I used a rat model of asphyxia-induced cardiac arrest to investigate the influence of post-resuscitation carbon dioxide level on neurological outcome.

The brain tissue was harvested 24 hour after cardiac arrest and used for western blotting.

Compared with the control group (normal level of CO2), the high CO2 level group demonstrated lower expression of Beclin 1, p62 and LAMP 2, while the LC3B II to LC3B I ratio was similar between the control and treatment groups.

As I could understand, the lower expression of Beclin 1 represented lower autophagic induction and lower expression of p62 and LAMP 2 represented higher autophagic degradation by autophagosome and autophagolysome, respectively, in the treatment group, compared with the control group. Finally, the similar ratios of LC3B II to LC3B I between control and treatment groups represented similar autophagosome formation rates.

Could it be possible that compared with control group, the autophagic induction was decreased and autophagic degradation was increased in the treatment group at the same time?