Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
复制标题
DOI：
10.1111/j.1349-7006.2004.tb03236.x
复制
发表时间：
2004-06-01
期刊：
影响因子：
5.7
通讯作者：
Tanaka, T
中科院分区：
文献类型：
--
作者：
Kohno, H;Suzuki, R;Tanaka, T
石榴籽油（PGO）含有70%以上的顺式(c)、反式(t)11、共轭亚麻酸（CLN） 13-18:3。我们之前的短期实验表明，含有丰富c9、t11、t13-CLN的苦椒籽油（BMO）可以抑制偶氮甲烷（AOM）诱导的结肠异常隐窝灶（ACF）的发生。在本研究中，我们研究了膳食中PGO对aom诱导的结肠恶性肿瘤发展的影响，并将其与共轭亚油酸（CLA）的影响进行了比较。为诱导6周龄雄性F344大鼠结肠肿瘤，每周皮下注射AOM （20 mg/kg体重）1次，连续注射2周。在AOM治疗前一周，他们开始食用含有0.01%，0.1%或1% PGO或1% CLA的饮食，持续32周。生物实验结束后（32周）对结肠肿瘤进行组织病理学评估。在第32周，AOM暴露导致结肠腺癌的发生率为81%，多样性为1.88 +/- 1.54。管理PGO饮食中显著地抑制发生率(PGO中耳炎+ 0.01%,44%,P < 0.05; PGO中耳炎+ 0.1%,38%,P < 0.01; PGO中耳炎+ 1%,56%)和多重性(PGO中耳炎+ 0.01%,0.56 + / - 0.73,P < 0.01; PGO中耳炎+ 0.1%,0.50 + / - 0.73,P < 0.005; PGO中耳炎+ 1%,0.88 + / - 0.96,P < 0.05)结肠腺癌,尽管明显的剂量反应关系没有观察到这些剂量水平。CLA喂养也轻微但不显著地降低了结肠腺癌的发生率和多样性。PGO对结肠肿瘤的抑制作用与结肠黏膜和肝脏脂质部分CLA含量的增加有关（c9, t11, 18:2）。此外，饮食中添加PGO可提高非肿瘤粘膜中过氧化物酶体增殖物激活受体(PPAR) γ蛋白的表达。这些结果表明，富含c9、t11、c13-CLN的PGO可以抑制aom诱导的结肠癌，其抑制作用部分与结肠和肝脏中CLA含量增加和/或结肠黏膜中PPARgamma蛋白表达增加有关。
Pomegranate (Punica granatum L.) seed oil (PGO) contains more than 70% cis(c),trans(t)11, c13-18:3 as conjugated linolenic acids (CLN). Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in c9, t11, t13-CLN, inhibited the occurrence of colonic aberrant crypt foci (ACF) induced by azoxymethane (AOM). In this study, we investigated the effect of dietary PGO on the development of AOM-induced colonic malignancies and compared it with that of conjugated linoleic acid (CLA). To induce colonic tumors, 6-week old male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks. One week before the AOM treatment they were started on diet containing 0.01%, 0.1%, or 1% PGO or 1% CLA for 32 weeks. Upon termination of the bioassay (32 weeks) colon tumors were evaluated histopathologically. AOM exposure produced colonic adenocarcinoma with an incidence of 81% and multiplicity of 1.88 +/- 1.54 at week 32. Administration of PGO in the diet significantly inhibited the incidence (AOM + 0.01% PGO, 44%, P < 0.05; AOM + 0.1% PGO, 38%, P < 0.01; AOM + 1% PGO, 56%) and the multiplicity (AOM + 0.01% PGO, 0.56 +/- 0.73, P < 0.01; AOM + 0.1% PGO, 0.50 +/- 0.73, P < 0.005; AOM + 1% PGO, 0.88 +/- 0.96, P < 0.05) of colonic adenocarcinomas, although a clear dose-response relationship was not observed at these dose levels. CLA feeding also slightly, but not significantly, reduced the incidence and multiplicity of colonic adenocarcinomas. The inhibition of colonic tumors by PGO was associated with an increased content of CLA (c9, t11, 18:2) in the lipid fraction of colonic mucosa and liver. Also, administration of PGO in the diet elevated expression of peroxisome proliferator-activated receptor (PPAR) gamma protein in the non-tumor mucosa. These results suggest that PGO rich in c9, t11, c13-CLN can suppress AOM-induced colon carcinogenesis, and the inhibition is associated in part with the increased content of CLA in the colon and liver and/or increased expression of PPARgamma protein in the colon mucosa.