Key result
Post-ischemia progesterone improves gastrointestinal transit to ~60% vs 46% while reducing inflammation.
Why the study?
Ischemia/reperfusion induced by aortic occlusion causes severe intestinal damage, inflammation, and motility impairment, and the modulatory effects of progesterone on these outcomes require evaluation.
Does progesterone treatment improve intestinal function and reduce inflammation in a rat model of ischemia/reperfusion induced by aortic occlusion?
RCT
randomized
Does progesterone treatment improve intestinal function and reduce inflammation in a rat model of ischemia/reperfusion induced by aortic occlusion?
Progesterone treatment mitigates intestinal injury, inflammation, and motility impairment following aortic occlusion-induced ischemia/reperfusion in rats.
Answers are grounded in this paper and cite their sources.
P4 may protect gut function after experimental aortic I/R; leaves open clinical translation in humans.
Aortic surgery induces severe ischemia and reperfusion. Ischemia/reperfusion (I/R) is a critical medical issue due to its high sensitivity tissue damage, inflammation, mucosal injury, and motility impairment. Studies have demonstrated that female sex hormones modulate the inflammatory response triggered by I/R. Progesterone (P4) had positive effects on intestines after trauma. We evaluated the effects of P4 on intestinal function and inflammation in a model of I/R by aortic occlusion. Methods Male Wistar rats were randomized to the following four groups: sham, surgically manipulated; IR, animals subjected to I/R; P4 pre, animals treated with P4 30 min before I/R and P4 post, treated immediately after flow reestablishment. I/R was induced by catheter 2F insufflation in the descending aorta, occluded for 30 min, followed by reperfusion for 2 h. Intestinal function, inflammatory and apoptosis markers, and mesenteric microcirculation were analyzed. Results Aortic occlusion led to systemic changes and intestinal homeostasis disruption. The I/R decreased the gastrointestinal transit (sham 69%, IR 46%, P = 0.0014) and the progesterone reduced impact induced by I/R (IR 46%, P4 post 60%, P = 0.0461). The treatment prevented the increase of epithelial mucosal barrier permeability and edema formation triggered by I/R (sham 0.2770 ng/mL vs. I/R 5.455 ng/mL, P = 0.0048) and (P4 pre 2.027 ng/mL, P = 0.0393). It also reduced inflammatory cell infiltration to intestinal tissue (IR 0.5876 vs. P4 pre 0.1818, P = 0.0003 and P4 post 0.1393 stained area/tissue area, P < 0.0001), modulating the release of inflammatory mediators and apoptosis markers (IR 0.1806 vs. P4 pre 0.0468, P = 0.0452). Conclusion Progesterone treatment was effective in modulating the neutrophil response and other inflammatory markers, decreased apoptosis, and improved gastrointestinal function triggered by I/R.
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Agostinho et al. (2025) conducted an RCT in Ischemia/reperfusion by aortic occlusion. Progesterone vs. Sham and untreated ischemia/reperfusion was evaluated on Gastrointestinal transit (p=0.0461). Progesterone treatment administered after ischemia/reperfusion improved gastrointestinal transit compared to untreated I/R (60% vs 46%, P=0.0461) and reduced inflammatory markers.
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