Study of mechanism on NF-κB mediates injection coryadlis decumbens pers par-ticipated in neuroprotection after ischemia reperfusion of rats
10.3969/j.issn.1000-484X.2016.08.023
- VernacularTitle:夏天无注射液参与脑缺血再灌注大鼠神经保护的NF－κB介导机制
- Author:
Zucai XU
;
Shasha ZHANG
;
Tao LIANG
;
Jing WANG
;
Yan PENG
;
Jun ZHANG
- Publication Type:Journal Article
- Keywords:
Injection coryadlis decumbens pers;
Cerebral ischemia reperfusion;
NF-κB;
Neuroprotection
- From:
Chinese Journal of Immunology
2016;32(8):1187-1191
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate themechanism on NF-κB mediates the injection coryadlis decumbens pers ( ICDP ) participated in neuroprotection after ischemia reperfusion of rats .Methods:The SD rats were rando mly divided into several groups as follows:Sham operation group,Model group,1.0 ml/kg ICDP group(Low-dose,ICDP-L),2.5 ml/kg ICDP group(Middle-dose,ICDP-M),5 ml/kg ICDP group(High-dose,ICDP-H),and NF-κB inhibitor group(BAY11-7082).24 h after anesthetize,the volume of infarct sections in different groups were detected by TCC staining ,and the phosphorylated NF-κB expression in rats brain was observed by im-munohistochemistry and Western blot .Results:The TTC staining showed that different concentration of ICDP and BAY 11-7082 could reduce the brain infarction volume significantly .There was no significant different effect among the ICDP-H group,ICDP-M group and inhibitor group ,however ,the effect in these three groups was more effective than that in the ICDP-M group.In addition ,the results of im-munohistochemistry indicated that phosphorylated NF-κB p65 expressed in brain tissue located mainly at the nucleus neuronal cells in the CA1 region of hippocampusin model rats ,and the expression of phosphorylated NF-κB were significantly reduced inICDP groups and BAY11-7082 group.Conclusion: The ICDP can reduce brain infarct volume after ischemia reperfusion of rats .The neuralprotection mechanism of ICDP may relative toinhibits thehyperphosphorylation of NF-κB.
