Mulberry leaf extract inhibits obesity and protects against diethylnitrosamine-induced hepatocellular carcinoma in rats

IF 3.3 3区 医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE
Yun-Ching Chang , Meng-Hsun Yu , Hui-Pei Huang , Dong-Hui Chen , Mon-Yuan Yang , Chau-Jong Wang
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Abstract

Mulberry leaf has been recognized as a traditional Chinese medicinal plant, which was distributed throughout the Asia. The aqueous extract of mulberry leaf extract (MLE) has various biologically active components such as polyphenols and flavonoids. However, the inhibitory effect of MLE in hepatocarcinogenesis is poorly understood. In this study, we determined the role of MLE supplementation in preventing hepatocarcinogenesis in a carcinogen-initiated high-fat diet (HFD)-promoted Sprague-Dawley (SD) rat model. The rats were fed an HFD to induce obesity and spontaneous hepatomas by administering 0.01% diethylnitrosamine (DEN) in their drinking water for 12 weeks (HD group), and also to fed MLE through oral ingestion at daily doses of 0.5%, 1%, or 2%. At the end of the 12-week experimental period, the liver tumors were analyzed to identify markers of oxidative stress and antioxidant enzyme activities, and their serum was analyzed to determine their nutritional status and liver function. Histopathological analysis revealed that MLE supplementation significantly suppressed the severity and incidence of hepatic tumors. Furthermore, compared with the HFD + DEN groups, the expression of protein kinase C (PKC)-α and Rac family small GTPase 1 (Rac1) was lower in the MLE groups. These findings suggest that MLE prevents obesity-enhanced, carcinogen-induced hepatocellular carcinoma development, potentially through the protein kinase C (PKC)α/Rac1 signaling pathway. MLE might be an effective chemoprevention modality for nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH)-related hepatocarcinogenesis.

Abstract Image

桑叶提取物可抑制肥胖,并保护大鼠免受亚硝胺诱发的肝细胞癌的危害
桑叶是一种传统的中药植物,分布于亚洲各地。桑叶水提取物(MLE)具有多种生物活性成分,如多酚和类黄酮。然而,桑叶提取物对肝癌发生的抑制作用却鲜为人知。在这项研究中,我们确定了补充 MLE 在致癌物质引发的高脂饮食(HFD)促进的 Sprague-Dawley (SD)大鼠模型中预防肝癌发生的作用。通过在饮用水中添加 0.01% 的二乙基亚硝胺 (DEN),给大鼠喂食高脂饮食诱发肥胖和自发性肝癌,为期 12 周(HD 组),同时通过口服 MLE,每日剂量为 0.5%、1% 或 2%。12 周实验结束时,对肝脏肿瘤进行分析,以确定氧化应激和抗氧化酶活性的标记物,并对血清进行分析,以确定其营养状况和肝功能。组织病理学分析表明,补充 MLE 能明显抑制肝肿瘤的严重程度和发病率。此外,与高纤维食物组+ DEN组相比,MLE组中蛋白激酶C(PKC)-α和Rac家族小GTP酶1(Rac1)的表达较低。这些研究结果表明,MLE可通过蛋白激酶C(PKC)α/Rac1信号通路阻止肥胖增强的、由致癌物质诱发的肝细胞癌的发展。MLE可能是一种有效的化学预防非酒精性脂肪肝(NAFLD)/非酒精性脂肪性肝炎(NASH)相关肝癌发生的方法。
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来源期刊
Journal of Traditional and Complementary Medicine
Journal of Traditional and Complementary Medicine Medicine-Complementary and Alternative Medicine
CiteScore
9.30
自引率
6.70%
发文量
78
审稿时长
66 days
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