Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain

Abstract

ABSTRACT. Inflammation plays an important role in cerebral ischemia reperfusion, which can cause severe damage to the brain and may lead to cerebral hemorrhage transformation. p38-mitogen-activated protein kinase (p38mapk) has been implicated in the etiology of a number of diseases because it is a cause of inflammation, but comparatively little research has been carried out into its role in the etiology of ischemia reperfusion. We investigated the expression of p38mapk in cerebral ischemia reperfusion to gain a better understanding of its potential role in hemorrhagic transformation (HT). One hundred rats were randomly divided into three groups: an ischemia reperfusion group, an ischemia group, and a sham-operated group. We carried out neurological deficit assessments, infarct volume measurements, histopathological examinations, and immunohistochemistry analyses. p38mapk was 2 Y.Q. Song et al. Genetics and Molecular Research 15 (3): gmr.15038492 overexpressed in the ischemia reperfusion group, which exhibited severe tissue damage and greater edema than the other two groups. These results suggest that p38mapk plays an important role in cerebral ischemia reperfusion, and may be one of the causes of HT.

Chemokine CCL2 contributes to BBB disruption via the p38 MAPK signaling pathway following acute intracerebral hemorrhage

“…The p-p38 MAPK signaling pathway has been implicated in the etiology of various diseases, and it plays an important role in ischemic stroke. 29 One basic study showed that occludin, a major component of the BBB, was regulated by p38 MAPK. 30 Moreover, increasing evidence has proven that p38 MAPK is a critical signal transduction pathway involved in changes in ICH and subarachnoid hemorrhage.…”

“…In our study, BBB disruption after ICH may have resulted from excessive p‐p38 MAPK and AQP4 overexpression. The p‐p38 MAPK signaling pathway has been implicated in the etiology of various diseases, and it plays an important role in ischemic stroke . One basic study showed that occludin, a major component of the BBB, was regulated by p38 MAPK .…”

Damage mechanism and therapy progress of the blood-brain barrier after ischemic stroke

“…4 Neuroinflammatory mechanism and related factors of BBB ischemic stroke injury the potential NOTCH3/NF-κB signaling pathway. The mitogen-activated protein kinase (MAPK) signaling pathway also plays a crucial role in ischemic strokes [83][84][85]. P38 MAPK regulates the synthesis of occludin proteins in the BBB structure [86].…”

The regulatory roles of circular RNAs via autophagy in ischemic stroke

“…In the early stage of stroke, activation of the p38 signaling pathway promotes Elk1, C/EBP homologous protein (CHOP10), leukocyte cell-derived chemotaxin-2 (LEF2C), and protein kinases MAPKK2/3 to maintain neuronal survival and play roles in anti-inflammatory and anti-apoptotic processes. In contrast, in the late stage of stroke, p38 MAPK is overactivated and promotes the expression of target genes activating transcription factors and caspases ( 106 – 108 ), promoting neuronal apoptosis; thus, differences in IS p38 MAPK signal molecules should be given different interventions. This viewpoint has been supported by relevant studies showing that rhizoma coptidis jiedu soup causes overactivation of ERK and inhibition of JNK, as well as that p38 MAPK signal induction protection autophagy is beneficial for treating IS.…”