2017
DOI: 10.3923/ijp.2017.1038.1046
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Protective Effect of Mesna on Intestinal Ischemia-reperfusion Injury by Nitric Oxide and Arginase in an Experimental Rat Model

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Cited by 4 publications
(3 citation statements)
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“…In retinal ischemia-reperfusion injury models, ARG-2 deletion leads to significantly reduced glial activation, reactive oxygen species formation and cell death by necroptosis leading to decreased ganglion cell loss, microvascular degeneration and preserved retinal morphology [8]. Similarly, in the small intestine [91] and liver [92], ARG blockade been shown to increase L-arginine bioavailability resulting in less injury in the latter following ischemia-reperfusion. Essentially, in reperfusion models of organs other than the brain, ARG upregulation following injury appears to have detrimental effects.…”
Section: Arg Response After Brain Injurymentioning
confidence: 99%
“…In retinal ischemia-reperfusion injury models, ARG-2 deletion leads to significantly reduced glial activation, reactive oxygen species formation and cell death by necroptosis leading to decreased ganglion cell loss, microvascular degeneration and preserved retinal morphology [8]. Similarly, in the small intestine [91] and liver [92], ARG blockade been shown to increase L-arginine bioavailability resulting in less injury in the latter following ischemia-reperfusion. Essentially, in reperfusion models of organs other than the brain, ARG upregulation following injury appears to have detrimental effects.…”
Section: Arg Response After Brain Injurymentioning
confidence: 99%
“…These beneficial outcomes of Mesna were built on inspection of the lung that demonstrated about normal structure apart from few mild changes. Similarly, Mesna could effectively counteract injury induced by I–R in the intestine 69 , liver 70 , spinal cord 71 , and kidney 72 .…”
Section: Discussionmentioning
confidence: 99%
“…Although mesna has been used effectively against IFS-induced cystitis, however; the symptoms of HC persist clinically in about 30% of cases. 10 Mesna cannot eradicate IFS-induced HC, which arises from direct contact of the toxic acrolein with the UB mucosa and induces the production of free radicals, RNS and ROS. Therefore, the protective agents against molecular damage in cases of HC should include various antioxidative enzymatic defense systems such as superoxide dismutase (SOD) and non-enzymatic antioxidants such as celery (Apium graveolens).…”
Section: Introductionmentioning
confidence: 99%