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1.
Cancer Research on Prevention and Treatment ; (12): 176-181, 2022.
Artigo em Chinês | WPRIM | ID: wpr-986497

RESUMO

With the continuous progress of tumor treatment methods in recent years, more and more emerging antitumor drugs have been approved to market and put into clinical use. In addition, some treatments that are in clinical trials such as gene therapy are also continuously making new breakthroughs. In this review, we mainly give a brief introduction to the novel antineoplastic therapies that have been clinically used in recent years, as well as the ones with remarkable efficacy and are expected to be approved for marketing.

2.
Experimental Neurobiology ; : 612-627, 2019.
Artigo em Inglês | WPRIM | ID: wpr-763785

RESUMO

Aldose reductase (AR) protein, a member of the NADPH-dependent aldo-keto reductase family, reduces a wide range of aldehydes and enhances cell survival by inhibition of oxidative stress. Oxidative stress is known as one of the major pathological factor in ischemia. Since the precise function of AR protein in ischemic injury is fully unclear, we examined the function of AR protein in hippocampal neuronal (HT-22) cells and in an animal model of ischemia in this study. Cell permeable Tat-AR protein was produced by fusion of protein transduction domain in Tat for delivery into the cells. Tat-AR protein transduced into HT-22 cells and significantly inhibited cell death and regulated the mitogen-activate protein kinases (MAPKs), Bcl-2, Bax, and Caspase-3 under oxidative stress condition. In an ischemic animal model, Tat-AR protein transduced into the brain tissues through the blood-brain barrier (BBB) and drastically decreased neuronal cell death in hippocampal CA1 region. These results indicate that transduced Tat-AR protein has protective effects against oxidative stress-induced neuronal cell death in vitro and in vivo, suggesting that Tat-AR protein could be used as potential therapeutic agent in ischemic injury.


Assuntos
Humanos , Aldeído Redutase , Aldeídos , Barreira Hematoencefálica , Encéfalo , Região CA1 Hipocampal , Caspase 3 , Morte Celular , Sobrevivência Celular , Técnicas In Vitro , Isquemia , Modelos Animais , Neurônios , Estresse Oxidativo , Oxirredutases , Proteínas Quinases
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