Effect and mechanism of picroside n on p38 mitogen activated protein kinase signal transduction pathway after cerebral ischemia/reperfusion in rats
10.16098/j.issn.0529-1356.2021.02.006
- Author:
Zhu-Qin YU
1
;
Guan-Xi WANG
1
;
Xiao-Lu WANG
2
;
Yue WANG
2
;
Ting-Ting WANG
2
;
Ting-Ting WANG
3
Author Information
1. Department of Internal Medicine, Songshan Hospital, Qingdao University Medical College
2. Institute of Integrative Medicine, Qingdao University Medical College
3. Department of Neurology, Qingdao Central Hospital
- Publication Type:Journal Article
- Keywords:
Brain;
Immunohistochemistry;
Ischemia/reperfusion injury;
p38 mitogen activated protein kinase signal transduction pathway;
Picroside II;
Rat;
Western blotting
- From:
Acta Anatomica Sinica
2021;52(2):196-204
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the neuroprotective effect and mechanism of picroside II on p38 mitogen activated protein kinase (p38 MAPK) signal transduction pathway after cerebral ischemia/reperfusion injury in rats. Methods A total of 150 healthy male Wistar rats were subject to establish middle cerebral artery occlusion/reperfusion (MCAO/R) models by inserting a monofilament thread. All rats were randomly divided into sham group, model group, picroside (Pier) group, anisomycin (Anis, agonist of p38 MAPK) group, Anis+Picr group, SB203580 (SB, inhibitor of p38 MAPK) group and SB+Picr group. The neurobehavioral function was evaluated by modified neurological severity score points (mNSS) test. The structure of neuron was observed using HE staining. The apoptotic cells were counted using TUNEL assay. The expression of phosphorylated p38 MAPK (p-p38 MAPK) in cortex was determined using the immunohistochemistry. And the expressions of p-p38 MAPK, phosphorylated MAPK activated protein kinase-2 (p-MK2), phosphorylated cytoplasm phospholipase A2 (p-cPLA2), interleukin-6 (IL-6) and tumor necrotic factor a (TNF-α) were determined by Western blotting. Results No neurological behavioral malfunction was found in sham group. In model group, the damage of neuron was worsened, while the neurobehavioral function score, apoptotic cell index and the expressions of p-p38 MAPK, p-MK2, p-cPLA2,IL-6 and TNF-α increased significantly than those in control group. No significant difference was found in TNF-α. In Pier group, SB group and SB+Picr group, the damage of neuron was lighter, the neurological behavioral function was improved, the number of apoptotic cells and the expressions of p-p38 MAPK, p- MK2, p-cPLA2 and IL-6 decreased significantly than those in model group. In Anis group and Anis + Pier group, the damage was worsen, the cerebral infarction was larger, and the expressions of p-p38 MAPK, p-MK2, p-cPLA2 and IL-6 increased significantly than those in control group. Conclusion Picroside II can protect the neuron from the apoptosis and inflammation reaction after MCAO/R by inhibiting p38 MAPK signal transduction pathway in rats.
