Influence of Sepsis on the Expression of Apoptotic Protease Caspase-3 in Hippocampus of Rats_West China Medical Journal

Authors：

 SUYun-jie ,  LIXi-hong , YANGXin , WANGJing , QUYi

Pediatric Intensive Care Unit, West China Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, P. R. China;

Corresponding?author：

LIXi-hong, Email: hilixihong@163.com

Keywords：

Sepsis; Hippocampus; Apoptosis; Caspase-3; Rats

DOI：

10.7507/1002-0179.20140309

Video：

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Objective To investigate the influence of sepsis on the expression of apoptotic protease caspase-3 in hippocampus neurons of rats. Methods Models of rats with sepsis were established by the cecal ligation and puncture (CLP) method. Eighty 30-day-old male Wistar rats were randomly divided into CLP group (n=50) and control group (n=30). In the CLP group, only CLP was performed on the rats. Ten rats in the CLP group and another 10 in the control group were taken at 6, 12, and 24 hours after operation, respectively. Five of them in each group were taken for neurobehavioral score, and the other five were killed and their brains were removed. Then the Western blot and immunohistochemistry staining were used to detect the expression changes of apoptosis protein caspase-3. Results In the control group, there were very low expression of apoptotic protease caspase-3 and high scores of neurological behavior. In the CLP group, the expression of apoptotic protease caspase-3 started to increase at the 6th hour, and reached the peak at the 24th hour after CLP, both of which were significantly higher than the control group (P<0.05). The scores of neurological behavior of the CLP group began to decline at 6h after CLP, and decreased gradually along with the time, and the scores were significantly lower at various time points after CLP in the CLP group than those in the control group (P<0.05). Conclusion The scores of neurological behavior decrease and the expression of apoptosis protease caspase-3 increase in the rat hippocampus with sepsis, and fluctuate with time change.

Citation： SUYun-jie, LIXi-hong, YANGXin, WANGJing, QUYi. Influence of Sepsis on the Expression of Apoptotic Protease Caspase-3 in Hippocampus of Rats. West China Medical Journal, 2014, 29(6): 1011-1014. doi: 10.7507/1002-0179.20140309 Copy

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1. LaRoche SM. Seizures and encephalopathy[J]. Semin Neurol, 2011, 31(2): 194-201.
2. Zhang LN, Wang XT, Ai YH, et al. Epidemiological features and risk factors of sepsis-associated encephalopathy in intensive care unit patients: 2008-2011[J]. Chin Med J (Engl), 2012, 125(5): 828-831.
3. Bariehello T, Fortunato JJ, Vitali AM, et al. Oxidative variables in the rat brain after sepsis induced by cecal ligation and perforation[J]. Crit Care Med, 2006, 34(3): 886-889.
4. d'Avila JC1, Santiago AP, Amancio RT, et al. Sepsis induces brain mitochondrial dysfunction[J]. Crit Care Med, 2008, 36(6): 1925-1932.
5. Rittirsch D, Huber-Lang MS, Flierl MA, et al. Immunodesign of experimental sepsis by cecal ligation and puncture[J]. Nat Protoc, 2009, 4(1): 31-36.
6. 張麗娜, 艾宇航, 郭曲練, 等. 膿毒癥相關性腦病大鼠動物模型的建立[J]. 中華急診醫學雜志, 2013, 22(7): 731-736.
7. Huang T, Long M, Huo B. Competitive binding to cuprous Ions of protein and BCA in the bicinchoninic acid protein assay[J]. Open Biomed Eng J, 2010, 4: 271-278.
8. Fry DE. Sepsis, systemic inflammatory response, and multiple organ dysfunction: the mystery continues[J]. Am Surg, 2012, 78(1): 1-8.
9. Kenzaka T, Okayama M, Kuroki S, et al. Importance of vital signs to the early diagnosis and severity of sepsis: association between vital signs and sequential organ failure assessment score in patients with sepsis[J]. Intern Med, 2012, 51(8): 871-876.
10. Gofton TE, Young GB. Sepsis-associated encephalopathy[J]. Nat Rev Neurol, 2012, 8(10): 557-566.
11. Ziaja M. Septic encephalopathy[J]. Curr Neurol Neurosci Rep, 2013, 13(10): 383.
12. Kuranaga E. Caspase signaling in animal development[J]. Dev Growth Differ, 2011, 53(2): 137-148.
13. Beier JI, Mcclain CJ. Mechanisms and cell signaling in alcoholic liver disease[J]. Biol Chem, 2010, 391(11): 1249-1264.
14. Hattori Y, Takano K, Teramae H, et al. Insights into sepsis therapeutic design based on the apoptotic death pathway[J]. J Pharmacol Sci, 2010, 114(4): 354-365.
15. Matsuda N, Takano Y, Kageyama S, et al. Silencing of caspase-8 and caspase-3 by RNA interference prevents vascular endothelial cell injury in mice with endotoxic shock[J]. Cardiovasc Res, 2007, 76(1): 132-140.
16. Comim CM, Barichello T, Grandgirard D, et al. Caspase-3 mediates in part hippocampal apoptosis in sepsis[J]. Mol Neurobiol, 2013, 47(1): 394-398.
17. 李寧, 王陽, 曾其毅. 膿毒癥早期大鼠腦線粒體損傷的研究[J]. 細胞與分子免疫學雜志, 2010, 26(4): 379-381.
18. Santos R, de Almodóvar CR, Bulteau AL, et al. Neurodegeneration, neurogenesis, and oxidative stres[J/OL]. Oxid Med Cell Longev, 2013. http://dx.doi.org/10.1155/2013/730581.
19. 王靜, 李熙鴻, 屈藝, 等. 細胞外信號調節激酶抑制劑PD98059對膿毒癥新生大鼠腦組織腫瘤壞死因子-α表達的影響[J]. 實用兒科臨床雜志, 2012, 27(24): 1888-1890.
20. Rim HK, Cho W, Sung SH, et al. Nodakenin suppresses lipopolysaccharide-induced inflammatory responses in macrophage cells by inhibiting tumor necrosis factor receptor-associated factor 6 and nuclear factor-κB pathways and protects mice from lethal endotoxin shock[J]. J Pharmacol Exp Ther, 2012, 342(3): 654-664.

West China Medical Journal

Influence of Sepsis on the Expression of Apoptotic Protease Caspase-3 in Hippocampus of Rats

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