Biosynthesis of Silver Nanoparticles Using Azadirachta indica and Their Antioxidant and Anticancer Effects in Cell Lines.

In the present study, silver nanoparticles (Ag-NPs) were synthesized using Azadirachta indica extract and evaluated for their in vitro antioxidant activity and cytotoxicity efficacy against MCF-7 and HeLa cells. The silver nanoparticles (Ag-NPs) were formed within 40 min and after preliminary confirmation by UV-visible spectroscopy (peak observed at 375 nm), they were characterized using a transmission electron microscope (TEM) and dynamic light scattering (DLS). The TEM images showed the spherical shape of the biosynthesized Ag-NPs with particle sizes in the range of 10 to 60 nm, and compositional analysis was carried out. The cytotoxicity and antioxidant activity of various concentrations of biosynthesized silver nanoparticles, Azadirachta indica extract, and a standard ranging from 0.2 to 1.0 mg/mL were evaluated. The 2,2-Diphenyl-1-picrylhydrazyl (DPPH) activity of the biosynthesized Ag-NPs and aqueous leaf extract increased in a dose-dependent manner, with average IC50 values of the biosynthesized Ag-NPs, aqueous leaf extract, and ascorbic acid (standard) of 0.70 ± 0.07, 1.63 ± 0.09, and 0.25 ± 0.09 mg/mL, respectively. Furthermore, higher cytotoxicity was exhibited in both the MCF-7 and HeLa cell lines in a dose-dependent manner. The average IC50 values of the biosynthesized Ag-NPs, aqueous leaf extract, and cisplatin (standard) were 0.90 ± 0.07, 1.85 ± 0.01, and 0.56 ± 0.08 mg/mL, respectively, with MCF-7 cell lines and 0.85 ± 0.01, 1.76 ± 0.08, 0.45 ± 0.10 mg/mL, respectively, with HeLa cell lines. Hence, this study resulted in an efficient green reductant for producing silver nanoparticles that possess cytotoxicity and antioxidant activity against MCF-7 and HeLa cells.

Biochemical and histopathological evaluation of Al2O3 nanomaterials in kidney of Wistar rats.

The present study was conducted to evaluate the response of kidneys in Wistar rats following long-term exposure to Al2O3 nanomaterials (NMs). To achieve this objective, Al2O3 of three different sizes (30 nm, 40 nm and bulk) was orally administered for 28 days to 9 groups of 10 Wistar rats each at the dose of 500, 1000 and 2000 mg/kg/rat. A tenth group of 10 rats received distilled water and served as control. After 28 days of exposure the animals were sacrificed and the serum was collected and tested for the activity levels of creatinine and urea following standard methods. Induction of oxidative stress was also investigated by assessing thiobarbituric acid reactive substances (TBARS) (MDA), protein carbonyl, reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) activities. A histopathological evaluation was also performed to determine the extent of kidney damage. The results showed that both serum creatinine and serum urea levels increased significantly in the treated rats compared to control animals. The increase was found to be more in Al2O3-30 nm treated rats followed by Al2O3-40 nm and Al2O3-bulk treated rats in a dose-dependent manner. Further administration of Al2O3 significantly increased the activities of TBARS, protein carbonyl, catalase and decreased the activities of GSH and SOD in a dose-dependent manner in the kidney of rats compared with the control group. Histopathological evaluation showed significant morphological alterations in kidney tissues of treated rats in accordance with biochemical parameters. Taken together, the results of this study demonstrate that Al2O3 is nephrotoxic and its toxicity may be mediated through oxidative stress. Further, the results suggest that prolonged oral exposure to Al2O3 NMs has the potential to cause biochemical and histological alterations in kidney of rats at high concentration.

Hepatotoxicity and Ultra Structural Changes in Wistar Rats treated with Al2O3 Nanomaterials.

The present study was designed to evaluate the hepatotoxicity of aluminium oxide (Al2O3). To achieve this objective, Al2O3 of three different sizes (30nm, 40nm and bulk) was orally administered for 28 days to 9 groups of 10 Wistar rats each, at the dose of 500, 1000 and 2000 mg/Kg/rat. A tenth group of 10 rats received distilled water and served as control. After 28 days of exposure, the animals were sacrificed and the serum was collected and tested for the activity levels of aminotransferases (AST or GOT and ALT or GPT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzymes following standard testing methods. Reduced glutathione (GSH) content was also measured in the liver tissue to study the oxidative stress. A histopathological evaluation was also performed to determine the extent of liver injury. Study results indicated that the activity of both the aminotransferases (AST and ALT), ALP and LDH increased significantly in Al2O3 treated rats compared to control animals. The increase was found to be more pronounced with Al2O3 - 30nm followed by Al2O3 - 40nm and Al2O3 - bulk treated rats in a dose dependent manner. However reduced glutathione content showed a decline in the activity. Ultra structural assessment showed significant morphological changes in the liver tissue in accordance with biochemical parameters. Taken together, the results of this study demonstrated that Al2O3 is hepatotoxic and the smaller size of this nanomaterial appeared to be the most toxic while the compound in the bulk form seemed to be the least toxic.

Combination of spices and herbal extract restores macrophage foam cell migration and abrogates the athero-inflammatory signalling cascade of atherogenesis.

The trapping of lipid-laden macrophages in the arterial intima is a critical but reversible step in atherogenesis. However, information about possible treatments for this condition is lacking. Here, we hypothesized that combining the polyphenol-rich fractions (PHC) of commonly consumed spices (Allium sativum L (Liliaceae), Zingiber officinale R (Zingiberaceae), Curcuma longa L (Zingiberaceae)) and herbs (Terminalia arjuna (R) W & A (Combretaceae) and Cyperus rotundus L (Cyperaceae)) prevents foam cell formation and atherogenesis. Using an in vitro foam cell formation assay, we found that PHC significantly inhibited lipid-laden macrophage foam cell formation compared to the depleted polyphenol fraction of PHC (F-PHC). We further observed that PHC attenuated the LDL and LPS induced CD36, p-FAK and PPAR-γ protein expression in macrophages and increased their migration. NK-κB-DNA interaction, TNF-α, ROS generation, and MMP9 and MMP2 protein expression were suppressed in PHC-treated macrophages. The anti-atherosclerotic activity of PHC was investigated in a high fat- and cholesterol-fed rabbit model. The inhibition of foam cell deposition within the aortic intima and atheroma formation confirmed the atheroprotective activity of PHC. Therefore, we conclude that the armoury of polyphenols in PHC attenuates the CD36 signalling cascade-mediated foam cell formation, enhances the migration of these cells and prevents atherogenesis.