Pretreatment with pPolyHb attenuates H₂O₂-induced endothelial cell injury through inhibition of JNK/p38 MAPK pathway by upregulation of heme oxygenase-1

Abstract

Polymerized porcine hemoglobin (pPolyHb) exhibits a protective effect on ischemia/reperfusion of organ grafts. A series of experiments were performed to explore the underlying cytoprotective mechanisms of pPolyHb pretreatment on H2O2-induced cell death and apoptosis. The results showed that the pretreatment augmented heme oxygenase-1 (HO-1) expression, and at the same time, decreased the phosphorylation of JNK/p38 mitogen-activated protein kinase (MAPK) and intracellular ROS generation in H2O2-treated HUVECs. Moreover, the inhibition of HO-1 expression by tin porphyrin (SnPP) abolished the protective effects of pPolyHb, which suggested that the cytoprotective effect of pPolyHb involves upregulating HO-1 and subsequently decreasing the phosphorylation of the JNK and p38 MAPK and ROS generation.

3,4,5‐O‐tricaffeoylquinic acid alleviates ionizing radiation‐induced injury in vitro and in vivo through regulating ROS/JNK/p38 signaling

“…Mitogen‐activated protein kinases regulate many cell physiological functions, such as cell proliferation and apoptosis, and are susceptible to stimulation by various physiological factors, including ROS 9,10,34 . Next, we explore whether the antiapoptotic effect of tCQA is related to the regulation of MAPK signaling pathway.…”

“…MAPKs control many physiological functions, such as cell growth, proliferation, and apoptosis. Xue 9 reported that polymerized porcine hemoglobin reduced the H 2 O 2 ‐induced endothelial cell damage by reducing the overproduction of ROS and subsequent phosphorylation of p38 MAPK; Gong 10 reported that Vaccarin prevents HUVEC inflammation and apoptosis induced by ox‐LDL by inhibiting ROS/p38 MAPK signaling. Therefore, inhibiting IR‐activated ROS/MAPK signaling pathway may be an effective strategy for the development of new radioprotective agents.…”