J
Jen-Kun Lin
Researcher at National Taiwan University
Publications - 268
Citations - 22357
Jen-Kun Lin is an academic researcher from National Taiwan University. The author has contributed to research in topics: Apoptosis & Kinase. The author has an hindex of 78, co-authored 268 publications receiving 21168 citations. Previous affiliations of Jen-Kun Lin include Academia Sinica & Chung Shan Medical University.
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Journal ArticleDOI
Stability of curcumin in buffer solutions and characterization of its degradation products
Ying-Jan Wang,Min-Hsiung Pan,Ann-Lii Cheng,Liang-In Lin,Yuan Soon Ho,Chang-Yao Hsieh,Jen-Kun Lin +6 more
TL;DR: It was shown that decomposition was pH-dependent and occurred faster at neutral-basic conditions and vanillin, ferulic acid, feruloyl methane were identified as minor degradation products and the amount of vanillin increased with incubation time.
Journal Article
Biotransformation of curcumin through reduction and glucuronidation in mice.
TL;DR: The results, together with previous findings, suggest that curcumin-glucuronoside, dihydrocurcumin - glucuronOSide, THC-gloucesteride, and THC are major metabolites ofCurcumin in vivo.
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Suppression of inducible cyclooxygenase and inducible nitric oxide synthase by apigenin and related flavonoids in mouse macrophages.
TL;DR: Results of further studies suggest that suppression of transcriptional activation of COX-2 and iNOS by apigenin might mainly be mediated through inhibition of IkB kinase activity.
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Suppression of nitric oxide synthase and the down-regulation of the activation of NFκB in macrophages by resveratrol
TL;DR: The flavonoids may be of value for inhibiting the enhanced expression of iNOS in inflammation through down‐regulation of NFκB binding activity.
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Involvement of reactive oxygen species and caspase 3 activation in arsenite-induced apoptosis
TL;DR: The results lead to a working hypothesis that arsenite‐induced apoptosis is triggered by the generation of hydrogen peroxide through activation of flavoprotein‐dependent superoxide‐producing enzymes (such as NADPH oxidase), and hydrogenperoxide might play a role as a mediator to induce apoptosis through release of cytochrome c to cytosol, activation of CPP32 protease, and PARP degradation.