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大鼠胃溃疡愈合过程中肝细胞生长因子的产生与激活

Production and activation of hepatocyte growth factor during the healing of rat gastric ulcers.

作者信息

Kinoshita Y, Kishi K, Asahara M, Matasushima Y, Wang H Y, Miyazawa K, Kitamura N, Chiba T

机构信息

Department of Medicine, Kobe University School of Medicine, Japan.

出版信息

Digestion. 1997;58(3):225-31. doi: 10.1159/000201448.

DOI:10.1159/000201448
PMID:9243117
Abstract

The hepatocyte growth factor has been reported to be a potent mitogen of various epithelial cells, including gastric mucosal cells. Therefore, production and activation of hepatocyte growth factor in the gastric wall were investigated to speculate on the possible role of this factor in the healing of gastric ulcer in rats. Indomethacin-induced gastric mucosal lesions and acetic acid induced ulcers were employed as models of acute gastric lesions and chronic ulcer, respectively. Immunoblot and Northern blot analyses indicate that experimentally induced gastric mucosal lesions stimulate not only the production of hepatocyte growth factor, but also the conversion to its active form. This conversion was accompanied by increased gene expression of hepatocyte growth factor activator in the stomach. In rats with acute mucosal lesions, hepatocyte growth factor activator mRNA was most abundant 6 h after induction of mucosal lesions. On the other hand, hepatocyte growth factor and hepatocyte growth factor activator mRNA levels were elevated until 15 days after the induction of chronic ulcers. In summary, it has been clarified that not only production, but also activation of hepatocyte growth factor is stimulated during gastric ulcer healing.

摘要

据报道,肝细胞生长因子是包括胃黏膜细胞在内的多种上皮细胞的强效促有丝分裂原。因此,研究了胃壁中肝细胞生长因子的产生和激活情况,以推测该因子在大鼠胃溃疡愈合中的可能作用。分别采用吲哚美辛诱导的胃黏膜损伤和乙酸诱导的溃疡作为急性胃损伤和慢性溃疡的模型。免疫印迹和Northern印迹分析表明,实验诱导的胃黏膜损伤不仅刺激肝细胞生长因子的产生,还刺激其向活性形式的转化。这种转化伴随着胃中肝细胞生长因子激活剂基因表达的增加。在急性黏膜损伤的大鼠中,黏膜损伤诱导后6小时肝细胞生长因子激活剂mRNA最为丰富。另一方面,在慢性溃疡诱导后15天内,肝细胞生长因子和肝细胞生长因子激活剂mRNA水平一直升高。总之,已经明确在胃溃疡愈合过程中,肝细胞生长因子不仅产生受到刺激,其激活也受到刺激。

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