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Chamomile confers protection against hydrogen peroxide-induced toxicity through activation of Nrf2-mediated defense response.


ABSTRACT: Oxidative stress plays an important role in the development of various human diseases. Aqueous chamomile extract is used as herbal medicine, in the form of tea, demonstrated to possess antiinflammatory and antioxidant properties. We demonstrate the cytoprotective effects of chamomile on hydrogen peroxide (H?O?)-induced cellular damage in macrophage RAW 264.7 cells. Pretreatment of cells with chamomile markedly attenuated H?O?-induced cell viability loss in a dose-dependent manner. The mechanisms by which chamomile-protected macrophages from oxidative stress was through the induction of several antioxidant enzymes including NAD(P)H:quinone oxidoreductase, superoxide dismutase, and catalase and increase nuclear accumulation of the transcription factor Nrf2 and its binding to antioxidant response elements. Furthermore, chamomile dose-dependently reduced H?O?-mediated increase in the intracellular levels of reactive oxygen species. Our results, for the first time, demonstrate that chamomile has protective effects against oxidative stress and might be beneficial to provide defense against cellular damage.

SUBMITTER: Bhaskaran N 

PROVIDER: S-EPMC4019961 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature

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Chamomile confers protection against hydrogen peroxide-induced toxicity through activation of Nrf2-mediated defense response.

Bhaskaran Natarajan N   Srivastava Janmejai K JK   Shukla Sanjeev S   Gupta Sanjay S  

Phytotherapy research : PTR 20120418 1


Oxidative stress plays an important role in the development of various human diseases. Aqueous chamomile extract is used as herbal medicine, in the form of tea, demonstrated to possess antiinflammatory and antioxidant properties. We demonstrate the cytoprotective effects of chamomile on hydrogen peroxide (H₂O₂)-induced cellular damage in macrophage RAW 264.7 cells. Pretreatment of cells with chamomile markedly attenuated H₂O₂-induced cell viability loss in a dose-dependent manner. The mechanisms  ...[more]

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