Effects of remote ischemic postconditioning on inflammation related factors of cerebral ischemia/reperfusion injury

doi:10.3969/j.issn.2095-4344.2015.49.006

Abstract

Abstract:

BACKGROUND: Although some studies have suggested that remote ischemic postconditioning plays a neuroprotective role, but the specific mechanism is still unknown.
OBJECTIVE: To investigate the protective effects of remote ischemic postconditioning on focal cerebral ischemia/reperfusion injury in rats.
METHODS: Focal cerebral ischemia/reperfusion injury rat models were established by occlusion of the middle cerebral artery using suture method and were subjected to remote ischemic postconditioning. Meanwhile, sham and ischemia/reperfusion groups were established as comparison. After 24 hours of ischemia/reperfusion, neurological function was graded to determine cerebral infarction volume and brain water content. The mRNA expression of interleukin 1β, interleukin-6, tumor necrosis factor α and monocyte chemoattractant protein 1 in brain tissue around ischemic area was detected by RT-PCR. The protein expression of Bcl-2 and Bax was detected by western blot analysis.
RESULTS AND CONCLUSION: Compared with ischemia/reperfusion group, the neurological function scores in the remote ischemic postconditioning group were slightly, but not significantly, decreased. Infarct volume and brain water content in remote ischemic postconditioning group were significantly decreased compared with those in ischemia/reperfusion group (P < 0.05). The mRNA expression of interleukin 1β, interleukin-6, tumor necrosis factor α and monocyte chemoattractant protein 1 and the protein expression of Bax in brain tissue around
ischemic area in ischemic postconditioning group were significantly decreased compared with those in ischemia/reperfusion group (P < 0.05). Bcl-2 protein expression significantly increased (P < 0.05). These results demonstrate that remote ischemic postconditioning can relieve focal cerebral ischemia/reperfusion injury in rats, the mechanism of which may be associated with reduction of inflammatory response.

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

CLC Number:

R318

Wang Ning, Li Xiao-ou, Ba Xiao-hong. Effects of remote ischemic postconditioning on inflammation related factors of cerebral ischemia/reperfusion injury[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(49): 7902-7907.

Figures/Tables 4

References

[1] Durukan A, Tatlisumak T. Preconditioning-induced ischemictolerance: a window into endogenous gearing for cerebroprotection. Exp Transl Stroke Med. 2010;2(1):2.

[2] Yannopoulos FS, Mkel T, Niemel E, et al. Improved cerebral recovery from hypothermic circulatory arrest after remote ischemic preconditioning. Ann Thorac Surg. 2010;90(1): 182-188.

[3] Ren C, Gao M, Dornbos D, et al. Remote ischemic post-conditioning reduced brain damage in experimental ischemia/reperfusion injury. Neurol Res. 2011;33(5): 514-519.

[4] Ren C, Yan Z, Wei D, et al. Limb remote ischemic postconditioning protects against focal ischemia in rats. Brain Res. 2009;1288:88-94.

[5] Peng B, Guo QL, He ZJ, et al. Remote ischemic postconditioning protects the brain from global cerebral ischemia/reperfusion injury by up-regulating endothelial nitric oxide synthase through the PI3K/Akt pathway. Brain Res. 2012;1445:92-102.

[6] Zhou Y, Fathali N, Lekic T, et al. Remote limb ischemic postconditioning protects against neonatal hypoxic- ischemic brain injury in rat pups by the opioid receptor/Akt pathway. Stroke. 2011;42(2):439-444.

[7] 严利,周文胜.脑缺血/再灌注损伤与高尔基体破裂的研究进展[J].中国实用神经疾病杂志,2015,3:70-72.

[8] Liu Q, Zhou S, Wang Y, et al. A feasible strategy for focal cerebral ischemia-reperfusion injury: remote ischemic postconditioning. Neural Regen Res. 2014;9(15): 1460-1463.

[9] Longa EZ, Weinstein PR, Carlotn S, et al. Reversible middle cerebral artery oclusion without craniotomy in rats. Stroke. 1989;20(1):84-91．

[10] Carty M, Bowie AG. Evaluating the role of Toll-like receptors in diseases of the central nervous system. Biochem Pharmacol. 2011;81:825-837.

[11] Pignataro G, Cuomo O, Vinciguerra A, et al. NCX as a key player in the neuroprotection exerted by ischemic preconditioning and postconditioning. Adv Exp Med Biol. 2013;961:223-240.

[12] Oppenheim JJ, Tewary P, de la Rosa G, et al. Alarmins initiate host defense. Adv Exp Med Biol. 2007;601:185-194.

[13] Qiu J, Xu J, Zheng Y, et al. High-mobility group box 1 promotes metalloproteinase-9 upregulation through Toll-like receptor 4 after cerebral ischemia. Stroke. 2010;41: 2077-2082.

[14] Facci L, Barbierato M, Marinelli C, et al. Toll-like receptors 2, -3 and -4 prime microglia but not astrocytes across central nervous system regions for ATP-dependent interleukin-1β release. Sci Rep. 2014;4:6824.

[15] Kim JH, Hong KW, Bae SS, et al. Probucol plus cilostazol attenuate ercholesterolemia induced exacerbation in ischemic brain injury via anti-inflammatory effects. Int J Mol Med. 2014;34(3):687-694.

[16] Luheshi NM, Kovacs KJ, Lopez-Castejon G, et al. Interleukin-1alpha expression precedes IL-1beta after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues. J Neuroinflammation. 2011;8:186.

[17] Emsley HC, Smith CJ, Georgiu RF, et al. Interleukin-6 and acute ischaemic stroke. Acta Neurol Scand. 2005;112:273-274.

[18] Buttini M, Appel K, Sauter A, et al. Expression of tumor necrosis factor alpha after focal cerebral ischaemia in the rat. Neuroscience. 1996;71(1):1-16.

[19] Del Zoppo GJ. The neurovascular unit, matrix proteases, and innate inflammation. Ann N Y Acad Sci. 2010;1207: 46-49.

[20] Kong Y, Rogers MR, Qin X. Effective neuroprotection by ischemic postconditioning is associated with a decreased expression of RGMa and inflammation mediators in ischemic rats. Neurochem Res. 2013;38(4):815-825.