Glutamine-mediated Modulation of XO/uric acid/NF-kB Signaling Pathway Ameliorates Intestinal I/R-induced Bacterial Translocation and Cardiorenal Inflammatory Injury.
Moses Agbomhere HamedOyedele Oladipo AdegboyegaOlalekan Isreal OjoTunmise Maryanne AkhigbeFolakemi Dorcas FajuyitanOmolade Christianah AdeyemoTomisin Folashade OdebunmiOluwapelumi Sarah AdeniyiIsaac Ayomide OmoleRoland Eghoghosoa AkhigbePublished in: Cell biochemistry and biophysics (2024)
This study explored the effect of intestinal ischaemia/reperfusion (I/R) on cardiorenal tissues. The involvement of xanthine oxidase/uric acid/NF-kB signaling in intestinal I/R was also investigated. In addition, the possible protective effect of glutamine was also evaluated. Twenty-four male Wistar rats were acclimatized and then randomly assigned to four groups (n = 6); sham-operated, glutamine-treated rats (GLUT), I/R, and I/R + GLUT. The sham-operated rats were sham-operated and received 0.5 mL of distilled water, GLUT rats were sham-operated and had 1 g/kg b.w. of glutamine, I/R animals had an intestinal I/R procedure and received 0.5 mL of distilled water, and the I/R + GLUT rats had an intestinal I/R procedure and also received 1 g/kg b.w. of glutamine. Treatments were daily and per os. Glutamine attenuated intestinal I/R-induced rise in intestinal and cardiorenal activities of creatinine kinase and lactate dehydrogenase and lactate level. More so, glutamine alleviated I/R-induced rise in malondialdehyde, xanthine oxidase, uric acid, myeloperoxidase, NF-kB, TNF-α, IL-1β, caspase 3 activity, and DNA fragmentation. Furthermore, glutamine suppressed I/R-induced decline in GSH levels and SOD and catalase activities. Moreover, glutamine improved intestinal, cardiac, and renal histology in animals subjected to intestinal I/R.
Keyphrases
- uric acid
- signaling pathway
- metabolic syndrome
- high glucose
- diabetic rats
- oxidative stress
- pi k akt
- heart failure
- clinical trial
- immune response
- acute myocardial infarction
- gene expression
- minimally invasive
- nuclear factor
- cell proliferation
- mass spectrometry
- brain injury
- percutaneous coronary intervention
- stress induced
- cell free
- atrial fibrillation
- high speed
- fluorescent probe