Figure 11.
A schematic pathway for KPR-induced HO-1 expression in HPAEpiCs. KPR attenuated LPS-induced ICAM-1 expression and lung monocyte/leukocyte accumulation through upregulation of HO-1 via enhanced p47phox/Nox2 activity, resulting in the accumulation of intracellular ROS. Imbalance in oxidative stress promoted the phosphorylation of c-Src/Pyk2/PKCα/p38α MAPK- and JNK1/2-dependent Nrf2 activation, which further binds with ARE on HO-1 promoter and suppresses the LPS-mediated inflammation in HPAEpiCs and in vivo. Thus, upregulation of the HO-1 by KPR exerts a potential strategy to protect against pulmonary inflammation.