Neurodegeneration Caused by Trimethyltin Via Inhibition of Tropomyosin-Receptor-Kinase B and Phosphoinositide 3-Kinase/Protein Kinase B Signaling Cascade  

Oleh:

Yen, Tran Phi Hoang ; Khoi, Nguyen Ngoc ; An, Duong Phuoc ; Van, Nguyen Thi Thu ; Quang, Do Minh

Jenis: Article from Journal - ilmiah nasional - terakreditasi DIKTI
Dalam koleksi: Indonesian Journal of Pharmacy vol. 25 no. 02 (Apr. 2014), page 61-67.
Topik: Trimethyltin; Neurodegeneration; TrkB Receptor; PI3K/Akt Pathway; Mice
Fulltext: I03 v25 n2 p61 kelik2017.pdf (807.53KB)

Ketersediaan

Perpustakaan FK Nomor Panggil: I03.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Trimethyltin (TMT, 2.4mg/kg, i.p) can trigger neuronal amage y 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 followed by PI3K/Akt cascade may play a part in the molecular mechanism by which TMT caused neurodegeneration in mice.

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