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DOI 10.1159/000490166

Медицинская библиотека · Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats.

Li Hangbing, Zhu Lin, Feng Jingwei, Hu Xiaotong, Li Chen, Zhang Bing

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Аннотация

BACKGROUND/AIMS: Hydrogen sulfide (H2S) can decrease blood-brain barrier (BBB) permeability after cardiac arrest (CA) and resuscitation; however, the underlying mechanisms are not understood clearly.

METHODS

We investigated the effects of inhalation of H2S on CA and resuscitation in a rat model of CA. We used Evans blue to detect the integrity of BBB and Western blot to assess the activation of protein kinase c (PKC) isozymes and the expression of Claudin-5, Occludin, and ZO-1. Neurological deficit scales and the 14-days survival rate were measured.

RESULTS

We determined that inhalation of 40 p.p.m or 80 p.p.m H2S significantly decreased brain water content and Evans blue leakage, ameliorated neurologic deficit scale and improved 14-days survival rate. H2S inhibited the activation of PKC-α, β I, β II and δ, impelled the activation of PKC-ε, and increased the expression of Claudin-5, Occludin and ZO-1.

CONCLUSIONS

H2S improved the integrity of BBB, mitigated brain edema; improved neurological outcome and 14-days survival rate in rats after CA and resuscitation. The beneficial effects of H2S may be associated with inhibiting the activation of PKC-α, β I, β II and δ, promoting the activation of PKC-ε, and increasing the expression of Claudin-5, Occludin and ZO-1.

Для цитирования: Li Hangbing, Zhu Lin, Feng Jingwei, Hu Xiaotong, Li Chen, Zhang Bing. Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats.. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2018. DOI: 10.1159/000490166.

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