CEG-AgNPs Ameliorates DMBA-Induced Mammary Carcinogenicity by Alleviating Cytokines Expression.

<b>Background and Objective:</b> For more than a decade, breast cancer has been one of the most common forms of cancer among women around the world. The present article aimed to evaluate the protective activity of CEG-AgNPs against DMBA-induced mammary carcinoma. <b>Materials and Methods:</b> In this experimental study, green synthesis and characterization of CEG-AgNPs were carried as well as IC₅₀ against Mcf7 cell line and LD₅₀ on mice were evaluated. A total of 24 adult albino mice were divided into four groups six rats in each. Group I was given an equal amount of distilled water, group II was received 80 mg kg¹ b.wt., DMBA for 4 weeks, groups III and IV were treated with CEG-AgNPs (28.1 and 70.25 mg kg¹) from the 5th week of DMBA administration for 4 weeks, respectively. <b>Results:</b> CEG-AgNPs were approximately 42.32±9.52 nm with a negative zeta potential of -17.44. It is IC₅₀ against the Mcf7 cell line and LD₅₀ is equal to 82.76 µg mL¹ and 1405 mg kg¹ b.wt., A significant normalization in plasma ALT, AST, AST and LDH as well as mammary MDA, TNF-α, IL-6, P53, SOD, GPx and GSH levels have been observed in CEG-AgNPs treated mice. Oral CEG-AgNPs administration has suppressed VEGF-C gene expression in DMBA-treated mice. <b>Conclusion:</b> The present results, biochemical, histological and MRI results showed that CEG-AgNPs have potent anticancer activity against DMBA-induced mammary carcinoma in mice by inducing the biosynthesizes of antioxidant biomarkers and suppression of cytokines gene expression.

Astaxanthin Attenuates D-Galactosamine-Induced Pancreatic Injury by Activating Antioxidant Enzymes and Inhibiting VEGF-C Gene Expression.

<b>Background and Objective:</b> Astaxanthin (3,3'-dihydroxy-ß-ß-carotene-4,4'-dione) is a carotenoid, commonly found in marine environments has been reported to possess versatile biological properties including anti-inflammatory and antioxidant. In this study, the pancreatic protective effect of astaxanthin was investigated in D-Galactosamine-induced pancreas injury in rats. <b>Materials and Methods:</b> In this experimental study, MTT assay was used to determine cytotoxic effects of the Astaxanthin on pnc1 cells. A total of 30 adult albino rats divided into 5 groups, six rats in each. Group I was given an equal amount of distilled water, group II was received 400 mg kg¹ b.wt. D-galactosamine on 15th day, groups III-V were treated with astaxanthin (50 and 100 mg kg¹) and/or silymarin (50 mg kg¹) for 14 days + 400 mg kg¹ b.wt. D-galactosamine on the 15th day, respectively. <b>Results:</b> IC₅₀of Astaxanthin against the pnc1 cell line was 92.9 µg mL¹. The daily oral administration of astaxanthin (50 and 100 mg kg¹) as well as silymarin (50 mg kg¹) for 14 days to rats treated with D-galactosamine resulted in a significant improvement in plasma AST, ALT, ALP as well as pancreatic TNF-α, IL-1ß, IL-10, NO and VEGF-C gene expression. On the other hand, inducible oral administration of astaxanthin increased the activity of pancreatic GSH, SOD, GPx, GR, CAT and the level of TBARs in D-galactosamine-treated pancreatic of rats. Furthermore, Astaxanthin almost normalized these effects in pancreatic tissue histoarchitecture and MRI examination. <b>Conclusion:</b> The obtained results showed that Astaxanthin protected experimental animals against D-galactosamine-induced pancreatic injury through activation of antioxidant enzymes and IL-10 and inhibition of VEGF-C activation.