English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Increasing lines of evidence show that activation of Kupffer cells plays a pivotal role in initiation and progression of alcoholic liver disease. Kupffer cell activation is evoked by endotoxin (lipopolysaccharide, LPS), which leads to rapid elevation of intracellular calcium accompanied by release of a variety of mediators including cytokines, eicosanoids and reactive radical species. Among them, TNF-alpha is a critical factor in the pathogenesis of alcoholic liver disease.  Thalidomide (alpha-N-phthalimidoglutarimide) was initially used as a sedative and antiemetic during pregnancy but was withdrawn from the market due to its teratogenic effects. Before it was banned, thalidomide was recognized to reduce dramatically symptoms associated with erythema nodosum leprosum, a complication of Hansen's disease. Subsequently, it was shown that thalidomide suppresses TNF-alpha production by macrophages and other cell types such as activated T cells [1,2], which was attributed to a mechanism of thalidomide action [3].  Accordingly, the purpose of this study was to determine whether thalidomide could prevent alcohol-induced liver injury. Here we report that thalidomide prevents liver damage caused by chronic ethanol exposure through not only suppression of TNF-alpha production but abrogation of Kupffer cell sensitization to LPS.

Thalidomide Prevents Alcoholic Liver Injury in Rats Through Inhibition of Kupffer Cell Sensitization.