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All Journal INDONESIAN JOURNAL OF PHARMACY
Tran Phi Hoang Yen
University of Ho Chi Minh City, Faculty of Medicine and Pharmacy. 41 Dinh Tien Hoang street, District 1, Ho Chi Minh City, Vietnam.
Medicine & Pharmacology

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INHIBITION OF TROPOMYOSIN-RECEPTOR-KINASE B AND PHOSPHOINOSITIDE 3-KINASE/PROTEIN KINASE B SIGNALING CASCADE Yen, Tran Phi Hoang
Indonesian Journal of Pharmacy Vol 25 No 2, 2014
Publisher : Faculty of Pharmacy Universitas Gadjah Mada, Yogyakarta, Skip Utara, 55281, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (826.908 KB) | DOI: 10.14499/indonesianjpharm25iss2pp61

Abstract

Trimethyltin (TMT, 2.4mg/kg, i.p) can trigger neuronal damage by inhibiting Tropomyosin receptor kinase B (TrkB receptor) following by phosphoinositide 3-kinase (PI3K)/protein kinase B or Akt signaling cascade. We examined hippocampal changes in TrkA/B phosphorylation  on Tyr490/Tyr516 of TMT-treated mice in a time-dependent manner. Phosphorylated PI3K (Tyr508), phosphorylated 3-phosphoinositide-dependent protein kinase 1 (PDK1, Ser241) and phosphorylated Akt (Ser473) were changed following by  TMT injury (from 3 hours until 7 days after injury). Treatment with 7,8-dihydroxyflavone (7,8-DHF), a specific agonist of TrkB, significantly attenuated the TMT-caused inhibition of phospho-TrkB, thereby increased in expressions of phospho-PI3K, phospho-PDK1 and phospho-Akt in TMT-treated mice, simultaneously 7,8-DHF showed a neuroprotective effect in observation of nuclear chromatic clumping by Cresyl violet- and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling- (TUNEL) staining in the hippocampal dentate gyrus (DG) of TMT-treated mice, as compared to saline-treated group. This finding suggests that inhibition of TrkB receptor following by PI3K/Akt cascade may play a part in the molecular mechanism by which TMT caused neurodegeneration in mice.
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