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Panax notoginseng and Ginsenoside‐Rg1 contribute to down‐regulation of P‐glycoprotein level after the cerebral ischemia/reperfusion in rats
Author(s) -
Yang Li,
Li Jie,
Wang Xiaojuan,
Yu Jianyun,
Chen Bo,
Guo Zeyun
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.705.8
Subject(s) - panax notoginseng , medicine , pharmacology , ischemia , p glycoprotein , ginsenoside , striatum , ginseng , cerebral infarction , cerebral cortex , brain ischemia , anesthesia , stroke (engine) , hippocampus , chemistry , pathology , multiple drug resistance , biochemistry , dopamine , alternative medicine , mechanical engineering , engineering , antibiotics
The blood‐brain barrier possesses active transporters carrying brain‐permeable xenobiotics, including many kinds of medicine, back into the blood against injuries. P‐glycoprotein(P‐gp), one kind of important multidrug resistance transporter, is upregulated on capillary endothelium after cerebral ischemia, which may refer as to protect the brain from the poison but may result in the treatment failure of the stroke. Panax notoginseng, a traditional Chinese medicine, has been used for thousands of years to treat ischemic patients. Panax notoginsenoside (PNS) is primarily composed of ginsenosides. Ginsenoside ‐Rg1 is an important part of saponin components in PNS. As such, here we aimed to study the role of PNS and ginsenosides Rg1 against overexpression of P‐glycoprotein in experiment induced cerebral ischemia–reperfusion (I/R) adult in rats. Male SD rats were randomly divided into sham‐injured, vehicle, PNS or Rg1 groups. The expression of P‐gp in cortex, hippocampus, striatum were detected by Imunohisochemistry, Western blot and RT‐PCR. The results show that PNS or Rg1 signicantly reduced P‐gp in cortex and striatum infarction area caused by cerebral I/R. The increased expressions of P‐gp caused by cerebral I/R were restored with PNS treatment groups, as well as in Rg1 treatment groups. These results suggest that PNS and Rg1 have similar roles in adjusting overexpression of P‐gp from ischemic/reperfusion damage. PNS could be considered as an inhibitor of P‐gp in brain injuries therapy strategy for use in the case of cerebral ischemic stroke.