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糙米醋“黑醋”提取物可抑制由氧化偶氮甲烷诱导的结肠异常隐窝灶的形成。

Extract of vinegar "Kurosu" from unpolished rice inhibits the development of colonic aberrant crypt foci induced by azoxymethane.

作者信息

Shimoji Y, Sugie S, Kohno H, Tanaka T, Nanda K, Tamura Y, Nishikawa Y, Hayashi R, Uenakai K, Ohigashi H

机构信息

Research Center, Tamanoi Vinegar Co. Ltd., Yamatokoriyama, Nara, Japan.

出版信息

J Exp Clin Cancer Res. 2003 Dec;22(4):591-7.

Abstract

The modifying effects of administrating an ethyl acetate extract of "Kurosu" (EK), a vinegar made from unpolished rice, on development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) were investigated in male F344 rats. We also assessed the effects of EK on proliferating cell nuclear antigen (PCNA) index in ACF, prostaglandin (PG) E2 expression in the colonic mucosa and activities of detoxifying enzymes of glutathione S-transferase (GST) and quinone reductase (QR) in the liver. To induce ACF, rats were given two weekly subcutaneous injections of AOM (20 mg/kg body wt). They also received drinking water containing 0, 0.05, 0.1 or 0.2% EK for 4 weeks, starting 1 week before the first dosing of AOM. AOM exposure produced 140 +/- 23 ACF/rat at the end of the study (week 4). EK administration dose-dependently inhibited ACF formation and inhibition by 0.2% EK was statistically significant (P < 0.002). Treatment with EK significantly lowered PCNA index in ACF and reduced PGE2 content in the colonic mucosa, while EK elevated liver GST and QR activities. These findings suggest that EK may be effective for inhibiting colonic ACF, through induction of liver GST and QR and possibly alteration of PGE2 production.

摘要

在雄性F344大鼠中,研究了由糙米制成的醋“黑醋”的乙酸乙酯提取物(EK)对氧化偶氮甲烷(AOM)诱导的结肠异常隐窝灶(ACF)发生的调节作用。我们还评估了EK对ACF中增殖细胞核抗原(PCNA)指数、结肠黏膜中前列腺素(PG)E2表达以及肝脏中谷胱甘肽S-转移酶(GST)和醌还原酶(QR)解毒酶活性的影响。为了诱导ACF,给大鼠每周皮下注射两次AOM(20mg/kg体重)。从首次给予AOM前1周开始,它们还饮用含0、0.05、0.1或0.2% EK的饮用水,持续4周。在研究结束时(第4周),AOM暴露使每只大鼠产生140±23个ACF。给予EK剂量依赖性地抑制ACF形成,0.2% EK的抑制作用具有统计学意义(P<0.002)。用EK处理可显著降低ACF中的PCNA指数,并降低结肠黏膜中的PGE2含量,而EK可提高肝脏GST和QR活性。这些发现表明,EK可能通过诱导肝脏GST和QR以及可能改变PGE2的产生来有效抑制结肠ACF。

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