Endoplasmic reticulum stress response in spontaneously @entity101 @entity35 is affected by XXXX reperfusion injury.

@entity21206 @entity296 @entity101 @entity21205 @entity741 @entity35 @entity24783 @entity46138
UNASSIGNED: Cell apoptosis induced by endoplasmic reticulum (ER) stress appears to be one of the main causes of @entity296 following @entity741 /reperfusion (MI/R). The @entity21206 ( @entity21206 ) pathway is the main pathway through which apoptosis is induced during ER stress. @entity21205 ( @entity21205 ) is an important protein involved in the @entity21206 pathway. The present study investigated the hypothesis that MI/R activates the @entity21206 pathway through signaling via a pathway involving PKR-like ER kinase (PERK), a-subunit of eukaryotic initiation factor 2 ( @entity46138 ) and @entity24783 ( @entity24783 ). Immunohistochemical staining of the heart tissues from spontaneously hypersensitive @entity35 indicated that MI/R injury increases @entity21206 and GPR78 protein expression levels. To further analyze the mechanism by which MI/R injury induces apoptosis by ER stress, the expression levels of five marker proteins involved in the hypothetical PERK- @entity46138 - @entity24783 pathway were detected, namely PERK, phosphorylated PERK (P-PERK), @entity46138 , phosphorylated @entity46138 (P- @entity46138 ) and @entity24783 . An increase in the collective expression levels of these proteins would indicate that apoptosis was induced by this signaling pathway. In addition, the study also explored whether @entity101 affects the signaling pathway of MI/R-induced @entity296 by treating spontaneously @entity101 @entity35 (SHRs) with captopril (an effective drug used to treat @entity101 ). @entity35 treated with captopril experienced a reduction in blood pressure to normal levels, but no marked differences in the expression levels of the tested proteins or in MI/R injury severity compared with those in untreated @entity35 . These results suggest that MI/R activates the @entity21206 pathway during ER stress by activating the PERK- @entity46138 - @entity24783 pathway and that @entity101 does not affect this signaling pathway.
