ObjectiveTo explore the effect of naringenin on the expression of vascular endothelial growth factor (VEGF) released by human fetal lung fibroblasts. MethodsHuman fetal lung fibroblast cells were divided into a control group,a cigarette smoke extract (CSE) group and a naringenin group. Cells in the naringenin group were incubated with different doses of naringenin for 2h. Then the naringenin group and the CSE group were incubated with CSE to adjust the final concentration of naringenin (5 μmol/L,10 μmol/L,and 20 μmol/L) and of CSE(5%). The concentration of VEGF was measured in human fetal lung fibroblasts after cultured for 24h,48h and 72h by enzyme-linked immunoabsorbent assay. Smad3 and p-Smad3 levels were detected by Western blot. ResultsELISA results showed that the CSE can significantly increase the VEGF expression,and naringenin can inhibit the increasing of the VEGF expression. Western blot results showed that the CSE can increase the p-Smad3 expression,and the naringenin can inhibit the increasing of the p-Smad3 expression. ConclusionNaringenin can inhibit phosphorylation of Smad3,and decrease the expression of VEGF released by human fetal lung fibroblasts.
ObjectiveTo investigate the effects of naringenin on the production of chemokines and its mechanism in human bronchial epithelial (HBE) cells. MethodsHBE cells were divided into a control group, a TNF-αgroup, a low-dose naringenin group, a moderate-dose naringenin group and a high-dose naringenin group. The Naringenin groups were incubated with different doses of naringenin (10, 5 and 2.5μmol/L, respectively) for 2 h. Then the naringenin groups and the TNF-αgroup were incubated with TNF-α. After 24 h of incubation, the levels of eotaxin and RANTES were determined by ELISA method, and IκBαdegradtion was detected by Western blot method. After incubated with TNF-αfor 30 min, NF-κB DNA-binding activity was detected by EMSA method. ResultsCompared with the control group, the levels of eotaxin and RANTES were significantly increased in the HBE cells stimulated with TNF-α. Naringenin had inhibitory effects on the expression of these chemokines. Naringenin abolished IκBαdegradation and reduced the DNA-binding activity of NF-κB. ConclusionNaringenin may inhibit the production of chemokines through inhibiting NF-κB pathway.