be found in the rhizome of ginger (Z. officinale) and has oral bioactivity. It activates TRPV1, with an EC₅₀ value of 5.0 µM. 8-Gingerol inhibits COX-2 and also suppresses the growth of H. pylori in vitro. Additionally, 8-Gingerol exhibits anticancer, antioxidant, and anti-inflammatory properties by inhibiting the epidermal growth factor receptor (EGFR) and modulating its downstream STAT3/ERK pathway to suppress the proliferation, migration, and invasion of colorectal cancer cells. 8-Gingerol also exerts immunosuppressive effects by inhibiting oxidative stress, inducing cell cycle arrest, promoting apoptosis, and regulating autophagy. Furthermore, 8-Gingerol has cardioprotective effects. 8-Gingerol is promising for research in the fields of cancer, infection, immunosuppression, and cardiovascular diseases. In Vitro:8-Gingerol (0-70 µM, 24-72 hours) can inhibit the proliferation of HCT116 and DLD1 colorectal cancer cells, induce G0/G1 phase cell cycle arrest, and significantly promote apoptosis in HCT116 cells^[3].
8-Gingerol (0-70 µM, 48 hours) significantly inhibits the migration and invasion abilities of the cells, and its effect is dependent on the EGFR/STAT3/ERK pathway^[3].
8-Gingerol (100 µM, 48 hours) can reduce the effective concentration of 5-FU in HCT116 and DLD1 colorectal cancer cells, and in combination treatment, it may help reduce the toxicity of 5-FU^[3].
8-Gingerol (40, 80 µg/mL, 24 hours) significantly inhibits the LPS (HY-D1056) and Concanavalin A (HY-P2149) induced splenocyte proliferation, exhibiting immunosuppressive effects^[4].
8-Gingerol (10, 20 µM, 48 hours) inhibits autophagy and apoptosis in myocardial fibrosis by regulating the PI3K/Akt/mTOR signaling pathway, showing significant cardioprotective effects^[5].
In Vivo:8-Gingerol (50, 100 mg/kg, i.p., once daily for 7 days) can suppress the humoral and cellular immune responses in mice, likely by directly inhibiting activated T cells and B cells^[4].
8-Gingerol (10, 20 mg/kg, i.p., once daily for 14 days) improves ISO-induced myocardial fibrosis in mice by regulating the PI3K/Akt/mTOR signaling pathway, inhibiting oxidative stress, apoptosis, and autophagy^[5].