期刊文献+

外源性bFGF对缺氧缺血新生大鼠脑c-Fos表达影响的研究

STUDY ON EFFECTS OF EXOGENOUS BASIC FTOROBLAST GROWTH FAC- TOR ON C - FOS EXPRESSION IN THE NEONATAL RAT BRAIN IN HYPOXIC - ISCHEMIC BRAIN DAMAGE
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摘要 探讨外源性碱性成纤维细胞生长因子(hFGF),对缺氧缺血性脑损伤(HIBD)新生大鼠脑c-fos基因蛋白产物(c-Fos)表达影响,研究原癌基因c-fos表达与HIBD的关系,采用免疫组织化学染色及定量图像分析方法,观察c-Fos表达强度、染色灰度及面积的变化。结果显示:正常生后7-14 d新生大鼠脑有c-Fos表达,以生后10 d最为明显;缺氧缺血20 min后即刻c-Fos表达增强,并于缺氧缺血后4 h达高峰,持续至72 h;脑内不同部位c-Fos表达时间、强度、灰度及面积不同。连续腹腔注射外源性bFGF 3 d后鼠脑c-Fos表达增强。结论:外源性bFGF可增强HIBD新生大鼠脑c-Fos的表达,bFGF及c-fos基因可能参与HIBD修复的病理生理过程。 To investigate the effects of exogenous basic fibroblast growth factor (bFGF) on c - fos gene protein expression (c - Fos) during hypoxic - ischeniic brain damage (HIBD) in neonatal rat brain and the relationship between c - Fos expression and HIBD. eicemunatin on c - Fos expression was done by immuno-histochemical staining and image quantitative analysis. Results showed that c - Fos was expressed in brain of normal neonate rats on postnatal day (PND) 7 to 14 with maximal expression on PND10. c - Fos expression were increased in different parts of brain immediately after hypoxia - ischemia (HI) for 20 min and peaked at 4 hours, and thereafter, its density gradually decreased, which lasted until 72 hr after HI insult, c - Fos expression was obvious in Ⅱ-Ⅴ layers of cortex, CA1 and DG of hippocampus, respectively . The time course, density of the expression, gray degree and area of c - Fos - positive cells varied with different cerebral areas, and that of thalamus was slightly increased. Expression of c - Fos was up -regulated by intraperitoneal bFGF administration. Conclusions: Exogenous bFGF up - regulates the expression of c - fos gene protein in neonate rat brain in HIBD. bFGF and c - fos gene may take part in pathophysiological process of HIBD.
出处 《新生儿科杂志》 2003年第1期15-19,共5页 The Journal of Neonatology
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  • 1Joyce MP, Barr GA. Ontogeny of Fos protein-like immunreactivityin the suprchiasmatic nucleus. Synaps 1995, 21(1): 54-59.
  • 2Walton M, Connor B, Lawlor P, et al. Neonatal death and survival in two models of hypoxic-ischemic brain damage. Brain Res Brain Res Rev 1999, 29(2-3 ): 137-168.
  • 3Cho S, Park EM, Kim Y, et al. Early c- fos induction after cerebral ischemia: a possible neuroprotective role. J Cereb Blood Flow Metab 2001, 21(5): 550-556.
  • 4Lee MC, Rho JL,kim MK, et al.e-Jun expression and apoptodic cell death in kainate- induced temporal lobe epilepsy.J Korean Med Sci 2001, 16(5): 649-656.
  • 5Liu x. Zhu XZ. Increased expression and nuclear accumulation of bFGF in primary cultured astrocytes following ischemic-like insults. Brain Res Mol Brain Res 1999, 71(2): 171- 177.
  • 6Iwata A, Masago A, Yamada K. Expression of basic fibroblast growth factor mRNA after transient focal ischemia: Comparison with expression of c-fos, c-jun, ang hsp70 mRNA. J Neurotrauma 1997,14(4): 201-210.
  • 7Ma J, QinJ, Hirt L, etal. Synagistic protective effect of caspase in hibitors and bFGF against brain injury induced by transient focal ischemia. Br J Pharmacol 2001, 133(3): 345-350.
  • 8Ay I, Sugimori H, Finklestein SP. Intravenous bFG F decreases DNA fragmentation and prevents down-regulation of bcl-2 expression in the ischemic brain following middle cerebral atery occlusion in rats. Brain Res Mol Brain Res 2001, 87(1): 71-80.
  • 9Caneras I, Rich CB, Jaworski JA, et al. Functional compo- ents of basic fibroblast growth factor signaling that inhibit lung elastin gene expression. Am J Physiol Lung Cell Mlo Physiol 2001, 281(4): L766-755.

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