[Researched of PJ34 which is protective effect on the glutamate-induced HT-22 cell damage].
OBJECTIVE
To poly ADP ribose polymerase inhibitors PJ34 on glutamate neurotoxicity induced protective effect, as PJ34 in ischemic cerebrovascular disease provide a reference for clinical applications.


METHODS
After the cultured HT-22 cells were treated with 5 mmol/L Glu induction treatment, divided into the PJ34 group subsequently given 50 micromol/L PARP inhibitor PJ34 protection effects processing. Inhibition rate of each group and the PARP activity of changes.


RESULTS
PJ34 group after 24 h, inhibition rate of HT-22 cells were markedly decreased (P<0.05). PJ34 PARP activity than the control group was significantly lower (P<0.05).


CONCLUSIONS
PJ34 PARP activity by reducing increased glutamate-induced HT-22 cell viability, and thus play a protective effect on cells.
Fan
Hong-bin
HB
Affiliated Hospital of Xuzhou Medical College, Xuzhou, China.
Wang
Yi-nan
YN
Geng
De-qin
DQ
D000818:Animals; D016923:Cell Death / Q000187:drug effects; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D018698:Glutamic Acid / Q000633:toxicity*; D051379:Mice; D010616:Phenanthrenes / Q000494:pharmacology*; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D020011:Protective Agents / Q000494:pharmacology*
D004791:Enzyme Inhibitors; C434926:N-(oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide hydrochloride; D010616:Phenanthrenes; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D020011:Protective Agents; D018698:Glutamic Acid