Protective Effect of Hesperidin on Sodium Arsenite-Induced Nephrotoxicity and Hepatotoxicity in Rats

Abstract

The present study was conducted to investigate the protective effects of hesperidin (HSP) against sodium arsenite (SA)-induced nephrotoxicity and hepatotoxicity in rats. Thirty-five male Sprague Dawley rats were divided into five groups as follows: control, HSP, SA, SA + HSP 100, and SA + HSP 200. Rats were orally gavaged with SA (10 mg/kg body weight) and HSP (100 and 200 mg/kg body weight) for 15 days. SA increased oxidative damage by decreasing antioxidant enzyme activities, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), and glutathione (GSH) level and increasing malondialdehyde (MDA) level in the kidney and liver tissues. In addition, it increased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and serum urea and creatinine levels. Furthermore, SA caused inflammation, apoptosis, and oxidative DNA damage by increasing tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), interleukin-1β (IL-1β), cysteine aspartate-specific protease-3 (caspase-3), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in the kidney and liver tissues and by increasing liver p53 and kidney interleukin-6 (IL-6) expressions. In other words, HSP administration reduced apoptosis, oxidative stress, inflammation, and oxidative DNA damage significantly in SA-induced kidney and liver tissues depending on dose. In this study, it was seen that HSP showed a protective effect against SA-induced kidney and liver toxicity.

Hesperidin ameliorates liver ischemia/reperfusion injury via activation of the Akt pathway

“…The antioxidant indicators, SOD, CAT, GPx and GSH, decreased significantly after liver i/R; however, these levels were increased by HDN treatment. These data suggested that HDN may ameliorate liver oxidative stress during liver I/R injury and were consistent with previous studies (36)(37)(38)(39). In a sepsis-induced lung injury model, Yuan et al (37) reported that oxidative stress was attenuated by HDN.…”

“…In a sepsis-induced lung injury model, Yuan et al (37) reported that oxidative stress was attenuated by HDN. In a sodium arsenite-induced nephrotoxicity and hepatotoxicity model, Turk et al (38) observed that HDN reduced oxidative stress and oxidative DNA damage depending on the dose. Similar results were observed in bilateral common carotid artery occlusion reperfusion injury (36) and in skeletal muscle I/R injury (39).…”

Hesperidin improves insulin resistance via down-regulation of inflammatory responses: Biochemical analysis and in silico validation

“…In present findings, hesperidin alone and in combination with orlistat has shown to regulate the serum levels of AST (P<0.001) and ALT (P<0.001) when compared with that of HFD group (Fig 4A and 4B). Correspondingly, hesperidin alone and in orlistat combination has also shown to improve the HFD-influenced kidney function biomarkers (Fig 4C and 4D) The effects of hesperidin alone and/or in combination on functional biomarkers of the kidney and/or liver also relate with some of the previously reported studies [22,62,63].…”

Hesperidin ameliorates hepatic dysfunction and dyslipidemia in male Wistar rats exposed to cadmium chloride

“…Hesperidin may have protective and healing effects on the structural integrity of the liver perhaps through opposing the oxidative damage effects of Cd on the lipid components of the hepatocyte membrane through the actions of ROS. Hesperidin has already been shown by others to have strong antioxidant potentials against oxidative damage in various tissues [ 25 , 56 , 57 ] and one of the well-known oxidative mechanism of Cd is by increase in membrane lipid peroxidation leading to elevation in MDA level [ 2 ]. We therefore deduce that the hepato-protective effect of hesperidin demonstrated in this present study against Cd toxicity may be through its scavenging action against various free radicals generated in vivo due to Cd detoxification process in the liver.…”