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表扶留醇通过调控 PI3K/AKT 通路改善 DMBA 诱导的白化大鼠乳腺癌。

Epifriedelinol Ameliorates DMBA-Induced Breast Cancer in Albino Rats by Regulating the PI3K/AKT Pathway.

机构信息

Department of Integrative Oncology, Tian Jin Cancer Hospital Airport Hospital.

Department of Integrative Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Tianjin; Tianjin's Clinical Research Center for Cancer; Key Laboratory of Cancer Immunology and Biotherapy.

出版信息

Tohoku J Exp Med. 2022 Jul 13;257(4):283-289. doi: 10.1620/tjem.2022.J030. Epub 2022 May 20.

DOI:10.1620/tjem.2022.J030
PMID:35598971
Abstract

We evaluated the protective effect of epifriedelinol against breast cancer and postulated an underlying mechanism. Breast cancer was induced by a single dose of 50 mg/kg 7,12-Dimethylbenanthracene (DMBA), and rats were treated with 100 or 200 mg/kg (i.p.) epifriedelinol for 4 weeks. We then evaluated the effect of epifriedelinol on tumor growth, oxidative stress and serum inflammatory cytokine levels in DMBA-induced breast cancer. Protein and mRNA levels were determined using western blotting and quantitative reverse transcription polymerase chain reaction, respectively. The tumor volume and weight were significantly (p < 0.01) decreased in the epifriedelinol-treated group compared to the negative control group. Epifriedelinol decreased the altered levels of oxidative stress and serum inflammatory cytokines in rats with DMBA-induced breast cancer. Protein levels of PI3K, AKT and mTOR and mRNA levels of PI3K, AKT, Map3k1, Erbb2 and Pdk1 were decreased in the mammary tissue of epifriedelinol-treated rats with DMBA-induced breast cancer. Apoptosis was significantly induced in the epifriedelinol-treated group compared to the negative control group. In conclusion, epifriedelinol ameliorates DMBA-induced breast cancer by regulating the PI3K/AKT pathway.

摘要

我们评估了表friedelinol 对乳腺癌的保护作用,并提出了一种潜在的机制。乳腺癌是由单次给予 50mg/kg 7,12-二甲基苯并蒽(DMBA)诱导的,大鼠用 100 或 200mg/kg(ip)表friedelinol 治疗 4 周。然后,我们评估了表friedelinol 对 DMBA 诱导的乳腺癌中肿瘤生长、氧化应激和血清炎症细胞因子水平的影响。使用 Western blot 和定量逆转录聚合酶链反应分别测定蛋白质和 mRNA 水平。与阴性对照组相比,表friedelinol 处理组的肿瘤体积和重量显著(p<0.01)降低。表friedelinol 降低了 DMBA 诱导的乳腺癌大鼠氧化应激和血清炎症细胞因子的改变水平。PI3K、AKT 和 mTOR 的蛋白水平以及 PI3K、AKT、Map3k1、Erbb2 和 Pdk1 的 mRNA 水平在 DMBA 诱导的乳腺癌大鼠的乳腺组织中降低。与阴性对照组相比,表friedelinol 处理组的细胞凋亡明显增加。总之,表friedelinol 通过调节 PI3K/AKT 通路改善 DMBA 诱导的乳腺癌。

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