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

• Main Authors: Hangbing Li, Lin Zhu, Jingwei Feng, Xiaotong Hu, Chen Li, Bing Zhang
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2018-05-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Blood-brain barrier; Cardiac arrest; Hydrogen sulfide; Protein kinase C; Tight junction
• Online Access: https://www.karger.com/Article/FullText/490166
• ISSN: 1015-8987; 1421-9778

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.