Alleviation of acute pancreatitis-associated lung injury by inhibiting the p38 mitogen-activated protein kinase pathway in pulmonary microvascular endothelial cells

Figure 1 p38 mitogen-activated protein kinase overactivation aggravates tumor necrosis factor-alpha-induced apoptosis and inflammatory cytokine expression in pulmonary microvascular endothelial cells. A: Western blotting confirmed that mitogen-activated protein kinase kinase (Glu) transfection constitutively activated p38 mitogen-activated protein kinase in pulmonary microvascular endothelial cells; B: Apoptotic rate in null and mitogen-activated protein kinase kinase (Glu) pulmonary microvascular endothelial cells stimulated with or without tumor necrosis factor-alpha for 24 h; C: Representative images of flow cytometry analysis for apoptosis; D: The expression level of interleukin-6 in each group; E: The expression level of interleukin-1β in each group. Data are expressed as mean ± SE of 3-4 samples per group; ^aP < 0.05; ^bP < 0.01. IL: Interleukin; MKK: Mitogen-activated protein kinase kinase; TNF-α: Tumor necrosis factor-alpha.