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1.
Biotechnol Appl Biochem ; 71(1): 132-146, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-37849075

RESUMO

Amyloid ß (Aß) plaque accumulation-mediated neuronal toxicity has been suggested to cause synaptic damage and consequent degeneration of brain cells in Alzheimer's disease (AD). With the increasing prerequisite of eco-friendly nanoparticles (NPs), research investigators are utilizing green approaches for the synthesis of zinc oxide (ZnO) NPs for pharmaceutical applications. In this present study, ZnO NPs were synthesized from Acanthus ilicifolius to assess the neuroprotective properties in the AD model of transgenic Caenorhabditis elegans strains CL2006 and CL4176 expressing Aß aggregation. Our findings revealed that the therapeutic effect of green-synthesized ZnO NPs is associated with antioxidant activity. We also found that ZnO NPs significantly enhance the C. elegan's lifespan, locomotion, pharyngeal pumping, chemotaxis behavior also diminish the ROS deposition and intracellular productionMoreover, thioflavin T staining demonstrated that ZnO NPs substantially attenuated the Aß deposition in the C. elegans strain as compared to untreated worms. With their antioxidant properties, the greenly synthesized ZnO NPs had a significant neuroprotective efficiency on Aß-induced toxicity by reducing Aß aggregation and specifically reducing the progression of paralysis in the C. elegans AD model. Our findings suggested that the biosynthesized ZnO NPs could be thought-provoking candidates for age-associated neurodegenerative disorders accompanied by oxidative stress.


Assuntos
Doença de Alzheimer , Nanopartículas , Fármacos Neuroprotetores , Óxido de Zinco , Animais , Peptídeos beta-Amiloides/toxicidade , Caenorhabditis elegans/metabolismo , Óxido de Zinco/farmacologia , Fármacos Neuroprotetores/farmacologia , Animais Geneticamente Modificados/metabolismo , Estresse Oxidativo , Doença de Alzheimer/tratamento farmacológico , Antioxidantes/farmacologia
2.
Curr Mol Pharmacol ; 16(3): 393-410, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-35490311

RESUMO

BACKGROUND AND OBJECTIVE: This investigation explores the neuroprotective effect of PIASA, a newly designed peptide, VCSVY, in in-silico and in opposition to rotenone stimulated oxidative stress, mitochondrial dysfunction, and apoptosis in an SH-SY5Y cellular model. METHODS: Docking and visualization of the PIASA and rotenone were progressed against mitochondrial respiratory complex I (MCI). The in-silico analysis showed PIASA to have interaction with the binding sites of rotenone, which may reduce the rotenone interaction and its toxicity too. The SH-SY5Y cells were segregated into four experimental groups: Group I: untreated control cells; Group II: rotenone-only (100 nM) treated cells; Group III: PIASA (5 µM) + rotenone (100 nM) treated cells; and Group IV: PIASA-only (5 µM) treated cells. RESULTS: We evaluated the cell viability, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), apoptosis (dual staining technique), nuclear morphological changes (Hoechst staining technique), the expressions of BAX, Bcl-2, cyt c, pro-caspase 3, and caspase 3, -6, -8, -9, and cleaved caspase 3 by western blot analysis. In SH-SY5Y cells, we further observed the cytotoxicity, oxidative stress and mitochondrial dysfunction in rotenone-only treated cells, whereas pretreatment of PIASA attenuated the rotenone-mediated toxicity. Moreover, rotenone toxicity is caused by complex I inhibition, which leads to mitochondrial dysfunction, increased BAX expression, while downregulating the Bcl-2 expression and cyt c release, and then finally, caspases activation. PIASA pretreatment prevented the cytotoxic effects via the normalization of apoptotic marker expressions influenced by rotenone. In addition, pre-clinical studies are acceptable in rodents to make use of PIASA as a revitalizing remedial agent, especially for PD in the future. CONCLUSION: Collectively, our results propose that PIASA mitigated rotenone-stimulated oxidative stress, mitochondrial dysfunction, and apoptosis in rotenone-induced SH-SY5Y cells.


Assuntos
Neuroblastoma , Rotenona , Humanos , Rotenona/toxicidade , Caspase 3/metabolismo , Caspase 3/farmacologia , Proteína X Associada a bcl-2/metabolismo , Proteína X Associada a bcl-2/farmacologia , Linhagem Celular Tumoral , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Sobrevivência Celular
3.
Environ Sci Pollut Res Int ; 25(11): 10328-10339, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28537028

RESUMO

Titanium dioxide nanoparticles are emerging as a biocompatible nanomaterial with multipurpose bioactivities. In this study, titanium dioxide (TiO2) nanoparticles were effectively synthesized using the aqueous leaf extracts of Parthenium hysterophorus prepared by microwave irradiation. TiO2 nanoparticles were fabricated by treating the P. hysterophorus leaf extracts with the TiO4 solution. Biologically active compounds such as alcohols, phenols, alkanes, and fluoroalkanes were involved in bioreduction of TiO4 into TiO2. The formation of green-engineered TiO2 nanoparticles was confirmed by UV-vis spectroscopy, Fourier transform infrared spectroscopy (FTIR), field emission scanning electron microscopy (FESEM), and energy-dispersive X-ray (EDX) spectroscopy and further characterized by X-ray diffraction (XRD) studies. UV-vis spectroscopy analysis showed maximum absorbance at 420 nm due to surface plasmon resonance of synthesized TiO2 NPs. FTIR spectrum of the engineered TiO2 NPs showed the presence of bioactive compounds in the leaf extract, which acted as capping and reducing agents. FESEM exhibited an average size of 20-50 nm and a spherical shape of TiO2 NPs. EDX analysis indicated the presence of TiO2 NPs by observing the peaks of titanium ions. XRD results pointed out the crystalline nature of engineered TiO2 NPs. The larvicidal activity of TiO2 NPs was studied on fourth instar larvae of dengue, Zika virus, and filariasis mosquito vectors Aedes aegypti and Culex quinquefasciatus. Antimicrobial efficacy of TiO2 NPs was assessed on clinically isolated pathogens Escherichia coli, Staphylococcus aureus, Pseudomonas aeruginosa, Klebsiella pneumoniae, Proteus vulgaris, and Staphylococcus epidermidis. Besides, we found that TiO2 NPs are able to quickly degrade the industrially harmful pigments methylene blue, methyl orange, crystal violet, and alizarin red dyes under sunlight illumination. Overall, this novel, simple, and eco-friendly approach can be of interest for the control of vector-borne diseases, as well as to formulate new bactericidal agents and to efficiently degrade dye solutions in the polluted areas.


Assuntos
Antibacterianos/farmacologia , Anti-Infecciosos/farmacologia , Compostos Azo/química , Inseticidas/química , Larva/efeitos dos fármacos , Extratos Vegetais/química , Prata/química , Titânio/química , Aedes , Animais , Antibacterianos/química , Anti-Infecciosos/química , Asteraceae , Culex , Mosquitos Vetores , Partenogênese , Difração de Raios X
4.
South Asian J Cancer ; 4(2): 83-7, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25992348

RESUMO

BACKGROUND: Hepatocellular carcinoma is one of the most common cancers and a lethal disease. In view of the limited treatment and a grave prognosis of liver cancer, preventive control has been emphasized. MATERIALS AND METHODS: The methanolic extract of roots of Cynodon dactylon was screened for its hepato-protective activity in diethyl nitrosamine (DEN) induced liver cancer in Swiss albino mice. The plant extract at a dose of 50 mg/kg was administered orally once a week, up to 30 days after DEN administration. The animals were sacrificed; blood sample and liver tissue were collected and used for enzyme assay such as, asparatate amino transferase (AST), alanine aminotransferase (ALT), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST). The liver marker enzymes AST and ALT produced significant results in the protective action. RESULTS: The antioxidant enzyme assay results concerning the improved activity of GPx, GST and CAT. These results concluded that enhanced levels of antioxidant enzyme and reduced amount of serum amino transaminase, which are suggested to be the major mechanisms of C. dactylon root extract in protecting the mice from hepatocarcinoma induced by DEN. These biochemical observations were supplemented by histopathological examination of liver sections. CONCLUSION: The methanolic extract of C. dactylon possesses significant anticancer properties.

5.
Artigo em Inglês | MEDLINE | ID: mdl-29264314

RESUMO

BACKGROUND: To explore the antioxidant and hepatoprotective effect of ethanolic Mangifera indica (EMI) and methanolic Mangifera indica (MMI) leaf extracts in mercuric chloride (HgCl2) induced toxicity in Swiss albino mice. MATERIALS AND METHODS: Toxicity in mice was induced with HgCl2 (5.0 mg/kg, i.p.), followed by oral intervention with EMI and MMI extracts (25 mg and 50 mg/kg. body wt.) for 30 days. RESULTS AND DISCUSSION: The extent of liver damage was assessed from the extents of histopathological, morphological, antioxidant and liver enzymes. Mercuric chloride-induced mice showed an increased cellular damage whereas leaf extracts of EMI and MMI-treated mice showed recovery of damaged hepatocytes. Mercuric chloride intoxicated mice exhibited a significant (p < 0.05) elevation in the liver enzymes (Aspartate amino transferase and Alanine amino transferase) and gradual decline in the cellular radical scavenging enzyme levels (Catalase, Glutathione-s-transferase and Glutathione peroxidase. The combined treatment with EMI and MMI leaf extracts significantly (p < 0.05) reversed these parameters. However, the effects of MMI leaf extract (50 mg/kg) were superior to those of EMI- treated mice possibly due to its potent radical scavenging property. These results suggest that oral supplementation of Mangifera indica extract remarkably reduces hepatotoxicity in mice possibly through its antioxidant potentials.How to cite this article: Karuppanan M, Krishnan M, Padarthi P, Namasivayam E. Hepatoprotec-tive and Antioxidant Effect of Mangifera Indica Leaf Extracts against Mercuric Chloride-induced Liver Toxicity in Mice. Euroasian J Hepato-Gastroenterol 2014;4(1):18-24.

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