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难消化物质减弱了禁食大鼠空肠黏膜细胞凋亡的变化。

Indigestible material attenuated changes in apoptosis in the fasted rat jejunal mucosa.

作者信息

Kakimoto Takashi, Fujise Takehiro, Shiraishi Ryosuke, Kuroki Tsukasa, Park Jae Myung, Ootani Akifumi, Sakata Yasuhisa, Tsunada Seiji, Iwakiri Ryuichi, Fujimoto Kazuma

机构信息

Department of Intestinal Medicine, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501, Japan.

出版信息

Exp Biol Med (Maywood). 2008 Mar;233(3):310-6. doi: 10.3181/0708-RM-228.

Abstract

We have previously demonstrated that fasting induced apoptosis and decreased cell proliferation in the rat intestinal mucosa. The aim was to investigate the effect of expanded polystyrene as indigestible material on apoptosis and cell proliferation in rat small intestinal mucosa during fasting. Male SD rats were divided into 3 groups. The first group was fed with chow and water ad libitum. The second group fasted for 72 hrs. The third group was fasted for 24 hrs and was fed expanded polystyrene. Intestinal apoptosis was evaluated by percent fragmented DNA assay, terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end-labeling (TUNEL) staining, and caspase-3 assay. Cell proliferation was analyzed by 5-bromo-2'-deoxyuridine (5-BrdU) uptake. Truncal vagotomy was performed to evaluate a role of the central nervous system. In the 72-hr fasted rat, mucosal height of the rat jejunum was decreased to 73% of that in rats fed ad libitum, and this decrease was partly restored to 90% in rats fed expanded polystyrene. The fragmented DNA was increased in fasted rats (28.0%) when compared with that in rats fed ad libitum (2.6%). The increase in fragmented DNA in fasted rats was recovered by feeding them expanded polystyrene (8.3%). TUNEL staining confirmed this result. The effect of polystyrene on apoptosis was decreased by truncal vagotomy. Expression of cleaved caspase-3 was increased in fasted rats, which was then decreased by feeding of expanded polystyrene. In contrast to apoptosis, feeding of expanded polystyrene had no reconstructive effect on 5-BrdU uptake in the intestinal epithelium, which was decreased by fasting to 60% of that in rats fed ad libitum. In conclusion, feeding of indigestible material partly restored the decrease in intestinal mucosal length in the fasted rats through the apoptotic pathway without any influence on BrdU uptake. Further exploration focused on the mechanism of this effect of indigestible material is required.

摘要

我们之前已经证明,禁食会诱导大鼠肠黏膜细胞凋亡并降低细胞增殖。本研究旨在探讨不可消化材料发泡聚苯乙烯对禁食期间大鼠小肠黏膜细胞凋亡和细胞增殖的影响。雄性SD大鼠分为3组。第一组大鼠自由进食普通饲料并饮水。第二组大鼠禁食72小时。第三组大鼠禁食24小时后喂食发泡聚苯乙烯。通过DNA片段化百分比分析、末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)染色以及半胱天冬酶-3检测来评估肠道细胞凋亡情况。通过5-溴-2'-脱氧尿苷(5-BrdU)掺入法分析细胞增殖情况。进行迷走神经切断术以评估中枢神经系统的作用。在禁食72小时的大鼠中,空肠黏膜高度降至自由进食大鼠的73%,而喂食发泡聚苯乙烯的大鼠这一降低情况部分恢复至90%。与自由进食大鼠(2.6%)相比,禁食大鼠的DNA片段化增加(28.0%)。喂食发泡聚苯乙烯可使禁食大鼠DNA片段化增加情况恢复(8.3%)。TUNEL染色证实了这一结果。迷走神经切断术可降低聚苯乙烯对细胞凋亡的影响。禁食大鼠中裂解的半胱天冬酶-3表达增加,喂食发泡聚苯乙烯后其表达降低。与细胞凋亡情况相反,喂食发泡聚苯乙烯对肠道上皮细胞中5-BrdU掺入无重建作用,禁食可使其降至自由进食大鼠的60%。总之,喂食不可消化材料通过凋亡途径部分恢复了禁食大鼠肠黏膜长度的减少,且对BrdU掺入无任何影响。需要进一步探索不可消化材料这种作用的机制。

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