Mitochondrial fission inhibitor aggravates OG D/Ri-nduced injury th roughi nhibition of autophga y
PENG Cheng
ZHANG Lei
RAO Wei
FEI Zhou
Abstract：Objective The objective of the research is to study the roles and mechanisms of mitochondrial fission inhibitor (Mdivi-1) in primary cultured cortex neurons of mice after Oxygen-glucose deprivation/Reperfusion (OGD/R) injury.Methods Occurrence of autophagy was detected after establishing OGD/R model in primary cultured cortex neurons.The mRNA and protein levels of autophagy-related genes were detected accompanied treatment with autophagy inhibitor (3-MA), autophagy agonist (rapamycin) and Mdivi-1.Moreover, the neural injury was measured.Results Following OGD/R treatment, autophagy was increased dependent on reperfusion times.And both levels of Beclin 1 and Microtubule-associated protein light chain 3 II ( LC3 II ) peaked at 24 h ( P<0.001, P<0.01).Results of cell counting kit-8 (CCK-8) after OGD/R treatment showed that Mdivi-1 could aggravate the injury (P <0.05), however, rapamycin could reduce not only the OGD/R injury (P <0.01), but also the aggravating damage induced by Mdivi-1 (P<0.05).Furthermore, Mdivi-1 significantly reduced the levels of Beclin 1 and LC3 II following OGD/R injury (P<0.05).Conclusion Mdivi-1 could aggravate the injury induced by OGD/R through inhibiting the occurrence of autophagy .
Keywords：Cerebral ischemia/reperfusion injuryMitochondrial fissionAutophagy
Publication Date：2016-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：4( 101-104 )