Article Publish Status: FREE
Abstract Title:

Myricetin protects cells against oxidative stress-induced apoptosis via regulation of PI3K/Akt and MAPK signaling pathways.

Abstract Source:

Int J Mol Sci. 2010 Nov 2 ;11(11):4348-60. Epub 2010 Nov 2. PMID: 21151442

Abstract Author(s):

Kyoung Ah Kang, Zhi Hong Wang, Rui Zhang, Mei Jing Piao, Ki Cheon Kim, Sam Sik Kang, Young Woo Kim, Jongsung Lee, Deokhoon Park, Jin Won Hyun

Article Affiliation:

Kyoung Ah Kang


Recently, we demonstrated that myricetin exhibits cytoprotective effects against H(2)O(2)-induced cell damage via its antioxidant properties. In the present study, myricetin was found to inhibit H(2)O(2)-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic bodies, nuclear fragmentation, sub-G(1) cell population, and disruption of mitochondrial membrane potential (Δψ(m)), which are increased in H(2)O(2)-treated cells. Western blot data showed that in H(2)O(2)-treated cells, myricetin increased the level of Bcl-2, which is an anti-apoptotic factor, and decreased the levels of Bax, active caspase-9 and -3, which are pro-apoptotic factors. And myricetin inhibited release of cytochrome c from mitochondria to cytosol in H(2)O(2)-treated cells. Myricetin-induced survival correlated with Akt activity, and the rescue of cells by myricetin treatment against H(2)O(2)-induced apoptosis was inhibited by the specific PI3K (phosphoinositol-3-kinase) inhibitor. Myricetin-mediated survival also inhibited the activation of p38 mitogen activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK), which are members of MAPK. Our studies suggest that myricetin prevents oxidative stress-induced apoptosis via regulation of PI3K/Akt and MAPK signaling pathways.

Study Type : In Vitro Study

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