The current study aimed to assess the antiulcerogenic impact of mesenchymal bone marrow stem cells (BMMSCs) against gastric ulcer induced by the use of piroxicam in rats and to compare this effect with the antiulcer drug “Pantoloc ®” proton pump inhibitors. The study included histological, histochemical, immunohistochemical and ultrastructural examination in stomach of rats in different study groups. In the ulcerated group, the glandular region of the stomach displayed clear mucosal lesions occurring as perforations along the stomach axis. In addition, stomach displayed degeneration of surface mucous cells accompanied by pyknosis, vacuolation among parietal cells in ishmus region, basal region with vacuolated chief cells and karyolitic nucleus of parietal cells. Moreover, Stomach sections of ulcer model rats showed intensive immunoreactivity to cytokeratin 20, Cox 2 and PCNA. Findings of the present study have shown that BMMSCs have an ameliorative effect against piroxicam-induced gastric ulcer in rats. Collectively, the proposed work has shown that BMMSCs have a curative capacity as an antiulcer due to their high antioxidant activity. Further studies are required in molecular levels to understand the mechanism of action during treatment.

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.

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-inflammatory 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 co-administration with AgNPs alleviates hepatic and renal oxidative insults ‎by decreasing MDA and NO levels with a significant 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 co-administration decreased the hepatic and ‎renal pro-inflammatory 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 findings were confirmed by the histopathological examination of hepatic and renal ‎tissues. Our data affirmed the protective effect of TQ against AgNPs cytotoxicity and proposed a ‎possible mechanism of TQ antioxidant, anti-inflammatory, 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.