Cell death induction (extrinsic versus intrinsic apoptotic pathway) by intestinal ischemia–reperfusion injury in rats is time-depended
link.springer.com shows its articles on its own site.
Read the article on link.springer.com ↗Article · Feb 2021 · 1 min read
In brief
In brief
Experimental study in rats demonstrating that intestinal ischemia-reperfusion injury triggers different apoptotic mechanisms depending on reperfusion duration. Early injury (24h) activates intrinsic mitochondrial pathway via Bax/Bcl-2, while delayed injury (48h) shifts to extrinsic death receptor pathway via TNF-α and Fas-FasL signaling.
Written by the GCMD Library team from the article.
Abstract
Purpose
We investigate the mechanism of intestinal cell apoptosis and its relation to the time of reperfusion in a rat model of intestinal ischemia–reperfusion (IR).
Methods
Rats were divided into 4 groups: Sham-24 and Sham-48 rats underwent laparotomy without an intentional ischemic intervention and were sacrificed 24 or 48 h hours later; IR-24 and IR-48 rats underwent occlusion of SMA and portal vein for 20 min followed by 24 or 48 h of reperfusion, respectively. Park’s injury score, cell proliferation and apoptosis were determined at sacrifice. Proliferation and apoptosis-related gene and protein expression were determined using Real-Time PCR, Western Blot and Immunohistochemistry.
Results
IR-24 rats demonstrated a strong increase in cell apoptosis along with an elevated Bax and decreased Bcl-2 expression and a decrease in cell proliferation (vs Sham-24). IR-48 group showed an increase in cell proliferation and a decrease in cell apoptosis compared to IR-24 animals. IR-48 rats demonstrated an increase in apoptotic rate that was accompanied by greater TNF-α mRNA, Fas mRNA and FasL mRNA compared to Sham-48 animals.
Conclusion
While cell apoptosis in IR-24 rats is regulated mainly by intrinsic apoptotic pathway, 48 h followed ischemia extrinsic apoptotic pathway is responsible for pro-apoptotic effects of IR injury.