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结肠炎症后,结肠传入神经的肽含量会降低。

The peptide content of colonic afferents decreases following colonic inflammation.

作者信息

Traub R J, Hutchcroft K, Gebhart G F

机构信息

Dept. Oral and Craniofacial Biological Sciences, University of Maryland Dental School, Baltimore 21201, USA.

出版信息

Peptides. 1999;20(2):267-73. doi: 10.1016/s0196-9781(98)00157-0.

DOI:10.1016/s0196-9781(98)00157-0
PMID:10422883
Abstract

Peripheral injury produces long term changes in peptide content in dorsal root ganglion (DRG) cells that contribute to the inflammatory process in the periphery and neuronal plasticity in the spinal cord. We report here the proportion of colonic afferents labeled for calcitonin gene-related peptide (CGRP), substance P (SP) or somatostatin (Som) in the T13-L2 and L6-S2 DRG and changes in the percentage of SP or CGRP labeled afferents 6, 24, and 72 h following induction of experimental colitis. Following injection of fluorogold (FG) into the descending colon, significantly more FG labeled DRG cells were observed in the T13-L2 than L6-S2 DRG. In noninflamed rats, in both spinal regions, 60-70% of the colonic afferents that were labeled with FG were double labeled for SP. Similar results were obtained when double labeling for CGRP. Only 20-30% of the FG labeled afferents were double labeled for Som. Following experimental colitis induced by intracolonic zymosan, there was a significant decrease in the percentage of cells double labeled for SP in the T13-L2 and L6-S2 DRG at 6, 24, and 72 h. The percentage of CGRP double labeled cells was decreased in the T13-L2 DRG at all time points, but only at 24 h in the L6-S2 DRG. The cell bodies of CGRP labeled colonic afferents were significantly larger than SP or Som in control rats. Inflammation did not affect the mean size of the double labeled cells. These results suggest that colonic inflammation increases SP and CGRP release in the spinal cord and the colon that is manifest as a decrease in peptide content in the cell bodies of the colonic afferents during the first 72 h following injury.

摘要

外周损伤会导致背根神经节(DRG)细胞中肽含量发生长期变化,这有助于外周的炎症过程和脊髓中的神经元可塑性。我们在此报告了在T13-L2和L6-S2背根神经节中,降钙素基因相关肽(CGRP)、P物质(SP)或生长抑素(Som)标记的结肠传入神经的比例,以及实验性结肠炎诱导后6、24和72小时,SP或CGRP标记的传入神经百分比的变化。将荧光金(FG)注入降结肠后,在T13-L2背根神经节中观察到的FG标记的DRG细胞明显多于L6-S2背根神经节。在未发炎的大鼠中,在两个脊髓区域,用FG标记的结肠传入神经中有60-70%同时被SP双重标记。对CGRP进行双重标记时也得到了类似结果。只有20-30%的FG标记传入神经被Som双重标记。在结肠内注射酵母聚糖诱导实验性结肠炎后,在6、24和72小时时,T13-L2和L6-S2背根神经节中被SP双重标记的细胞百分比显著下降。在所有时间点,T13-L2背根神经节中CGRP双重标记细胞的百分比均下降,但在L6-S2背根神经节中仅在24小时时下降。在对照大鼠中,CGRP标记的结肠传入神经的细胞体明显大于SP或Som标记的细胞体。炎症并未影响双重标记细胞的平均大小。这些结果表明,结肠炎症会增加脊髓和结肠中SP和CGRP的释放,这表现为损伤后最初72小时内结肠传入神经细胞体中肽含量的下降。

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