Quercetin Attenuates Pancreatic and Renal D-Galactose-Induced Aging-Related Oxidative Alterations in Rats

Abstract

Aging is an oxidative stress-associated process that progresses with age. Our aim is to delay or attenuate these oxidative alterations and to keep individuals healthy as they age using natural compounds supplementation. Therefore, we conducted the present study to investigate the protective potentials of quercetin against D-galactose (D-gal)-associated oxidative alterations that were induced experimentally in male Wistar rats. Forty-five rats were randomly allocated into five groups of nine rats each. The groups were a control group that was reared on a basal diet and injected subcutaneously with 120 mg D-gal dissolved in physiological saline solution (0.9% NaCl) per kg body weight daily and quercetin-treated groups that received the same basal diet and subcutaneous daily D-gal injections were supplemented orally with 25, 50, and 100 mg of quercetin per kg body weight for 42 days. Pancreatic and renal samples were subjected to histopathological, immunohistochemical, and relative mRNA expression assessments. Aging (p53, p21, IL-6, and IL-8), apoptotic (Bax, CASP-3, and caspase-3 protein), proliferative (Ki67 protein), antiapoptotic (Bcl2 and Bcl2 protein), inflammatory (NF-κB, IL-1β, and TNF-α), antioxidant (SOD1), and functional markers (GCLC and GCLM genes and insulin, glucagon, and podocin proteins) were determined to evaluate the oxidative alterations induced by D-gal and the protective role of quercetin. D-gal caused oxidative alterations of the pancreas and kidneys observed via upregulations of aging, apoptotic, and inflammatory markers and downregulated the antiapoptotic, proliferative, antioxidant, and functional markers. Quercetin potentially attenuated these aging-related oxidative alterations in a dose-dependent manner. Finally, we can conclude that quercetin supplementation is considered as a promising natural protective compound that could be used to delay the aging process and to maintain human health.

Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats

“…This may be explained by the ability of quercetin to reduce the ROS therefore inhibiting lipid peroxidation and preventing the formation of MDA [ 33 ]. This was attributed to the catechol group (B ring) and the OH group at position 3 of the A and C ring, which have optimal free-radical scavenging [ 17 ].…”

“…Quercetin (3, 3′, 4′, 5, 7-pentahydroxyflavone) is a flavonoid present in fruits (apples, berries, cherries and red grapes) and vegetables (onions and broccoli) in addition to many seeds, buckwheat, nuts, flowers, barks, green tea and olive oil [ 10 ]. Quercetin has plentiful valuable effects comprising anti-inflammatory, anti-oxidant, anti-mutagenic, anti-ischemic, anti-viral and anti-aging effects [ 11 , 12 , 13 , 14 , 15 , 16 , 17 ]. Quercetin is lipophilic and can penetrate the blood-brain barrier (BBB) [ 18 ].…”

“…Quercetin is lipophilic and can penetrate the blood-brain barrier (BBB) [ 18 ]. Furthermore, quercetin exhibits a potential anti-oxidant role by the enhancement of reduced glutathione (GSH) and the upregulation of copper-zinc superoxide dismutase (SOD1) [ 17 ]. Quercetin can chelate iron, inhibiting Fenton’s reaction and inhibiting ROS generation [ 19 ].…”

Molecular Mechanisms Underlying Protective Role of Quercetin on Copper Sulfate-Induced Nephrotoxicity in Mice

“…Quercetin has many biological functions including anti-oxidant, antiinflammatory, and immune-regulatory activities (17)(18)(19). Quercetin supplementation had been shown to attenuate D-Galactose-induced renal damage in rats and aflatoxin B1-induced neurotoxicity in mice through the inhibition of oxidative stress (20,21). A recent study also showed that quercetin supplementation could inhibit lipopolysaccharide (LPS)-induced inflammation in a proximal tubular cell line human kidney 2 (HK-2) cells which derived from normal human kidney (22).…”

Protective effects of quercetin against cisplatin induced urogenital organ toxicity

“…Park et al had investigated quercetin against ischemic brain injury and demonstrated that ischemia-induced glutamate and caspase-3 increases were effectively suppressed [25]. Examining the effects of quercetin supplementation against aging caused by D-galactose in the pancreatic and kidney tissues, El-Far and colleagues reported that this substance may be effective in preventing aging-related oxidant damage and suppress apoptotic and inflammatory events [26]. Furthermore, in doxorubicin-induced cardiotoxicity, quercetin treatment, by increasing the antioxidant levels, suppressed ROS formation and caspase activity and thereby corrected the mitochondrial function [27].…”