Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

详细信息    查看全文

• 作者：Dong Won Kim ; Jae-Chul Lee ; Jeong-Hwi Cho ; Joon Ha Park…
• 关键词：Sublethal and lethal ischemia ; CA1 region ; Pyramidal neurons ; Delayed neuronal death ; Inflammation
• 刊名：Neurochemical Research
• 出版年：2015
• 出版时间：September 2015
• 年：2015
• 卷：40
• 期：9
• 页码：1984-1995
• 全文大小：7,361 KB
• 参考文献：1.Olson EE, McKeon RJ (2004) Characterization of cellular and neurological damage following unilateral hypoxia/ischemia. J Neurol Sci 227:7-9CrossRef PubMed
  2.Kirino T (1982) Delayed neuronal death in the gerbil hippocampus following ischemia. Brain Res 239:57-9CrossRef PubMed
  3.Lipton P (1999) Ischemic cell death in brain neurons. Physiol Rev 79:1431-568PubMed
  4.Abe K, Aoki M, Kawagoe J, Yoshida T, Hattori A, Kogure K, Itoyama Y (1995) Ischemic delayed neuronal death. A mitochondrial hypothesis. Stroke 26:1478-489CrossRef PubMed
  5.Kato H, Kogure K, Araki T, Itoyama Y (1995) Induction of Jun-like immunoreactivity in astrocytes in gerbil hippocampus with ischemic tolerance. Neurosci Lett 189:13-6CrossRef PubMed
  6.Kirino T, Nakagomi T, Kanemitsu H, Tamura A (1996) Ischemic tolerance. Adv Neurol 71:505-11PubMed
  7.Nakamura H, Katsumata T, Nishiyama Y, Otori T, Katsura K, Katayama Y (2006) Effect of ischemic preconditioning on cerebral blood flow after subsequent lethal ischemia in gerbils. Life Sci 78:1713-719CrossRef PubMed
  8.Amantea D, Nappi G, Bernardi G, Bagetta G, Corasaniti MT (2009) Post-ischemic brain damage: pathophysiology and role of inflammatory mediators. FEBS J 276:13-6CrossRef PubMed
  9.Danton GH, Dietrich WD (2003) Inflammatory mechanisms after ischemia and stroke. J Neuropathol Exp Neurol 62:127-36PubMed
  10.Hanisch UK, Quirion R (1995) Interleukin-2 as a neuroregulatory cytokine. Brain Res Brain Res Rev 21:246-84CrossRef PubMed
  11.Araujo DM, Lapchak PA (1994) Induction of immune system mediators in the hippocampal formation in Alzheimer’s and Parkinson’s diseases: selective effects on specific interleukins and interleukin receptors. Neuroscience 61:745-54CrossRef PubMed
  12.Liu T, Clark RK, McDonnell PC, Young PR, White RF, Barone FC, Feuerstein GZ (1994) Tumor necrosis factor-alpha expression in ischemic neurons. Stroke 25:1481-488CrossRef PubMed
  13.Barone FC, Arvin B, White RF, Miller A, Webb CL, Willette RN, Lysko PG, Feuerstein GZ (1997) Tumor necrosis factor-alpha. A mediator of focal ischemic brain injury. Stroke 28:1233-244CrossRef PubMed
  14.Yang MS, Park EJ, Sohn S, Kwon HJ, Shin WH, Pyo HK, Jin B, Choi KS, Jou I, Joe EH (2002) Interleukin-13 and -4 induce death of activated microglia. Glia 38:273-80CrossRef PubMed
  15.Opal SM, DePalo VA (2000) Anti-inflammatory cytokines. Chest 117:1162-172CrossRef PubMed
  16.Yang MS, Ji KA, Jeon SB, Jin BK, Kim SU, Jou I, Joe E (2006) Interleukin-13 enhances cyclooxygenase-2 expression in activated rat brain microglia: implications for death of activated microglia. J Immunol 177:1323-329CrossRef PubMed
  17.Bogdan C, Thuring H, Dlaska M, Rollinghoff M, Weiss G (1997) Mechanism of suppression of macrophage nitric oxide release by IL-13: influence of the macrophage population. J Immunol 159:4506-513PubMed
  18.Yu JT, Lee CH, Yoo KY, Choi JH, Li H, Park OK, Yan B, Hwang IK, Kwon YG, Kim YM, Won MH (2010) Maintenance of anti-inflammatory cytokines and reduction of glial activation in the ischemic hippocampal CA1 region preconditioned with lipopolysaccharide. J Neurol Sci 296:69-8CrossRef PubMed
  19.Chang CY, Kuan YH, Li JR, Chen WY, Ou YC, Pan HC, Liao SL, Raung SL, Chang CJ, Chen CJ (2013) Docosahexaenoic acid reduces cellular inflammatory response following permanent focal cerebral ischemia in rats. J Nutr Biochem 24:2127-137CrossRef PubMed
  20.Park JH, Park O, Cho JH, Chen BH, Kim IH, Ahn JH, Lee JC, Yan BC, Yoo KY, Lee CH, Hwang IK, Kwon SH, Lee YL, Won MH, Choi JH (2014) Anti-inflammatory effect of tanshinone I in neuroprotection against cerebral ischemia-reperfusion injury in the gerbil hippocampus. Neurochem Res 39:1300-312CrossRef PubMed
  21.Kim IH, Yoo KY, Park JH, Yan BC, Ahn JH, Lee JC, Kwon HM, Kim JD, Kim YM, You SG, Kang IJ, Won MH (2014) Comparison of neuroprotective effects of extract and fractions from Agarum clathratum against experimentally induced transient cerebral ischemic damage. Pharm Biol 52:335-43CrossRef PubMed
  22.Candelario-Jalil E, Alvarez D, Merino N, Leon OS (2003) Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils. Neurosci Res 47:245-53CrossRef PubMed
  23.Lee JC, Kim IH, Cho GS, Park JH, Ahn JH, Yan BC, Kwon HM, Kim YM, Cheon SH, Cho JH, Lee HY, Won MH, Seo JY (2014) Ischemic preconditioning-induced neuroprotection against transient cerebral ischemic damage via attenuating ubiquitin aggregation. J Neurol Sci 336:74-2CrossRef PubMed
  24.Kirino T, Sano K (1984) Selective vulnerability in the gerbil hippocampus following transient ischemia. Acta Neuropathol 62:201-08CrossRef PubMed
  25.Buiatti de Araujo FL, Bertolino G, Rodrigues Funayama CA, Coimbra NC, Eduardo de Araujo J (2008) Influence of treadmill training on motor performance and organization of exploratory behavior in Meriones unguiculatus with unilateral ischemic stroke: histological correlates
• 作者单位：Dong Won Kim (1) (2)
  Jae-Chul Lee (3)
  Jeong-Hwi Cho (3)
  Joon Ha Park (3)
  Ji Hyeon Ahn (3)
  Bai Hui Chen (4)
  Bich-Na Shin (4)
  Hyun-Jin Tae (5)
  Jeong Yeol Seo (1)
  Jun Hwi Cho (2)
  Il Jun Kang (6)
  Seongkweon Hong (7)
  Young-Myeong Kim (8)
  Moo-Ho Won (3)
  In Hye Kim (3)
  
  1. Department of Emergency Medicine, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon, 200-702, South Korea
  2. Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea
  3. Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea
  4. Department of Physiology, College of Medicine, Hallym University, Chuncheon, 200-702, South Korea
  5. Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, 200-702, South Korea
  6. Department of Food Science and Nutrition, Hallym University, Chuncheon, 200-702, South Korea
  7. Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea
  8. Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

Ischemic preconditioning (IPC) induced by sublethal transient cerebral ischemia could reduce neuronal damage/death following a subsequent lethal transient cerebral ischemia. We, in this study, compared expressions of interleukin (IL)-2 and tumor necrosis factor (TNF)-α as pro-inflammatory cytokines, and IL-4 and IL-13 as anti-inflammatory cytokines in the gerbil hippocampal CA1 region between animals with lethal ischemia and ones with IPC followed by lethal ischemia. In the animals with lethal ischemia, pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region were dead at 5 days post-ischemia; however, IPC protected the CA1 pyramidal neurons from lethal ischemic injury. Expressions of all cytokines were significantly decreased in the SP after lethal ischemia and hardly detected in the SP at 5 days post-ischemia because the CA1 pyramidal neurons were dead. IPC increased expressions of anti-inflammatory cytokines (IL-4 and IL-13) in the stratum pyramidale of the CA1 region following no lethal ischemia (sham-operation), and the increased expressions of IL-4 and IL-13 by IPC were continuously maintained is the SP of the CA1 region after lethal ischemia. However, pro-inflammatory cytokines (IL-2 and TNF-α) in the SP of the CA1 region were similar those in the sham-operated animals with IPC, and the IL-4 and IL-13 expressions in the SP were maintained after lethal ischemia. In conclusion, this study shows that anti-inflammatory cytokines significantly increased and longer maintained by IPC and this might be closely associated with neuroprotection after lethal transient cerebral ischemia. Keywords Sublethal and lethal ischemia CA1 region Pyramidal neurons Delayed neuronal death Inflammation