Taurine Attenuates Multiple Organ Injury Induced by Intestinal Ischemia Reperfusion in Rats

Zhang, Feng; Tong, Lei; Qiao, Haiquan; Dong, Xuesong; Qiao, Guojun; Jiang, Hongchi; Sun, Xueying

doi:10.1016/j.jss.2007.12.781

Cited by 38 publications

(31 citation statements)

References 41 publications

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“…Moreover, the macrophages of taut Ϫ/Ϫ mice appear to change their stability in response to malaria, as circumstantially indicated by the increased systemic levels of TNF-␣ and IL-1␤, which are produced primarily by macrophages. This accords with other data showing, conversely, that taurine is able to dampen the effect of proinflammatory cytokines, including IL-1␤ (12) and TNF-␣ (10,24,33,34,44,47,60).…”

Section: Discussionsupporting

confidence: 92%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

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Deletion of the taurine transporter gene (taut) results in lowered levels of taurine, the most abundant amino acid in mammals. Here, we show that taut ؊/؊ mice have lost their ability to self-heal blood-stage infections with Plasmodium chabaudi malaria. All taut ؊/؊ mice succumb to infections during crisis, while about 90% of the control taut ؉/؉ mice survive. The latter retain unchanged taurine levels even at peak parasitemia. Deletion of taut, however, results in the lowering of circulating taurine levels from 540 to 264 mol/liter, and infections cause additional lowering to 192 mol/liter. Peak parasitemia levels in taut ؊/؊ mice are approximately 60% higher than those in taut ؉/؉ mice, an elevation that is associated with increased systemic tumor necrosis factor alpha (TNF-␣) and interleukin-1␤ (IL-1␤) levels, as well as with liver injuries. The latter manifest as increased systemic ammonia levels, a perturbed capacity to entrap injected particles, and increased expression of genes encoding TNF-␣, IL-1␤, IL-6, inducible nitric oxide synthase (iNOS), NF-B, and vitamin D receptor (VDR). Autopsy reveals multiorgan failure as the cause of death for malaria-infected taut ؊/؊ mice. Our data indicate that taut-controlled taurine homeostasis is essential for resistance to P. chabaudi malaria. Taurine deficiency due to taut deletion, however, impairs the eryptosis of P. chabaudi-parasitized erythrocytes and expedites increases in systemic TNF-␣, IL-1␤, and ammonia levels, presumably contributing to multiorgan failure in P. chabaudi-infected taut ؊/؊ mice.

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Section: Discussionsupporting

confidence: 92%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

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“…The intestinal IR can result in collapse of the systemic circulation (e.g., hypovolemic and septic shock) as well demonstrate [2][3][4][5] .…”

Section: ■ Introductionmentioning

confidence: 99%

“…TNFalpha), and a large amount of nitric oxide (NO) from inducible NO synthase (iNOS), thus, leading to the inflammatory injury and cell apoptosis [5][6][7] . The local and systemic inflammatory responses were caused by generation of a variety of proinflammatory mediators, such as TNF-alpha and oxygen free radicals in the circulation results in the systemic inflammatory response syndrome, one of major causes for morbidity and mortality during illness in general 5,8 . Activated polymorphonuclear neutrophils (PMN) and proinflammatory cytokines are then released into the systemic circulation, interact with the vascular endothelium of distant organs, therefore, contributing to the systemic inflammatory response 8,9 .…”

Section: ■ Introductionmentioning

confidence: 99%

Effect of atenolol pre-treatment in heart damage in a model of intestinal ischemia-reperfusion

et al. 2017

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1 AbstractPurpose: To investigate the effects of atenolol in inflammatory mediator and oxidative stress in a myocardial injury by intestinal ischemia/reperfusion in rat model. Methods: Adult Wistar male rats were randomly (n=8), anesthetized and divided in: Sham: submitted to operation only; group SS+IR: intravenous saline infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); group AT+IR: intravenous atenolol infusion (2 mg/kg) following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); and group AT+I+AT+R: intravenous atenolol infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and in the time 45 minutes other atenolol doses were administrated and the artery was open for 120 minutes (reperfusion), all animals were submitted to muscular relaxation for mechanical ventilation. In the end of experiment the animals were euthanized and the hearts tissue were morphology analyzed by histology and malondialdehyde by ELISA, and the plasma were analyzed for tumor necrosis factor-alpha by ELISA. Results:The group SS+IR demonstrated the higher malondialdehyde levels when compared with the atenolol treated-groups (p=0.001) in the heart tissue. The tumor necrosis factoralpha level in plasma decrease in the treated groups when compared with SS+IR group (p=0.001). Histology analyses demonstrate pyknosis, edema, cellular vacuolization, presence of inflammatory infiltrate and band contraction in the heart tissue of the rats. Conclusion: Atenolol significantly reduce the degree of cardiac damage after intestinal ischemia-reperfusion.

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“…İntestinal dokunun reperfüzyonu nötrofillerin aktivasyonu, mitokondriyal elektron transport zinciri, ksantin oksidaz metabolizması ile ortaya çıkan SOR'nin oluşumunu, interstisyel ödem ve mukozanın fonksiyonel ve yapısal hasarını tetikler (3). İ/R mukozal bariyer fonksiyonunu bozarak mukozal ve vasküler permeabilite artışı, bakteriyel translokasyon ve sonuçta sistemik inflamatuar cevap ve çoklu organ yetmezliğine neden olmaktadır (3,4). Çeşitli inflamatuar ve oksidatif mediatörler intestinal İ/R sonrası sistemik dolaşıma salınmakta ve akut akciğer hasarına neden olmaktadır (1,5,6).…”

Section: Introductionunclassified