AIM To explore the molecular mechanism of curcumin in alleviating oxidative low-density lipoprotein (ox-LDL) induced cell damage by inhibiting insulin-like growth factor 2 (IGF2), so as to elucidate the role of curcumin in treating atherosclerosis.
METHODS Cell model was created by ox-LDL induced Human umbilical vein endothelial cells (HUVECs), and the expression level of IGF2 mRNA was detected by qRT-PCR. CCK8 and EdU were used to detect cell viability and proliferation. The apoptosis rate was measured by flow cytometry. The levels of IGF2, Bax and Bcl-2 were tested by Western blotting. The concentrations of TNF-α, IL-1β and IL-6 were determined by ELISA.
RESULTS Compared with the control group, IGF2 mRNA and protein level in ox-LDL group were increased (P<0.05, P<0.01), together with decreased cell proliferation level (P<0.01). The results also reported increased apoptosis rate (P<0.01), increased Bax protein level, as well as decreased Bcl-2 protein level (P<0.01); The observation also included increased concentrations of TNF-α, IL-1β and IL-6 (P<0.01), coupled with increased p-p65/p65 level (P<0.01). Compared with ox-LDL group, the group of ox-LDL with added curcumin showed decreased IGF2 mRNA and protein level (P<0.05, P<0.01), increased cell proliferation level (P<0.01), decreased cell apoptosis rate (P<0.05), decreased Bax protein level (P<0.01) and elevated Bcl-2 protein level (P<0.05); The concentrations of TNF-α, IL-1β and IL-6 dropped (P<0.05, P<0.01); The p-p65/p65 level was decreased (P<0.01). In comparison, the ox-LDL+ curcumin +oe-IGF2 group showed increased IGF2 mRNA and protein expression (P<0.01), reduced cell proliferation level (P<0.01), and the rise of cell apoptosis rate (P<0.05) and Bax protein level (P<0.01). Bcl-2 protein level declined (P<0.01); The concentrations of TNF-α, IL-1β and IL-6 were increased (P<0.05, P<0.01); The p-p65/p65 level was elevated (P<0.01).
CONCLUSION Curcumin alleviates ox-LDL-induced apoptosis and inflammation by inhibiting IGF2-mediated NF-κB pathway.
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