Figure 4
Delphinidin inhibits T lymphocyte proliferation through ERα-dependent mechanism. (A) Histograms show the percentage of proliferation of cells exposed to either 10−2 g/L of delphinidin (Del), 5 µg/mL PHA or both in presence or in absence of nonselective estrogen receptor antagonist (Fulvestrant 100 nM) for 48 h. Data are the mean ± SEM (n = 8). (B) Western blot of phosphorylated ERK1/2 in T cells exposed to either 10−2 g/L of delphinidin, 5 µg/mL PHA or both for 24 h in presence of fulvestrant. Histograms show densitometric analysis of phosphorylated ERK1/2 normalized to total ERK1/2 expression, Data are the mean ± SEM (n = 6). (C) Representative traces (left) and histograms (right) showing the effect of 10−2 g/L of delphinidin alone or after activation by 1 µM thapsigargine (TG) on [Ca2+]i in Ca2+-containing PSS in presence of Ful (100 nM). (D) Representative traces (left) and histograms (right) showing the effect of delphinidin on [Ca2+]i increase induced by 1.25 mM of CaCl2 after depletion of intracellular stores in Ca2+-free PSS by thapsigargin in presence of fulvestrant. Data are the mean ± SEM (n = 7). (E) Histograms show the percentage of proliferation of cells isolated from ERα WT or KO mice exposed to either 10−2 g/L of delphinidin, 5 µg/mL PHA or both for 48 h. (F) Representative traces (left) and histograms (right) showing the effect of 10−2 g/L of delphinidin (Del) alone or after activation by 1 µM thapsigargin (TG) on [Ca2+]i in Ca2+-containing PSS of cells isolated from ERα WT mice. (G) Same experiments on cells isolated from ERα KO mice. Data are the mean ± SEM (n = 4). *P < 0.05, **P < 0.01 and ***P < 0.001 versus control group.
