Format

Send to

Choose Destination
Environ Toxicol Pharmacol. 2015 Mar;39(2):990-6. doi: 10.1016/j.etap.2015.02.014. Epub 2015 Mar 10.

Anti-hyperplasia effects of Rosa rugosa polyphenols in rats with hyperplasia of mammary gland.

Author information

1
Department of Pharmacy, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; College of Pharmacy, Hubei University of Chinese Medicine, Wuhan, China.
2
Department of Pharmacy, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
3
Department of Pharmacy, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: shanghuchuan@126.com.
4
Department of Pharmacy, Wuhan Sixth Hospital, Wuhan, China.

Abstract

Rosa rugosa (Thunb.) is used in Chinese traditional medicine with the functions of promoting blood circulation, relieving the depressed liver and attenuating breast disorders. This study was to investigate the anti-hyperplasia effects of the polyphenols-rich fraction from R. rugosa (FRR) in rat. Rat model of hyperplasia of mammary gland (HMG) was induced by intramuscularly injected with estrogen (0.5mg/kg/d) for 25 days, and followed with progestogen (5mg/kg/d) for another 5 days. Meanwhile, FRR was orally given for 30 days. Then, the levels of estradiol and oxidative stress were assessed. The mammary expressions of AKT and JNK were evaluated by Western blot analysis. The expressions of NFκB-p65, COX-2 and VEGF were measured by immunohistochemical analysis. The whole results indicated that FRR could exert anti-hyperplasia effects in rat via modulating the mammary expression of JNK and AKT, as well as alleviating the NFκB related oxidative stress and inflammatory responses.

KEYWORDS:

Hyperplasia of mammary gland; Inflammatory responses; Oxidative stress; Rosa rugosa (Thunb.)

PMID:
25828785
DOI:
10.1016/j.etap.2015.02.014
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center