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2.
Pharmacol Rep ; 67(5): 996-1009, 2015 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-26398396

RESUMEN

Lung cancer is the major cause of overall cancer deaths, and chemoprevention is a promising strategy to control this disease. Benzo(a)pyrene [B(a)P], a polycyclic aromatic hydrocarbon, is one among the principal constituents of tobacco smoke that plays a key role in lung carcinogenesis. The B(a)P induced lung cancer in mice offers a relevant model to study the effect of natural products and has been widely used by many researchers and found considerable success in ameliorating the pathophysiological changes of lung cancer. Currently available synthetic drugs that constitute the pharmacological armamentarium are themselves effective in managing the condition but not without setbacks. These hunches have accelerated the requisite for natural products, which may be used as dietary supplement to prevent the progress of lung cancer. Besides, these agents also supplement the conventional treatment and offer better management of the condition with less side effects. In the context of soaring interest toward dietary phytochemicals as newer pharmacological interventions for lung cancer, in the present review, we are attempting to give a silhouette of mechanisms of B(a)P induced lung carcinogenesis and the role of dietary phytochemicals in chemoprevention.


Asunto(s)
Anticarcinógenos/farmacología , Benzo(a)pireno/toxicidad , Carcinógenos/toxicidad , Dieta , Neoplasias Pulmonares/inducido químicamente , Neoplasias Pulmonares/prevención & control , Fitoquímicos/farmacología , Animales , Quimioprevención , Humanos , Neoplasias Pulmonares/patología
3.
Neurochem Int ; 76: 70-81, 2014 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-25049175

RESUMEN

The highly conserved abundant nuclear protein poly(ADP-ribose)polymerase1 (PARP1) functions at the center of cellular stress response and is mainly implied in DNA damage repair mechanism. Apart from its involvement in DNA damage repair, it does sway multiple vital cellular processes such as cell death pathways, cell aging, insulator function, chromatin modification, transcription and mitotic apparatus function. Since brain is the principal organ vulnerable to oxidative stress and inflammatory responses, upon stress encounters robust DNA damage can occur and intense PARP1 activation may result that will lead to various CNS diseases. In the context of soaring interest towards PARP1 as a therapeutic target for newer pharmacological interventions, here in the present review, we are attempting to give a silhouette of the role of PARP1 in the neurological diseases and the potential of its inhibitors to enter clinical translation, along with its structural and functional aspects.


Asunto(s)
Enfermedades del Sistema Nervioso/tratamiento farmacológico , Poli(ADP-Ribosa) Polimerasas/efectos de los fármacos , Investigación Biomédica Traslacional , Daño del ADN , Reparación del ADN , Homeostasis , Humanos , Poli(ADP-Ribosa) Polimerasa-1 , Poli(ADP-Ribosa) Polimerasas/metabolismo
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