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Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were div...
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2023
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| LEADER | 00000njm a2000000a 4500 | ||
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| 001 | oai:repository.ui.edu.ng:123456789/13542 | ||
| 042 | |a dc | ||
| 720 | |a Akinrinde, A. S. |e author | ||
| 720 | |a Ajibade, T. O. |e author | ||
| 720 | |a Adetona, M. O. |e author | ||
| 720 | |a Oyagbemi, A. A. |e author | ||
| 720 | |a Adedapo, A. D. A. |e author | ||
| 720 | |a Larbie, C. |e author | ||
| 720 | |a Omobowale, T. O. |e author | ||
| 720 | |a Ola-Davies, O. E. |e author | ||
| 720 | |a Adedapo, A. A. |e author | ||
| 720 | |a Saba, A. B. |e author | ||
| 720 | |a Oguntibeju, O. O. |e author | ||
| 720 | |a Yakubu, M. A. |e author | ||
| 260 | |c 2023 | ||
| 520 | |a Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress. | ||
| 024 | 8 | |a 1119-5096 | |
| 024 | 8 | |a ui_art_akinrinde_glycine_2023 | |
| 024 | 8 | |a African Journal of Biomedical Research 26, pp. 281-289 | |
| 024 | 8 | |a https://repository.ui.edu.ng/handle/123456789/13542 | |
| 653 | |a Kidneys | ||
| 653 | |a Diclofenac | ||
| 653 | |a Glycine | ||
| 653 | |a immunohistochemistry | ||
| 653 | |a receptors | ||
| 653 | |a blood pressure | ||
| 245 | 0 | 0 | |a Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor |