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逍遥解郁方通过PI3K/Akt信号通路减轻乳腺导管上皮不典型增生

Xiaotan Jieyu Prescription Alleviates Breast Precancerous Lesions through PI3K/Akt Signaling Pathway.

作者信息

Zhao Jing, Pang Tao, Jiao Jian-Peng, Wang Bin, Liu Xuan, Xiu Li-Juan, Sun Da-Zhi, Yue Xiao-Qiang, Yu Chao-Qin

机构信息

Department of Traditional Chinese Medicine, Changzheng Hospital, Navy Medical University, Shanghai 200003, China.

Department of Pharmacy, Changzheng Hospital, Navy Medical University, Shanghai 200003, China.

出版信息

Evid Based Complement Alternat Med. 2020 Aug 12;2020:4129461. doi: 10.1155/2020/4129461. eCollection 2020.

Abstract

METHODS

The successfully established breast precancerous lesion rat model and normal healthy rats were randomly assigned into the blank (BLA), model (MOD), XTJY-low (LD), XTJY-medium (MD), XTJY-high (HD), and tamoxifen (TAM) groups. Different concentrations of XTJY and saline were supplied by intragastric administration for 4 consecutive weeks to assess the protective effect of XTJY on the progress of the breast precancerous lesion in rats involving the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway.

RESULTS

In this study, it determined that 10 mg/each rat DMBA-combined estrogen and progesterone induction for 10 weeks was the optimal condition for the establishment of the breast precancerous lesion rat model. In vivo administration of XTJY or TAM was found to inhibit the development of the breast precancerous lesion, and the occurrence rate of breast invasive carcinomas was decreased by about 50%. Furthermore, XTJY or TAM markedly reduced protein expressions of PI3K and p-Akt and increased protein expressions of PTEN.

CONCLUSION

These data indicated that XTJY can significantly alleviate the development of breast precancerous lesions by inhibiting the activation of the PI3K/Akt signaling pathway. XTJY may be a promising drug for the treatment of precancerous lesions in breast cancer.

摘要

方法

将成功建立的乳腺癌前病变大鼠模型和正常健康大鼠随机分为空白组(BLA)、模型组(MOD)、消癌解毒方低剂量组(LD)、消癌解毒方中剂量组(MD)、消癌解毒方高剂量组(HD)和他莫昔芬组(TAM)。连续4周通过灌胃给予不同浓度的消癌解毒方和生理盐水,以评估消癌解毒方对大鼠乳腺癌前病变进展的保护作用,该作用涉及磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)信号通路。

结果

本研究确定,每只大鼠10 mg二甲基苯并蒽联合雌激素和孕激素诱导10周是建立乳腺癌前病变大鼠模型的最佳条件。发现体内给予消癌解毒方或他莫昔芬可抑制乳腺癌前病变的发展,乳腺浸润癌的发生率降低约50%。此外,消癌解毒方或他莫昔芬显著降低PI3K和p-Akt的蛋白表达,并增加PTEN的蛋白表达。

结论

这些数据表明,消癌解毒方可通过抑制PI3K/Akt信号通路的激活来显著缓解乳腺癌前病变的发展。消癌解毒方可能是一种有前途的治疗乳腺癌前病变的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95e/7441443/f78538e69382/ECAM2020-4129461.001.jpg

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