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	Flavonoid genistein protects bone marrow sinusoidal blood vessels from damage by methotrexate therapy in rats
	Hassanshahi, Mohammadhossein1,2; Su, Yu-Wen1,2; Khabbazi, Samira1,2; Fan, Chia-Ming1,2; Chen, Ke-Ming3; Wang, Ju-Fang4; Qian, Airong5; Howe, Peter R.6,7; Yan, De-Wen8; Zhou, Hou-De9
刊名	JOURNAL OF CELLULAR PHYSIOLOGY
	2019-07-01
卷号	234期号:7页码:11276-11286
关键词	angiogenesis apoptosis bone marrow sinusoidal endothelial cells (BM SECs) genistein
ISSN号	0021-9541
DOI	10.1002/jcp.27785
通讯作者	Xian, Cory J.(cory.xian@unisa.edu.au)
英文摘要	Cancer chemotherapy can cause significant damage to the bone marrow (BM) microvascular (sinusoidal) system. Investigations must now address whether and how BM sinusoidal endothelial cells (SECs) can be protected during chemotherapy. Herein we examined the potential protective effects of genistein, a soy-derived flavonoid, against BM sinusoidal damage caused by treatment with methotrexate (MTX). The groups of young adult rats were gavaged daily with genistein (20mg/kg) or placebo. After 1 week, rats also received daily injections of MTX (0.75mg/kg) or saline for 5 days and were killed after a further 4 days. Histological analyses showed that BM sinusoids were markedly dilated (p<0.001) in the MTX-alone group but were unaffected or less dilated in the genistein+MTX group. In control rats, genistein significantly enhanced expression of vascular endothelial growth factor (VEGF; p<0.01), particularly in osteoblasts, and angiogenesis marker CD31 (p<0.001) in bone. In MTX-treated rats, genistein suppressed MTX-induced apoptosis of BM SECs (p<0.001 vs MTX alone group) and tended to increase expression of CD31 and VEGF (p<0.05). Our in vitro studies showed that genistein in certain concentrations protected cultured SECs from MTX cytotoxic effects. Genistein enhanced tube formation of cultured SECs, which is associated with its ability to induce expression of endothelial nitric oxide synthase and production of nitric oxide. These data suggest that genistein can protect BM sinusoids during MTX therapy, which is associated, at least partially, with its indirect effect of promoting VEGF expression in osteoblasts and its direct effect of enhancing nitric oxide production in SECs.
收录类别	SCI
WOS关键词	NITRIC-OXIDE SYNTHASE ; PHYTOESTROGEN GENISTEIN ; EXPRESSION ; ANGIOGENESIS ; CHEMOTHERAPY ; MECHANISMS ; CELLS ; DIFFERENTIATION ; HEMATOPOIESIS ; REGENERATION
WOS研究方向	Cell Biology ; Physiology
WOS类目	Cell Biology ; Physiology
语种	英语
出版者	WILEY
WOS记录号	WOS:000462645700127
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2555508
专题	寒区旱区环境与工程研究所
通讯作者	Xian, Cory J.
作者单位	1.Univ South Australia, Sch Pharm & Med Sci, GPO Box 2471, Adelaide, SA 5001, Australia 2.Univ South Australia, UniSA Canc Res Inst, GPO Box 2471, Adelaide, SA 5001, Australia 3.Lanzhou Gen Hosp CPLA, Inst Orthopaed, Lanzhou, Gansu, Peoples R China 4.Chinese Acad Sci, Inst Modern Phys, Lanzhou, Gansu, Peoples R China 5.Northwestern Polytech Univ, Key Lab Space Biosci & Biotechnol, Sch Life Sci, Lab Bone Metab, Xian, Shaanxi, Peoples R China 6.Univ Southern Queensland, Inst Resilient Reg, Springfield, Qld, Australia 7.Univ Newcastle, Clin Nutr Res Ctr, Callaghan, NSW, Australia 8.Shenzhen Univ, Affiliated Hosp 1, Dept Endocrinol, Shenzhen, Guangdong, Peoples R China 9.Cent S Univ, Xiangya Hosp 2, Natl Clin Res Ctr Metab Dis, Dept Endocrinol & Metab, Changsha, Hunan, Peoples R China
推荐引用方式 GB/T 7714	Hassanshahi, Mohammadhossein,Su, Yu-Wen,Khabbazi, Samira,et al. Flavonoid genistein protects bone marrow sinusoidal blood vessels from damage by methotrexate therapy in rats[J]. JOURNAL OF CELLULAR PHYSIOLOGY,2019,234(7):11276-11286.
APA	Hassanshahi, Mohammadhossein.,Su, Yu-Wen.,Khabbazi, Samira.,Fan, Chia-Ming.,Chen, Ke-Ming.,...&Xian, Cory J..(2019).Flavonoid genistein protects bone marrow sinusoidal blood vessels from damage by methotrexate therapy in rats.JOURNAL OF CELLULAR PHYSIOLOGY,234(7),11276-11286.
MLA	Hassanshahi, Mohammadhossein,et al."Flavonoid genistein protects bone marrow sinusoidal blood vessels from damage by methotrexate therapy in rats".JOURNAL OF CELLULAR PHYSIOLOGY 234.7(2019):11276-11286.

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