Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Apr 4;2017:6891645. doi: 10.1155/2017/6891645

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2017 Di Ma et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

Mechanism of the anti-inflammatory effects of ischemic postconditioning (IPO). Ischemic postconditioning places stress on the cell, triggering endogenous protective mechanisms. Immunosuppression is reduced by decreasing peripheral humoral immunity. Intracellular: ischemic postconditioning places stress on the cell, triggering endogenous protective mechanisms. Reduction of mitochondrial cytochrome C results in immunosuppression, which leads to a decrease in the levels of inflammatory cytokines and chemokines. IL-1β: interleukin 1 beta; TNF-α: tumor necrosis factor alpha; TLR-2: toll-like receptor 2; TLR-4: toll-like receptor 4; Cyto C: cytochrome C; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells.