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The aim of this study is to investigate the protective effects of thymoquinone (TQ) and ebselen (Eb) on arsenic (As)-induced renal toxicity in female rats. Sodium arsenite was orally administrated at a dose of 20 mg/kg body weight daily for 28 days, either alone or 1 h before TQ (10 mg/kg) or Eb (5 mg/kg) administration. Renal tissue As concentration and oxidative stress markers, including lipid peroxidation (LPO), nitrite/nitrate, and glutathione (GSH) levels, were determined. In addition to the oxidative stress response, antioxidant enzyme activities including that of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were measured. Exposure to As elicited a significant increase in As concentration and significant modifications to the redox state of the kidney, as was evidenced by a significant elevation in LPO and nitrite/nitrate concentration, with a concomitant reduction in GSH content and antioxidant enzyme activity. The oxidant/antioxidant imbalance observed in As toxicity was associated with a significant elevation in renal tumor necrosis factor α, interleukin 6, B-cell lymphoma 2 (Bcl-2)-associated X protein, and caspase 3 levels, in addition to a significant decrease in Bcl-2 levels. Post-administration of TQ and Eb markedly prevented As-induced oxidative stress, inflammation, apoptosis, and As accumulation in the renal tissue and reduced histological renal damage. These findings demonstrate that TQ, the main bioactive phytochemical constituent of Nigella sativa seed oil, and Eb, an organoselenium compound, could significantly inhibit As-induced oxidative damage, apoptosis, and inflammation, and significantly attenuate the accumulation of As in renal tissues by facilitating As biomethylation and excretion.

Purpose Selenium nanoparticles (SeNPs) have recently gained much attention in nanomedicine applications owing to their unique biological properties. Biosynthesis of SeNPs using nutraceuticals as lycopene (LYC) maximizes their stability and bioactivities. In this context, this study aimed to elucidate the renoprotective activity of SeNPs coated with LYC (LYC-SeNPs) in the acute kidney injury (AKI) model. Methods Rats were divided into six groups: control, AKI (glycerol-treated), AKI+sodium selenite (Na 2 SeO 3 ; 0.5 mg/kg), AKI+LYC (10 mg/kg), AKI+LYC-SeNPs (0.5 mg/kg) and treated for 14 days. Results Glycerol treatment evoked significant increases in rhabdomyolysis-related markers (creatine kinase and LDH). Furthermore, relative kidney weight, Kim-1, neutrophil gelatinase-associated lipocalin (NGAL), serum urea, and creatinine in the AKI group were elevated. Glycerol-injected rats displayed declines in reduced glutathione level, and superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities, paralleled with downregulations in Nfe2l2 and Hmox-1 expressions and high renal MDA and NO contents. Glycerol-induced renal inflammation was evident by rises in TNF-α, IL-1β, IL-6, and upregulated Nos2 expression. Also, apoptotic (elevated caspase-3, Bax, and cytochrome-c with lowered Bcl-2) and necroptotic (elevated Pipk3 expression) changes were reported in damaged renal tissue. Co-treatment with Na 2 SeO 3 , LYC, or LYC-SeNPs restored the biochemical, molecular, and histological alterations in AKI. In comparison with Na 2 SeO 3 or LYC treatment, LYC-SeNPs had the best nephroprotective profile. Conclusion Our findings authentically revealed that LYC-SeNPs co-administration could be a prospective candidate against AKI-mediated renal damage via antioxidant, anti-inflammatory, anti-apoptotic and anti-necroptotic activities.

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Silver nanoparticles (AgNPs) are the most common nanomaterials in consumer products. Therefore, it has been crucial to control AgNPs toxicological effects to improve their safety and increase the outcome of their applications. This work investigated the possible protective effect of thymoquinone (TQ) against AgNPs-induced hepatic and renal cytotoxicity in rats. Serum markers of liver and kidney functions as well as liver and kidney oxidative stress status, pro-in ammatory cytokines, apoptosis markers, and histopathology were assessed. TQ reversed AgNPs-induced elevation in serum liver and kidney function markers, including aspartate transaminase, alanine transaminase, urea, and creatinine. Moreover, TQ coadministration with AgNPs alleviates hepatic and renal oxidative insults by decreasing MDA and NO levels with a signi cant increase in the activity of antioxidant enzymes (superoxide dismutase, catalase, and glutathione recycling enzymes peroxidase and reductase) compared to AgNPs-treated rats. Besides, TQ upregulated hepatic and renal Nrf2 gene expression in AgNPs intoxicated rats. Furthermore, TQ coadministration decreased the hepatic and renal pro-in ammatory mediators represented by, IL-1β, TNF-α, TGF-β, and NF-κB levels. Besides, TQ co-administration decreased apoptotic protein (Bax) levels and increased the anti-apoptotic protein (Bcl-2) levels. These ndings were con rmed by the histopathological examination of hepatic and renal tissues. Our data a rmed the protective effect of TQ against AgNPs cytotoxicity and proposed a possible mechanism of TQ antioxidant, anti-in ammatory, and anti-apoptotic effects. Consequently, we could conclude that using TQ might control AgNPs toxicological effects, improve their safety, and increase the outcome of their applications.

Thymoquinone (TQ) is an active constituent in Nigella sativa, and is extensively reported for its distinguished antioxidant, and anti-in ammatory bioactivities. Despite the local protective response of the acute in ammation, it contributes to the development of various disease conditions such as cell death, organ damage, or genesis of tumors. Hence, in this study, the effects of orally administered TQ (50 and 100 mg/kg) for 14 days against edema development, oxidative stress, and in ammation were investigated in paw edema induced by carrageenan in mice. Indomethacin (10 mg/kg) was used as a reference drug. The results revealed that TQ reduced the paw edema volume in a time-dependent manner, attenuated acetic acid-provoked writhing movements, and reduced xylene-triggered ear edema.Hematological ndings revealed marked normalization of altered counts of WBCs, and platelets. Furthermore, paw tissue levels of MDA and NO showed marked decreases together with increases Nrf2, GSH, SOD, CAT, GPx, and GR after TQ administration. Additionally, TQ decreased the levels of proin ammatory mediators, such as IL-1b, TNF-α, IL-6, MCP-1, CRP, MPO, and NF-κB in the in amed paw tissue. Moreover, appreciable decreases were recorded in COX-2 and its product (PGE-2) as well as the immune reaction of TNF-α in TQ-treated mice. Histopathological ndings further validated the potential antioedematous, anti-in ammatory power of TQ in in amed tissues. Conclusively, the obtained ndings encourage the potent application of TQ to subside the acute in ammatory events because of its striking antioxidant and anti-in ammatory properties in the in amed paw tissue.