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Researchers from Sichuan University Detail New Studies and Findings in the Area of Inflammation (Silymarin attenuates cigarette smoke extract-induced...

Health & Medicine Week

12-16-16

Researchers from Sichuan University Detail New Studies and Findings in the Area of Inflammation (Silymarin attenuates cigarette smoke extract-induced inflammation via simultaneous inhibition of autophagy and ERK/p38 MAPK pathway in human ...)

By a News Reporter-Staff News Editor at Health & Medicine Week -- Data detailed on Inflammation have been presented. According to news reporting originating from Chengdu, People's Republic of China, by NewsRx correspondents, research stated, "Cigarette smoke (CS) is a major risk of chronic obstructive pulmonary disease (COPD), contributing to airway inflammation. Our previous study revealed that silymarin had an anti-inflammatory effect in CS-exposed mice."

Our news editors obtained a quote from the research from Sichuan University, "In this study, we attempt to further elucidate the molecular mechanisms of silymarin in CS extract (CSE)-induced inflammation using human bronchial epithelial cells. Silymarin significantly suppressed autophagy activation and the activity of ERK/p38 mitogen-activated protein kinase (MAPK) pathway in Beas-2B cells. We also observed that inhibiting the activity of ERK with specific inhibitor U0126 led to reduced autophagic level, while knockdown of autophagic gene Beclin-1 and Atg5 decreased the levels of ERK and p38 phosphorylation. Moreover, silymarin attenuated CSE-induced upregulation of inflammatory cytokines TNF-alpha, IL-6 and IL-8 which could also be dampened by ERK/p38 MAPK inhibitors and siRNAs for Beclin-1 and Atg5. Finally, we validated decreased levels of both autophagy and inflammatory cytokines (TNF-alpha and KC) in CS-exposed mice after silymarin treatment. The present research has demonstrated that CSE-induced autophagy in bronchial epithelia, in synergism with ERK MAPK pathway, may initiate and exaggerate airway inflammation."

According to the news editors, the research concluded: "Silymarin could attenuate inflammatory responses through intervening in the crosstalk between autophagy and ERK MAPK pathway, and might be an ideal agent treating inflammatory pulmonary diseases."

For more information on this research see: Silymarin attenuates cigarette smoke extract-induced inflammation via simultaneous inhibition of autophagy and ERK/p38 MAPK pathway in human bronchial epithelial cells. Scientific Reports, 2016;6():1-10. Scientific Reports can be contacted at: Nature Publishing Group, Macmillan Building, 4 Crinan St, London N1 9XW, England. (Nature Publishing Group - www.nature.com/; Scientific Reports - www.nature.com/srep/)

The news editors report that additional information may be obtained by contacting F.Q. Wen, Sichuan University, West China Hosp, State Key Lab Biotherapy China, Div Pulm Dis, Chengdu 610041, Sichuan, People's Republic of China. Additional authors for this research include J. Hu, T. Wang, X. Zhang, L. Liu, H. Wang, Y.Q. Wu, D. Xu and F.Q. Wen (see also Inflammation).

Keywords for this news article include: Chengdu, People's Republic of China, Asia, Epithelial Cells, Inflammation, Sichuan University.

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2016, NewsRx LLC

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