IL-6 attenuates trimethyltin-induced cognitive dysfunction via activation of JAK2/STAT3, M1 mAChR and ERK signaling network-Reference-Cited by-同舟云学术

IL-6 attenuates trimethyltin-induced cognitive dysfunction via activation of JAK2/STAT3, M1 mAChR and ERK signaling network

Published:2013-06 Issue:6 Volume:25 Page:1348-1360
ISSN:0898-6568
Container-title:Cellular Signalling
language:en
Short-container-title:Cellular Signalling

Author:

Kim Beom Keun,Tran Haong-Yen Phi,Shin Eun-Joo,Lee Chaeyoung,Chung Yoon Hee,Jeong Ji Hoon,Bach Jae-Hyung,Kim Won-Ki,Park Dae Hoon,Saito Kuniaki,Nabeshima Toshitaka,Kim Hyoung-Chun

Publisher

Elsevier BV

Subject

Cell Biology

Reference48 articles.

1. Trimethyltin syndrome as a hippocampal degeneration model: temporal changes and neurochemical features of seizure susceptibility and learning impairment

2. Ascorbate attenuates trimethyltin-induced oxidative burden and neuronal degeneration in the rat hippocampus by maintaining glutathione homeostasis

3. Dextromethorphan attenuates trimethyltin-induced neurotoxicity via σ1 receptor activation in rats

4. Role of oxidative stress in epileptic seizures

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