Relationship between apoptosis and lipid absorption in rat intestine

大鼠肠道细胞凋亡与脂质吸收的关系

• 批准号: 10470137
• 负责人: FUJIMOTO Kazuma
• 金额: $ 5.5万
• 依托单位: Saga Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10470137/
• 关键词: cell death; ischemia-reperfusion; intestinal function; lipid absorption; long chain fatty acids; immunohistochemical stain; 免疫組織染色; 中性脂肪; 絨毛; 糖尿病; 粘膜肥厚; 摂食行動; 増殖因子

The purpose of this study is to assess a relationship between apoptosis and lipid absorption in rat intestinal mucosa after ischemia-reperfusion. In intestinal lymph fistula rats, the superior mesenteric artery was isolated and occluded for 15 min or 60 min. After ischemia-reperfusion, a lipid test meal containing radioactive triolein was infused at 3 ml per h for 8 h. Radioactive lipid in lymph, lumen, intestinal wall, portal and systemic blood, epididymal fat pads and liver was determined. Ratios of fragmented DNA to total DNA, electrophoresis, and immunohistochemical staining were examined after ischemia-reperfusion for evaluation of mucosal apoptosis. Lymph radioactive lipid output was markedly depressed in the experimental rats 3 and 6 h after reperfusion. This reduction in lipid output in lymph appeared to be the result of an increased portal transport of the infused radioactive lipid rather than a deficiency of digestion or absorption of infused triolein. Percent fragmented DNA significantly increased just after ischemia and peaked at 1 h after reperfusion in the jejunum and ileum. These increases were significantly higher in the 60 min ischemia group as compared to the 15 min ischemia group. This increase of apoptosis recovered 6 h after reperfusion. The results were corroborated by Percent fragmented DNA significantly increased just after ischemia and peaked at 1 h after reperfusion in the jejunum and ileum. These increases were significantly higher in the 60 min ischemia group as compared to the 15 min ischemia group. The results were corroborated by histological evaluations of the intestine under the same conditions. The intestinal lipid absorption is sensitive to the deleterious effects of ischemia followed by reperfusion and therefore it may be used as a functional assessment of the small intestinal apoptosis after ischemia-reperfusion induced injuries.

本研究旨在探讨缺血再灌注后大鼠肠黏膜细胞凋亡与脂质吸收的关系。在肠淋巴瘘大鼠中，分离肠系膜上动脉并闭塞15 min或60 min。缺血再灌注后，以每小时3 ml的速度注入含放射性三油酸的脂质试验粉，持续8 h。测定淋巴、管腔、肠壁、门静脉和全身血液、附睾脂肪垫和肝脏中的放射性脂质。缺血再灌注后检测碎片DNA与总DNA的比值、电泳和免疫组织化学染色，以评估粘膜凋亡。再灌注后3、6 h，实验大鼠淋巴放射性脂质输出明显下降。淋巴中脂质输出的减少似乎是由于注入的放射性脂质的门静脉运输增加，而不是由于注入的三油苷消化或吸收不足。空肠和回肠DNA片段率在缺血后显著增加，再灌注后1 h达到峰值。这些增加在60分钟缺血组明显高于15分钟缺血组。再灌注6小时后，细胞凋亡的增加恢复。空肠和回肠DNA片段率在缺血后显著升高，再灌注后1 h达到峰值。这些增加在60分钟缺血组明显高于15分钟缺血组。在相同条件下对肠道的组织学评价证实了这一结果。小肠脂质吸收对缺血再灌注后的有害影响敏感，可作为缺血再灌注损伤后小肠细胞凋亡的功能评价指标。

项目成果

Noda T,et al.: "Suppression of apoptosis is responsible for increased thickness of intestinal mucosa is strptozotocin induced diabetic rats"Metabolism. (in press).

Noda T等人：“链脲佐菌素诱导的糖尿病大鼠肠粘膜厚度增加是细胞凋亡受到抑制的原因”代谢。

Kashiwagi Y,et al.: "Loss of diurnal variation of ornithine decarboxylase and apoptosis in small intestine of Mongolian gerbils"J.Gastroenterol.. (in press).

Kashiwagi Y 等人：“蒙古沙鼠小肠鸟氨酸脱羧酶昼夜变化的丧失和细胞凋亡”J.Gastroenterol..（出版中）。

Kashiwagi Y., et al.: "Loss of diurnal variation of ornithine decarboxylase and apoptosis in small intestine of Mongolian gerbils"J. Gastroenterol.. (in press).

Kashiwagi Y., et al.：“蒙古沙鼠小肠鸟氨酸脱羧酶昼夜变化的丧失和细胞凋亡”J.

Yoshida, et al.: "Histaminergic effect on apoptosis of rat small intestinal mucosa after ischemia-reperfusion"Dig. Dis. Sci. (in press).

Yoshida 等人：“组胺能对缺血再灌注后大鼠小肠粘膜细胞凋亡的影响”Dig。

Noda T., et al.: "Suppression of apoptosis is responsible for increased thickness of intestinal mucosa is strptozotocin induced diabetic rats"Metabolism. (in press).

Noda T.等人：“链脲佐菌素诱导的糖尿病大鼠肠粘膜厚度增加是由细胞凋亡的抑制引起的”代谢。