Effects about TMP to expression of proteins relating with JNK signal transduction pathways on cultured rat hippocampal neurons after anoxia-reoxygenation
10.3969/j.issn.1006-5725.2015.13.008
- VernacularTitle:川芎嗪对缺氧／复氧海马神经元JNK通路相关蛋白表达的影响
- Author:
Yun WANG
;
Wuhua MA
- Publication Type:Journal Article
- Keywords:
Tetramethylpyrazine;
JNK pathways;
Caspases-1;
Bad
- From:
The Journal of Practical Medicine
2015;(13):2095-2097
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects about Tetramethyl -pyrazine (TMP)to Bad, Caspases-1 protein relating with JNK signal transduction pathways on cultured rat hippocampal neurons after anoxia-reoxygenation. Methods Rat hippocampal neurons were cultured in vitro and observed respectively on 7 ~ 9 days. Neurons were exposed to TMP in three different concentration (60,200,800 μg/mL) and JNK inhibitors (10 μmol/L). Control/normal groups were set in each experiment, except for the normal group. After 1 hour of treatment, the rat hippocampal neurons were placed in an incubator with 90%N2 + 10% CO2 for 2 hours to induce anoxia. Then, the rat hippocampal neurons were placed in an incubator with 5% CO2+95%air to establish reoxygenation. Bad, Caspases-1 protein were examined by Western Blot. Results After neurons with 60,200, 800 μg/mL TMP and 10 μmol/L JNK inhibitors on damage induced by anoxia-reoxygenation , the Bad , Caspases-1 protein are lower than the control group. But the 200 μg/mL group is better than 60 800 μg/mL groups. Conclusions Through the JNK signal transduction pathways, the Caspases-1, Bad protein expressions are lower than the control group. So TMP has obvious inhibitory action to rat hippocampal neuronal damage induced by anoxia-reoxygenation.
