The effect of focal cerebral ischemia-reperfusion injury on TLR4 and NF-κB signaling pathway.
The effect of focal cerebral ischemia-reperfusion injury on TLR4 and NF-κB signaling pathway.
复制标题
局灶性脑缺血再灌注损伤对TLR4和NF-κB信号通路的影响。
DOI:
10.3892/etm.2017.5463
复制
发表时间:
2018-01
影响因子:
2.7
通讯作者:
Xu B
中科院分区:
文献类型:
--
作者:
Chen J;Yang C;Xu X;Yang Y;Xu B
The present study analyzed the change of Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) expression in focal cerebral ischemia-reperfusion injury model. A sample of 36 Sprague-Dawley rats were randomly selected and divided into sham operation group (group S), control group (group C) and Chrysanthemum ester group (NF-κB inhibitor, group CE), each group consisted of 12 rats. The rat model of focal cerebral ischemia-reperfusion was established. The physiological indexes and neurological severity score of rats was recorded by a double-blind method. The cerebral infarction area was evaluated by triphenyltetrazole oxide (TTC) staining on brain slices. Apoptosis was evaluated by TUNEL staining. Semi-quantitative PCR and western blot analysis was used to measure the expression of TLR4 and NF-κB. The neurological severity score of rats in group C and CE were found to be significantly lower than group S (P<0.01). The TTC staining results showed that group C and CE had different levels of cerebral infarction but the area of infarction in group CE was significantly lower than group C (P<0.01). In addition, the number of TUNEL positive cells in group CE was significantly lower than group C (P<0.01). Semi-quantitative PCR and westernblot analysis results showed that the expression of NF-κB and TLR4 of group S was significantly lower than that of group C and group CE (P<0.01), the relative expression of NF-κB and TLR4 of group CE was significantly lower than that of group C (P<0.01). Moreover, the expression of NF-κB p65/p50 of group CE and group C was significantly higher than that of group S (P<0.01). This study concludes that the focal cerebral ischemia-reperfusion injury in rats can cause brain damage and cell apoptosis. This effect might be associated to the increased expression of NF-κB and TLR4, and the activation of TLR4/NF-κB signaling pathway.
登录
查看更多内容
影响因子:
2.2
作者:
Crivera, Concetta;Nelson, Winnie W.;Witt, Edward A.
通讯作者:
Witt, Edward A.
影响因子:
2.9
作者:
Gauberti, Maxime;Obiang, Pauline;Orset, Cyrille
通讯作者:
Orset, Cyrille
DOI:
10.1073/pnas.1522459113
发表时间:
2016-04-12
影响因子:
11.1
作者:
Levitz, Joshua;Royal, Perrine;Sandoz, Guillaume
通讯作者:
Sandoz, Guillaume
DOI:
10.6061/clinics/2015(12)07
发表时间:
2015-12
期刊:
Clinics (Sao Paulo, Brazil)
影响因子:
--
作者:
Oshiro AH;Otsuki DA;Hamaji MW;Rosa KT;Ida KK;Fantoni DT;Auler JO Jr
通讯作者:
Auler JO Jr
影响因子:
7.3
作者:
Vivier, Delphine;Bennis, Khalil;Ducki, Sylvie
通讯作者:
Ducki, Sylvie