Qingnao dripping pills mediate immune-inflammatory response and MAPK signaling pathway after acute ischemic stroke in rats
The aim of the present study was to examine the neuroprotective effect of Qingnao dripping pills (QNDP), especially the infiltration of neutrophils and macrophages, as well as the mitogen-activated protein kinase (MAPK) signal pathway. Adult male Sprague–Dawley rats were randomized to three groups:...
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Published in | Journal of pharmacological sciences Vol. 139; no. 3; pp. 143 - 150 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Japan
Elsevier B.V
01.03.2019
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | The aim of the present study was to examine the neuroprotective effect of Qingnao dripping pills (QNDP), especially the infiltration of neutrophils and macrophages, as well as the mitogen-activated protein kinase (MAPK) signal pathway. Adult male Sprague–Dawley rats were randomized to three groups: sham, MCAO, and QNDP. After 24 h of ischemia and reperfusion, neurological deficit scores and infarct volume were measured. Macrophages and neutrophil infiltration in the ischemic brain were respectively determined with CD68 and MPO immunofluorescence and western blot. The proteins involved in MAPK signaling (SAPK/JNK, P-SAPK/JNK, p38, P-p38, ERK1/2, and P-ERK1/2) were measured by western blotting. In vitro ischemic paradigm (oxygen-glucose deprivation) was performed in SH-SY5Y cells to evaluate the effects of QNDP. The viability and death ration of cells induced OGD/R was measured by MTT and LDH assay. The proteins involved in MAPK signaling were measured by western blotting. The results showed that QNDP treatment significantly improved the neurological deficit scores and reduced infarct size. In addition, QNDP treatment inhibited the number of CD68- and MPO-positive cells in the ischemic brain. It inhibited the MAPK signaling pathway in the ischemic brain and SH- SY5Y cells induced OGD/R. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1347-8613 1347-8648 |
DOI: | 10.1016/j.jphs.2018.12.009 |