Mechanism of action of butylphalide against the injury following oxygen glucose deprivation/reoxygenation in rat cortical neurons.
- Author:
Li-Rong WU
1
;
Yong LUO
Author Information
1. First Affiliated Hospital, Chongqing Medical University, Key Lab of Neurology in Chongqing, Chongqing 400016, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Antioxidants;
pharmacology;
Benzofurans;
pharmacology;
Cell Hypoxia;
Cerebral Cortex;
cytology;
metabolism;
Drugs, Chinese Herbal;
pharmacology;
Female;
Glucose;
deficiency;
metabolism;
L-Lactate Dehydrogenase;
metabolism;
Male;
Neurons;
drug effects;
metabolism;
Neuroprotective Agents;
pharmacology;
Nitric Oxide Synthase Type II;
biosynthesis;
genetics;
Pyrrolidines;
pharmacology;
RNA, Messenger;
metabolism;
Rats;
Rats, Wistar;
Thiocarbamates;
pharmacology;
Transcription Factor RelA;
metabolism
- From:
Acta Pharmaceutica Sinica
2008;43(4):366-370
- CountryChina
- Language:Chinese
-
Abstract:
To explore the mechanism of action of butylphalide (NBP) against the injury following oxygen glucose deprivation/reoxygenation (OGD/R) in rat cortical neurons, neurons of Wistar newborn rats were prepared by filtering through a mesh, centrifugation and trypsogen digestion. A simple, stable and reliable in vitro model of OGD/R of neurons was established. We studied the activation, the nuclear translocation of NF-kappaB p65 and the mRNA expression of iNOS affected by NBP in each group neuron by RT-PCR. NBP is proved to be able to add cellular vigor and decrease LDH release. The mRNA expression of iNOS in neurons after OGD 4 h/R 8 h decreased when treated with NBP. There is statistical difference between each concentration of NBP that it adds cellular vigor, decreases LDH release and expression of iNOS in neurons after OGD 4 h/R 8 h. There is also statistical difference between NBP (100 micromol x L(-1)) and PDTC (100 micromol x L(-1)). It is proved that NBP can protect neurons, block upregulation of iNOS mRNA, and restrain activation of NF-kappaB in neurons.
