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      Protective Effect of Curcumin against Sodium Salicylate-Induced Oxidative Kidney Damage, Nuclear Factor-Kappa Dysregulation, and Apoptotic Consequences in Rats

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          Abstract

          This study examined the effect of sodium salicylates (SS), alone and in combination with curcumin (CUR), on kidney function and architecture in rats. Five rat groups were given 1 mL physiological saline/rat orally, 1 mL olive oil/rat orally, 50 mg CUR/kg bwt orally, 300 mg SS/kg bwt intraperitoneally, or CUR+SS for 15 days. The hematological indices, serum protein profile, serum electrolytes balance, oxidative stress, and lipid peroxidation of kidney tissues were assessed. The histopathological examination and immune expression of Caspase-3 and nuclear factor kappa (NF-κB) were conducted. The findings showed that SS injection induced nephrotoxic activity, including increased serum urea, creatinine, and uric acid levels. It also caused apparent pathological alterations with increased Caspase-3 and NF-κB immuno-expression. In addition, thrombocytopenia, leukocytosis, neutrophilia, hyponatremia, hypochloremia, hypocalcemia, and hypomagnesemia but not hyperkalemia and hyperphosphatemia were evident in SS-injected rats. Moreover, SS exposure increased serum α1 globulin, renal tissue malondialdehyde, and Caspase-3 levels but superoxide dismutase, glutathione peroxidase, and Bcl-2 levels declined. Meanwhile, CUR significantly counteracted the SS harmful impacts on kidneys but SS+CUR co-administration induced an anemic condition. Overall, CUR has an evident protective role against SS-induced renal damage, but the disturbed hematological alterations should be carefully taken into consideration in their combined use.

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          Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction.

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            Reactive oxygen species in inflammation and tissue injury.

            Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
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              Free radicals in the physiological control of cell function.

              At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish "redox homeostasis." Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman (J Gerontol 11: 298-300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Antioxidants (Basel)
                Antioxidants (Basel)
                antioxidants
                Antioxidants
                MDPI
                2076-3921
                21 May 2021
                June 2021
                : 10
                : 6
                : 826
                Affiliations
                [1 ]Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt
                [2 ]Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt; atiaanatomy@ 123456gmail.com
                [3 ]Clinical Laboratory Sciences Department, Turabah University College, Taif University, Turabah 21995, Saudi Arabia; a.ahdhahrani@ 123456tu.edu.sa (A.A.); mmsoliman@ 123456tu.edu.sa (M.M.S.)
                [4 ]Department of Histology and Cytology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt; rasharagab2006@ 123456yahoo.com
                [5 ]Department of Clinical Pathology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt; waffa.clinical@ 123456yahoo.com
                [6 ]Pharmacology Department, Faculty of Pharmacy, Future University, City of the Future 41639, Egypt; Bayan.saffaf@ 123456fue.edu.eg
                [7 ]Department of Biochemistry, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt; dr.mmeldeib@ 123456yahoo.com
                Author notes
                [* ]Correspondence: yasminafor@ 123456zu.edu.eg ; Fax: +20-55-228-4283
                Author information
                https://orcid.org/0000-0002-3646-6385
                https://orcid.org/0000-0001-7208-7123
                https://orcid.org/0000-0003-3105-8662
                Article
                antioxidants-10-00826
                10.3390/antiox10060826
                8224369
                34064189
                24a94c8c-4530-4318-b61e-f2ca47fc6145
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                : 24 April 2021
                : 17 May 2021
                Categories
                Article

                curcumin,sodium salicylate,kidney,anemia,nf-kappa b,caspase-3
                curcumin, sodium salicylate, kidney, anemia, nf-kappa b, caspase-3

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