Estradiol prevented intestinal ischemia and reperfusion-induced changes in intestinal permeability and motility in male rats

Abstract

OBJECTIVES: Ischemia and reperfusion (I/R) in the intestine could lead to severe endothelial injury, compromising intestinal motility. Reportedly, estradiol can control local and systemic inflammation induced by I/R injury. Thus, we investigated the effects of estradiol treatment on local repercussions in an intestinal I/R model. METHODS: Rats were subjected to ischemia via the occlusion of the superior mesenteric artery (45 min) followed by reperfusion (2h). Thirty minutes after ischemia induction (E30), 17β-estradiol (E2) was administered as a single dose (280 μg/kg, intravenous). Sham-operated animals were used as controls. RESULTS: I/R injury decreased intestinal motility and increased intestinal permeability, accompanied by reduced mesenteric endothelial nitric oxide synthase (eNOS) and endothelin (ET) protein expression. Additionally, the levels of serum injury markers and inflammatory mediators were elevated. Estradiol treatment improved intestinal motility, reduced intestinal permeability, and increased eNOS and ET expression. Levels of injury markers and inflammatory mediators were also reduced following estradiol treatment. CONCLUSION: Collectively, our findings indicate that estradiol treatment can modulate the deleterious intestinal effects of I/R injury. Thus, estradiol mediates the improvement in gut barrier functions and prevents intestinal dysfunction, which may reduce the systemic inflammatory response.

Mucosal Recovery after Intestinal Transplantation in the Rat: A Sequential Histological and Molecular Assessment

“…Although the physical loss of the epithelial barrier appears short-lived, it is likely that altered permeability and bacterial translocation may persist until the near-complete restoration of the mucosa and its intercellular mucus stores. Previous studies indicated that bacterial translocation depended on multiple factors, including the extent of injury, bacterial strains in the intestine, and motility [26][27][28]. This is in line with our previous findings in the same animal model when lipopolysaccharide reached the highest circulating levels after 24 h of reperfusion [29] and suggests that increased permeability for bacteria and bacterial products may persist, despite the apparent morphological recovery.…”

When less is more: Experimental Bishop–Koop technique for reduction in the use of laboratory animals for intestinal pathophysiological studies

“…In addition, SI morphological damage and villus recovery were comparable with several previous results published by our group and others. 15–19,40 In the present study, we observed the greatest damage at 30–60 min post-reperfusion in both the BK-IIRI and OSMA groups, with denuded villi and loss of villi (scores 4 and 5, respectively, on the Park/Chiu score) as the main characteristic lesions. The kinetic study facilitated the recovery of the intestinal mucosa, with edema (Park/Chiu score 1–2) as the predominant lesion at 24 h post-reperfusion and slight intestinal damage at 1 week after IIRI (Figure 5c).…”

“…For example, in the SI, superior mesenteric artery clamping model is currently used to evaluate IIRI, requiring one animal for each sample and study time. 15–29 The same situation occurs in the field of experimental colitis, where old and recent scientific articles use one animal in each LI sample collection. 30–37 For the reasons mentioned above, it is a challenge to develop models that enable reducing the number of animals involved in these studies.…”

Estrogen Alleviates Posthemorrhagic Shock Mesenteric Lymph-Mediated Lung Injury Through Autophagy Inhibition

“…Hence, intestinal barrier dysfunction caused by intestinal injury and consequently intestinal-derived infection via the mesenteric lymphatic pathway has become an important mechanism of organ damage. Studies have shown that E2 treatment could play beneficial roles in reducing intestinal permeability and inflammatory response after hemorrhagic shock or intestinal ischemia-reperfusion (37–40). The current results also showed E2 intervention significantly inhibited hemorrhagic shock–induced intestinal ischemia and intestinal villi irregularity, edema, and truncation, suggesting that E2 treatment alleviated intestinal injury.…”