Remifentanil preconditioning alleviating brain damage of cerebral ischemia reperfusion rats by regulating the JNK signal pathway and TNF-α/TNFR1 signal pathway

被引:43
作者
Zhang, Yan [1 ]
Li, Yan-Wei [2 ]
Wang, Ya-Xin [1 ]
Zhang, Hong-Tao [1 ]
Zhang, Xiao-Mei [3 ]
Liang, Yu [1 ]
Zhang, Xiu-Shan [1 ]
Wang, Wen-Sheng [1 ]
Liu, Hai-Gen [1 ]
Zhang, Yi [4 ]
Zhang, Ling [4 ]
Zheng, Yu-Hua [5 ]
机构
[1] Tianjin Huanhu Hosp, Dept Anesthesiol, Tianjin 300060, Peoples R China
[2] Tianjin Med Univ, Hosp 2, Dept Nephrol, Tianjin 300211, Peoples R China
[3] Tianjin First Ctr Hosp, Dept Anesthesiol, Tianjin 300192, Peoples R China
[4] Tianjin Huanhu Hosp, Dept Pharm, Tianjin 300060, Peoples R China
[5] Tianjin Nan Kai Hosp, Dept Anesthesiol, Tianjin 300100, Peoples R China
关键词
Cerebral ischemia/reperfusion; Remifentanil preconditioning; TNF-alpha/TNFR1; JNK signal pathways; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; CYTOCHROME-C; FACTOR-ALPHA; ISCHEMIA/REPERFUSION INJURY; INDUCED APOPTOSIS; CELL-DEATH; PROTEIN; BAX; RELEASE;
D O I
10.1007/s11033-013-2819-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Tumor necrosis factor (TNF) and the TNF receptor (TNFR) superfamily play very important roles for cell death as well as normal immune regulation. Previous studies have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. The purpose of this investigation was to examine the protective effect of remifentanil preconditioning in cerebral ischemia/reperfusion injury (CIR) and its possible molecular mechanism. Results showed that Remifentanil pretreatment significantly decreased the CD4(+) and increased the CD8(+) in cerebral tissues. Additionally, CD4(+)/CD8(+) in CIR + Remifentanil group was markedly lower than that in CIR group. TNF-alpha and TNFR1 in CIR + Remifentanil group rats was found to be significant lower than that in CIR group rats. The expression levels of Cyt-c, caspase-3, caspase-9 and pJNK proteins in brain of CIR + Remifentanil group rats were found to significantly decreased compared to CIR group rats. In addition, decreased ROS level indirectly inhibit JNK activation and cell death in CIR rat receiving Remifentanil preconditioning. From current experiment results, at least two signal pathways involve into the process of Remifentanil preconditioning inhibiting cerebral damage induced by ischemia reperfusion. The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways. Taken together, this study indicated that regulation of the TNF-alpha/TNFR1 and JNK signal pathways may provide a new therapy for cerebral damage induced by ischemia and reperfusion.
引用
收藏
页码:6997 / 7006
页数:10
相关论文
共 74 条
[1]   Peripheral blood CD4(+)CD8(+) lymphocytes in cynomolgus monkeys are of resting memory T lineage [J].
Akari, H ;
Terao, K ;
Murayama, Y ;
Nam, KH ;
Yoshikawa, Y .
INTERNATIONAL IMMUNOLOGY, 1997, 9 (04) :591-597
[2]   The role of caspase 3 and BclxL in the action of interleukin 7 (IL-7):: A survival factor in activated human T cells [J].
Amos, CL ;
Woetmann, A ;
Nielsen, M ;
Geisler, C ;
Odum, N ;
Brown, BL ;
Dobson, PRM .
CYTOKINE, 1998, 10 (09) :662-668
[3]   Poliovirus induces Bax-dependent cell death mediated by c-Jun NH2-terminal kinase [J].
Autret, Arnaud ;
Martin-Latil, Sandra ;
Mousson, Laurence ;
Wirotius, Aurelie ;
Petit, Frederic ;
Arnoult, Damien ;
Colbere-Garapin, Florence ;
Estaquier, Jerome ;
Blondel, Bruno .
JOURNAL OF VIROLOGY, 2007, 81 (14) :7504-7516
[4]   Tumour necrosis factor and cancer [J].
Balkwill, Frances .
NATURE REVIEWS CANCER, 2009, 9 (05) :361-371
[5]   Tumor necrosis factor-alpha - A mediator of focal ischemic brain injury [J].
Barone, FC ;
Arvin, B ;
White, RF ;
Miller, A ;
Webb, CL ;
Willette, RN ;
Lysko, PG ;
Feuerstein, GZ .
STROKE, 1997, 28 (06) :1233-1244
[6]   Identification of novel polymorphisms in the human TNFR1 gene:: distribution in acute leukemia patients and healthy individuals [J].
Bazzoni, F ;
Gatto, L ;
Lenzi, L ;
Vinante, F ;
Pizzolo, G ;
Zanolin, E ;
De Gironcoli, M .
IMMUNOGENETICS, 2000, 51 (02) :159-163
[7]  
Bester DJ, 2012, J FOOD AGRIC ENVIRON, V10, P29
[8]   Prion protein protects human neurons against Bax-mediated apoptosis [J].
Bounhar, Y ;
Zhang, Y ;
Goodyer, CG ;
LeBlanc, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (42) :39145-39149
[9]   TNF-mediated inflammatory disease [J].
Bradley, J. R. .
JOURNAL OF PATHOLOGY, 2008, 214 (02) :149-160
[10]   Apoptotic signaling pathways: Caspases and stress-activated protein kinases [J].
Cho, SG ;
Choi, EJ .
JOURNAL OF BIOCHEMISTRY AND MOLECULAR BIOLOGY, 2002, 35 (01) :24-27