Gum Acacia Improves Renal Function and Ameliorates Systemic Inflammation, Oxidative and Nitrosative Stress in Streptozotocin-Induced Diabetes in Rats with Adenine-Induced Chronic Kidney Disease

Abstract

Background/Aims: The effect of treatment with gum acacia (GA), a prebiotic shown previously to ameliorate chronic kidney disease (CKD), in diabetic and non – diabetic rats with adenine – induced CKD has been investigated using several conventional and novel physiological, biochemical, and histopathological parameters. Methods: Diabetes mellitus was induced in rats by a single injection of streptozotocin (STZ). Diabetic and non – diabetic rats were randomly divided into several groups, and given either normal food or food mixed with adenine (0.25% w/w, for five weeks) to induce CKD. Some of these groups were also concomitantly treated orally with GA in the drinking water (15% w/w). Results: Rats fed adenine alone exhibited physiological (decreased body weight, increased food and water intake and urine output), biochemical (increase in urinary albumin/creatinine ratio, plasma urea and, creatinine, indoxyl sulfate and phosphorus), inflammatory biomarkers (increased in neutrophil gelatinase-associated lipocalin, transforming growth factor beta -1, tumor necrosis factor alpha, adiponectin, cystatin C and interleukin-1β), oxidative biomarkers (8-isoprostane, 8 -hydroxy -2-deoxy guanosine), nitrosative stress biomarkers (nitrite and nitrate) and histopathological (increase in tubular necrosis and fibrosis) signs of CKD. STZ - induced diabetes alone worsened most of the renal function tests measured. Administration of adenine in STZ – diabetic rats further worsened the renal damage induced by adenine alone. GA significantly ameliorated the renal actions of adenine and STZ, given either singly or in combination, especially with regards to the histopathological damage. Conclusion: GA is a useful dietary agent in attenuating the progression of CKD in rats with streptozotocin-induced diabetes.

Neurological sequel of chronic kidney disease: From diminished Acetylcholinesterase activity to mitochondrial dysfunctions, oxidative stress and inflammation in mice brain

“…8), astrocytosis (Fig. 13) and calcium dysregulation in the cortex and hippocampus of the CKD mice may contribute to the observed depressive behaviour, since these inflammatory factors along with other associated pathophysiologies, which are prevalent in adenine model of CKD as well 56,60,98 , have been implicated in causing depression 99–109 .…”

Increment of Lysosomal Biogenesis by Combined Extracts of Gum Arabic, Parsley, and Corn Silk: A Reparative Mechanism in Mice Renal Cells

“…However, the increasing frequency of prescribing mixtures of these herbs by practitioners of natural medicine calls for careful examination [ 10 ]. The use of these herbs results in a general improvement in the urinary system wellbeing through the reduction in blood urea nitrogen (BUN) and creatinine concentration [ 11 ], but the precise signaling cascades they elicit to repair renal cells remain obscure. Therefore, the benefits of combining the extracts of gum Arabic, parsley, and corn silk on the urinary system following a single one-off dose of amikacin are worth investigation.…”

Peer Review #2 of "Metabolomic and biochemical characterization of a new model of the transition of acute kidney injury to chronic kidney disease induced by folic acid (v0.2)"

“…Manuscript to be reviewed the prevention of damage by regulation of the expression of anti-oxidant enzymes (Mori et al 2005). Models that have evaluated a single phase of CKD induced by adenine demonstrated an increase in serum NGAL levels relative to controls (Al Za'abi et al 2018;Ali et al 2018;. Another study that evaluated a three-phase model of CKD induced by adenine reported a significant increase in serum and urinary NGAL only in the presence of the damage inducer (Gil et al 2016).…”

“…Cys-C has been proposed as a marker of renal function because it is freely filtered by the glomerulus and subsequently reabsorbed and degraded by proximal tubular cells (McMahon & Waikar 2013). Several studies of adenine-induced kidney damage have reported an increase in serum levels of Cys-C compared with the control group (Al Za'abi et al 2018;Ali et al 2015;Ali et al 2018;Ali et al 2017;Bokenkamp et al 2001;Thakur et al 2018); however, these studies reported only one phase of kidney damage. In the present study, it was found that the serum levels of Cys-C increased in each phase as the degree of renal damage increased, although histological evaluation suggested that the damage induced by FA in this study did not affect the structure of the glomerulus.…”

“…The elevation of pro-inflammatory cytokines such as IL-1, IL-6 and TNF- is common in CKD (Furuichi et al 2009) and has been used as a predictor of mortality in patients with kidney disease (Castillo-Rodriguez et al 2017). Elevation in the expression of genes for these cytokines has also been reported in various models of kidney damage including IRI (Le Clef et al 2016), adenine (Ali et al 2018) and 5/6 nephrectomy (Agharazii et al 2015). In the present study, an elevation of the serum values of IL-1, IL-6 and TNF- was observed as the degree of renal damage induced by FA progressed; this is consistent with the histological findings of an increase in inflammatory infiltrates as the degree of kidney damage increased.…”