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1.
Food Funct ; 15(8): 4310-4322, 2024 Apr 22.
Artigo em Inglês | MEDLINE | ID: mdl-38529619

RESUMO

Background: Alzheimer's disease (AD) exerts tremendous pressure on families and society due to its unknown etiology and lack of effective treatment options. Our previous study had shown that Se-methylselenocysteine (SMC) improved the cognition and synaptic plasticity of triple-transgenic AD (3 × Tg-AD) mice and alleviated the related pathological indicators. We are dedicated to investigating the therapeutic effects and molecular mechanisms of SMC on mitochondrial function in 3 × Tg-AD mice. Methods: Transmission electron microscopy (TEM), western blotting (WB), mitochondrial membrane potential (ΔΨm), mitochondrial swelling test, and mitochondrial oxygen consumption test were used to evaluate the mitochondrial morphology and function. Mitophagy flux and autophagy flux were assessed with immunofluorescence, TEM and WB. The Morris water maze test was applied to detect the behavioral ability of mice. Results: The destroyed mitochondrial morphology and function were repaired by SMC through ameliorating mitochondrial energy metabolism, mitochondrial biogenesis and mitochondrial fusion/fission balance in 3 × Tg-AD mice. In addition, SMC ameliorated mitochondria by activating mitophagy flux via the BNIP3/NIX pathway and triggering autophagy flux by suppressing the Ras/Raf/MEK/ERK/mTOR pathway. SMC remarkably increased the cognitive ability of AD mice. Conclusions: This research indicated that SMC might exert its therapeutic effect by protecting mitochondria in 3 × Tg-AD mice.


Assuntos
Doença de Alzheimer , Autofagia , Modelos Animais de Doenças , Camundongos Transgênicos , Mitocôndrias , Mitofagia , Selenocisteína , Selenocisteína/análogos & derivados , Animais , Doença de Alzheimer/tratamento farmacológico , Doença de Alzheimer/metabolismo , Mitofagia/efeitos dos fármacos , Camundongos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Selenocisteína/farmacologia , Autofagia/efeitos dos fármacos , Masculino , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos
2.
Biomed Pharmacother ; 133: 111079, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33378976

RESUMO

Non-small cell lung cancer (NSCLC) remains by far the single most common malignancy of lung cancer which causes more and more mortality in recent years. NSCLC accounts for more than 80 % of lung cancers, and the vast majority of patients were found to be in advanced inoperable stages. Chemotherapy used to be the main treatment for NSCLC, but due to its obvious side effects. Chemotherapy gradually withdrew from the stage of history. In recent years, cellular and molecular biotechnology has developed rapidly, and researchers have begun to target key genes and regulatory molecules for treatment. Targeted drugs have also emerged. The purpose of this review is to introduce important research achievements in recent years and the treatment progress of new drugs.


Assuntos
Antineoplásicos/uso terapêutico , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Inibidores de Proteínas Quinases/uso terapêutico , Proteínas Tirosina Quinases/antagonistas & inibidores , Proteínas Proto-Oncogênicas p21(ras)/antagonistas & inibidores , Animais , Antineoplásicos/efeitos adversos , Carcinoma Pulmonar de Células não Pequenas/enzimologia , Carcinoma Pulmonar de Células não Pequenas/patologia , Humanos , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/patologia , Terapia de Alvo Molecular , Medicina de Precisão , Inibidores de Proteínas Quinases/efeitos adversos , Proteínas Tirosina Quinases/genética , Proteínas Tirosina Quinases/metabolismo , Proteínas Proto-Oncogênicas p21(ras)/genética , Proteínas Proto-Oncogênicas p21(ras)/metabolismo , Transdução de Sinais , Resultado do Tratamento
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