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.

Antitumor and Protective Activity of TVLE against CdCl2-Induced Renal Damage in Rats.

<b>Background and Objective:</b> Cadmium is a heavy metal that has a wide range of applications in human existence. Cadmium may bind to the protein metallothionein and decrease kidney function once it enters the body. The purpose of this study was to investigate the renal protective activity of TVLE against CdCl₂-induced renal toxicity in rats. <b>Materials and Methods:</b> TVLE was prepared and characterized using instrumental analysis and spectral data. Furthermore, the IC₅₀ of TVLE against the Vero renal carcinoma cell line was calculated. Adult albino rats were used to assess the renal protective activity of TVLE (150 and 300 mg kg¹ b.wt.) in CdCl₂-treated rats. <b>Results:</b> IC₅₀of TVLE against Vero cell line equals 148.25 µg mL¹. The daily oral administration of TVLE at concentrations of 150 and 300 mg kg¹ b.wt. for 21 days to CdCl₂-treated rates resulted in a significant improvement in tumour volume and tumour weight, urea, creatinine, uric acid, TNF-α, NOx, TBARs, GSH, CAT, SOD, GPx and VEGF-C gene expression in CdCl₂-treated rats. Furthermore, TVLE almost normalized these effects in renal histoarchitecture. <b>Conclusion:</b> The biochemical, histological and MRI examinations of the current study suggested that TVLE have renal protective activity against CdCl₂-induced renal toxicity in rats.

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.