Figure 5
From: Iron-Overload triggers ADAM-17 mediated inflammation in Severe Alcoholic Hepatitis
Effect of Iron or Fenton can be reversed by iron chelation in THP1 derived macrophages. (A) Relative expression of oxidative-stress, inflammation and iron-regulation genes in THP1-macrophages treated with 50 uM-Fecl2 in presence or absence of 150-uM Kelfer ([*] = p < 0.05). (B) Relative expression of oxidative-stress, inflammation and iron-regulation genes in THP1-macrophages treated with 50 uM-Fenton in presence or absence of 150 uM Kelfer ([*] = p < 0.05). (C) Relative expression of ADAM17, CD163 and associated genes in THP1-macrophages treated with 50 uM-Fecl2 in presence or absence of 150 uM Kelfer. The lower panel documents protein expression validation of ADAM17, CD163 and ADAM10 in the same condition ([*] = p < 0.05). (D) Relative expression of ADAM17, CD163 and associated genes in THP1-macrophages treated with 50 uM-Fenton in presence or absence of 150 uM Kelfer. The lower panel documents protein expression validation of ADAM17, CD163 and ADAM10 in the same condition ([*] = p < 0.05). (E) Relative expression of apoptosis, ER-stress and autophagy genes in THP1-macrophages treated with 50 uM-Fecl2 in presence or absence of 150 uM Kelfer ([*] = p < 0.05). (F) Relative expression of apoptosis, ER-stress and autophagy genes in THP1-macrophages treated with 50 uM-Fenton in presence or absence of 150 uM Kelfer ([*] = p < 0.05).
