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Due to their exceptional physicochemical features, green synthesized silver nanoparticles (AgNPs) have been of considerable interest in cancer treatment. In the present study, for the first time, we aimed to green synthesize AgNPs from Euphorbia retusa and explore their anticancer potential on human breast cancer (MCF‐7) cells. First, the green synthesized AgNPs (EU‐AgNPs) were well characterized by UV–visible spectroscopy, Fourier transmission infrared (FTIR) spectrum, XRD, scanning and transmission electron microscopy (SEM and TEM), and EDX techniques. The characterization data exhibited that EU‐AgNPs were spherical in shape and crystalline in nature with an average size of 17.8 nm. FTIR results established the presence of active metabolites in EU‐AgNPs. Second, the anticancer effect of EU‐AgNPs was evaluated against MCF‐7 cells by MTT and neutral red uptake (NRU) assays. Moreover, morphological changes, ROS production, MMP, and apoptotic marker genes were also studied upon exposure to cytotoxic doses of EU‐AgNPs. Our results showed that EU‐AgNPs induce cytotoxicity in a concentration‐dependent manner, with an IC50 value of 40 μg/mL. Morphological changes in MCF‐7 cells exposed to EU‐AgNPs also confirm their cytotoxic effects. Increased ROS and decreased MMP levels revealed that EU‐AgNPs induced oxidative stress and mitochondrial membrane dysfunction. Moreover, ROS–mediated apoptosis was confirmed by elevated levels of proapoptotic marker genes (p53, Bax, caspase‐3, and caspase‐9) and reduced levels of an antiapoptotic gene (Bcl‐2). Altogether, these findings suggested that EU‐AgNPs could induce potential anticancer effects through ROS–mediated apoptosis in MCF‐7 cells. Significance Statement: This study reports the green synthesis of silver nanoparticles (EU‐AgNPs) via a single‐step reduction of silver ions using the Euphorbia retusa plant. The green synthesized EU‐AgNPs were well characterized by various analytical techniques and possess cytotoxic potential against human breast cancer (MCF‐7) cells. This study showed that EU‐AgNPs can induce apoptotic cell death via reactive oxygen species–mediated mitochondrial pathway in MCF‐7 cells. Therefore, EU‐AgNPs may play an important role in the development of new therapeutic agents for the treatment of cancer. [ABSTRACT FROM AUTHOR]

Two half‐sandwich organometallic ruthenium (II) complexes containing analogs of aminobenzimidazole of molecular formula [η6‐p‐cymene)Ru (LH)Cl2] 1 and [η6‐p‐cymene)Ru (LMe)Cl2] 2, where LH and LMe represent 2‐aminobenzimidazole and 2‐amino‐1‐methylbenzimidazole, respectively, have been synthesized and characterized by FT‐IR, NMR (1H, 13C), ESI‐MS, elemental analysis, and single X‐ray crystallography (for 1). Both complexes 1 and 2 were studied for human serum albumin (HSA) binding affinity using intrinsic, synchronous, three‐dimensional (3D) fluorescence, thermodynamics parameter, and Förster resonance energy transfer (FRET) analysis. The Stern–Volmer constant (KSV) values are of the order of ×105 M−1 and increases in KSV with temperature ascertained the static quenching. The molecular docking of both the complexes with HSA was carried out to ascertain the binding sites/pockets. Furthermore, compounds were evaluated for their cytotoxic potential against three human cancer cell lines, namely, HeLa, HepG2, MCF‐7, and non‐tumorigenic HEK293 cells. The IC50 value of 2 was found to <10 μM against Hela and HepG2 cancer cells and has better cytotoxic properties than cisplatin (a standard drug), yet showed minimal toxicity against HEK293 cells. These results suggest further investigation for the development of ruthenium complex 2 as potential anticancer therapeutics. [ABSTRACT FROM AUTHOR]

Oxidative stress is known to induce cytotoxicity and apoptosis in endothelial cells and indorse development of atherosclerosis. The aim of this research was to assess the cytoprotective effects of ethanolic extract of Nigella sativa (NSE) against H2O2‐induced cell death in human umbilical vein endothelial cells (HUVECs) and also study the probable mechanisms through which NSE exhibited cyto‐protection. The cytotoxicity was measured by exposing the HUVECs with NSE (10–200 μg/ml) and H2O2 (25–1000 μM) for 24 h. Then, the HUVECs were pretreated with noncytotoxic doses (10–50 μg/ml) of NSE for 24 h before administration of 200 μM H2O2 for 24 h. The MTT, NRU, and morphological assays were performed to assess the cytotoxicity and cyto‐protection. Potential antioxidant activity of NSE on oxidative stress marker (glutathione [GSH] and lipid peroxidation [LPO]) was also evaluated. The fluorescence probe, DCF‐DA, and Rh123 were applied to measure the reactive oxygen species (ROS) level and mitochondrial membrane potential. Moreover, flow cytometric analysis and comet assay were used to study the cell cycle arrest and DNA damage, respectively. The concentrations (10, 30, and 50 μg/ml) of NSE were found to protect HUVECs against H2O2 (200 μM)‐induced cytotoxicity in HUVECs. Pretreatment of HUVECs with NSE significantly reduced the LPO and ROS levels and restored the GSH and loss of MMP induced by H2O2. Furthermore, NSE inhibited H2O2‐induced cell cycle arrest and cellular DNA damage in HUVECs. Altogether, these results suggest that NSE can prevent H2O2‐induced cell death, and NSE could be a potential candidate that can prevent HUVECs against toxicants. The aim of this research was to assess the cytoprotective effects of Nigella sativa (NSE) against H2O2‐induced cell death in human umbilical vein endothelial cells (HUVECs). The concentrations (10, 30, and 50 μg/ml) of NSE were found to protect HUVECs against H2O2 (200 μM)‐induced cytotoxicity in HUVECs. Pretreatment with NSE significantly reduced the LPO and ROS levels and restored the GSH and loss of MMP induced by H2O2. Furthermore, NSE inhibited H2O2‐induced cell cycle arrest and DNA damage in HUVECs. [ABSTRACT FROM AUTHOR]

Background: Cancer is one of the major causes of death worldwide. The plant-derived natural products have received considerable attention in recent years due to their diverse pharmacological properties including anticancer effects. Nepeta deflersiana (ND) is used in the folk medicine as antiseptic, carminative, antimicrobial, antioxidant, and for treating rheumatic disorders. However, the anticancer activity of ND chloroform extract has not been explored so far. Objectives: The present study was aimed to investigate the anticancer activities of chloroform Nepeta deflersiana extract and various sub-fractions (ND-1–ND-15) of ND against human breast cancer cells (MCF-7) and human lung cancer cells (A-549). Materials and Methods: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and neutral red uptake assays, and cellular morphological alterations using phase contrast light microscope were studied. Cells were exposed with 10–1000 μg/ml of sub-fractions of ND for 24 h. Results: Results showed that selected sub-fractions of the chloroform extract significantly reduced the cell viability of MCF-7 and A-549 cells, and altered the cellular morphology in a concentration-dependent manner. Among the sub-fractions, ND-10 fraction showed relatively higher cytotoxicity compared to other fractions whereas, ND-1 did not cause any cytotoxicity even at higher concentrations. The A-549 cells were found to be more sensitive to growth inhibition by all the extracts as compared to the MCF-7 cells. Conclusion: The present study provides preliminary screening of anticancer activities of chloroform extract and sub-fractions of ND, which can be further used for the development of a potential therapeutic anticancer agent. [ABSTRACT FROM AUTHOR]

Context: Garden cress [Lepidium sativum(Brassicaceae)] has been widely used to treat a number of ailments in traditional medicine. The pharmacological and preventive potential ofLepidium sativum, such as anti-inflammatory, antipyretic, antihypertensive, anti-ashthamatic, anticancer, and anti-oxidant, are well known. Objective: The present investigation was designed to study the protective effects of chloroform extract ofLepidium sativumseed (LSE) against oxidative stress and cytotoxicity induced by hydrogen peroxide (H2O2) in human liver cells (HepG2). Materials and methods: Cytotoxicity of LSE and H2O2was identified by (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), neutral red uptake (NRU) assays, and morphological changes in HepG2. The cells were pre-exposed to biologically safe concentrations (5–25 μg/ml) of LSE for 24 h, and then cytotoxic (0.25 mM) concentration of H2O2was added. After 24 h of the exposures, cell viability by MTT, NRU assays, and morphological changes in HepG2 were evaluated. Further, protective effects of LSE on reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), lipid peroxidation (LPO), and reduced glutathione (GSH) levels induced by H2O2were studied. Results: Pre-exposure of LSE significantly attenuated the loss of cell viability up to 48% at 25 µg/ml concentration against H2O2(LD50value = 2.5 mM). Results also showed that LSE at 25 µg/ml concentration significantly inhibited the induction of ROS generation (45%) and LPO (56%), and increases the MMP (55%) and GSH levels (46%). Discussion and conclusion: The study suggests the cytoprotective effects of LSE against H2O2-induced toxicity in HepG2. The results also demonstrate the anti-oxidative nature of LSE. [ABSTRACT FROM PUBLISHER]

Background: Cancer is one of the major causes of death worldwide. The plant-derived natural products have received considerable attention in recent years due to their diverse pharmacological properties including anticancer effects. Nepeta deflersiana (ND) is used in the folk medicine as antiseptic, carminative, antimicrobial, antioxidant, and for treating rheumatic disorders. However, the anticancer activity of ND chloroform extract has not been explored so far. Objectives: The present study was aimed to investigate the anticancer activities of chloroform Nepeta deflersiana extract and various sub-fractions (ND-1-ND-15) of ND against human breast cancer cells (MCF-7) and human lung cancer cells (A-549). Materials and Methods: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and neutral red uptake assays, and cellular morphological alterations using phase contrast light microscope were studied. Cells were exposed with 10-1000 μg/ml of sub-fractions of ND for 24 h. Results: Results showed that selected sub-fractions of the chloroform extract significantly reduced the cell viability of MCF-7 and A-549 cells, and altered the cellular morphology in a concentration-dependent manner. Among the sub-fractions, ND-10 fraction showed relatively higher cytotoxicity compared to other fractions whereas, ND-1 did not cause any cytotoxicity even at higher concentrations. The A-549 cells were found to be more sensitive to growth inhibition by all the extracts as compared to the MCF-7 cells. Conclusion: The present study provides preliminary screening of anticancer activities of chloroform extract and sub-fractions of ND, which can be further used for the development of a potential therapeutic anticancer agent. [ABSTRACT FROM AUTHOR]

Oxidative stress is known to induce cytotoxicity and apoptosis in endothelial cells and indorse development of atherosclerosis. The aim of this research was to assess the cytoprotective effects of ethanolic extract of Nigella sativa (NSE) against H 2 O 2 -induced cell death in human umbilical vein endothelial cells (HUVECs) and also study the probable mechanisms through which NSE exhibited cyto-protection. The cytotoxicity was measured by exposing the HUVECs with NSE (10-200 μg/ml) and H 2 O 2 (25-1000 μM) for 24 h. Then, the HUVECs were pretreated with noncytotoxic doses (10-50 μg/ml) of NSE for 24 h before administration of 200 μM H 2 O 2 for 24 h. The MTT, NRU, and morphological assays were performed to assess the cytotoxicity and cyto-protection. Potential antioxidant activity of NSE on oxidative stress marker (glutathione [GSH] and lipid peroxidation [LPO]) was also evaluated. The fluorescence probe, DCF-DA, and Rh123 were applied to measure the reactive oxygen species (ROS) level and mitochondrial membrane potential. Moreover, flow cytometric analysis and comet assay were used to study the cell cycle arrest and DNA damage, respectively. The concentrations (10, 30, and 50 μg/ml) of NSE were found to protect HUVECs against H 2 O 2 (200 μM)-induced cytotoxicity in HUVECs. Pretreatment of HUVECs with NSE significantly reduced the LPO and ROS levels and restored the GSH and loss of MMP induced by H 2 O 2 . Furthermore, NSE inhibited H 2 O 2 -induced cell cycle arrest and cellular DNA damage in HUVECs. Altogether, these results suggest that NSE can prevent H 2 O 2 -induced cell death, and NSE could be a potential candidate that can prevent HUVECs against toxicants., (© 2020 John Wiley & Sons, Ltd.)