Sodium tanshinone IIA silate inhibits oxygen-glucose deprivation/recovery-induced cardiomyocyte apoptosis via suppression of the NF-B/TNF- pathway

doi:10.1111/bph.12185

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	Sodium tanshinone IIA silate inhibits oxygen-glucose deprivation/recovery-induced cardiomyocyte apoptosis via suppression of the NF-B/TNF- pathway
	Wu, Wen-Yu 1,2; Wang, Wen-Yi 1,2; Ma, Yan-Ling 1,2; Yan, Hong 1,2; Wang, Xin-Bo 1,2; Qin, Yin-Lin 3; Su, Mei 3; Chen, Tao 3; Wang, Yi-Ping2
刊名	BRITISH JOURNAL OF PHARMACOLOGY
	2013-07
卷号	169 期号:5 页码:1058-1071
关键词	myocardial cell apoptosis sodium tanshinone IIA silate NF-B TNF- PI3K Akt
ISSN号	0007-1188
DOI	10.1111/bph.12185
文献子类	Article
英文摘要	Background and Purpose Inhibition of apoptosis may attenuate the irreversible injury associated with reperfusion. In the current study, we focused on the cytoprotective effects and the underlying mechanism of sodium tanshinone IIA silate (STS) against damage induced by oxygen-glucose deprivation/recovery (OGD/R). in H9c2 cardiomyocytes and the underlying mechanisms. Experimental Approach We used a model of cardiac ischaemia/reperfusion, OGD/R in H9c2 cardiomyocytes, to assess the cardioprotective effects of STS. Apoptosis of cells was measured with Hoechst 33342-based fluorescence microscopy, and annexin V-FITC-based flow cytometry. Caspase-3 and caspase-8 activities and mitochondrial membrane potential were also measured using commercial kits. TNF- in the cell culture supernatant fractions were measured with sandwich elisa, and protein levels assayed using Western blot. Key Results STS inhibited OGD/R-induced apoptosis by suppressing JNK-mediated activation of NF-B, TNF- expression, activation of caspase-3 and caspase-8 and the Bax/Bcl-2 ratio. Additionally, positive feedback between NF-B and TNF- and amplification of TNF- were inhibited, suggesting that STS plays a protective role against apoptosis in cardiomyocytes, even upon activation of pro-inflammatory cytokines. Interestingly, the cytoprotective effects of STS on OGD/R-induced apoptosis and promotion of cell survival were attenuated after inhibition of PI3K. Conclusion and Implications The inhibitory effects of STS on TNF- and positive feedback signalling of the NF-B/TNF- pathways may play important roles in myocardial protection against ischaemia/reperfusion. These protective effects of STS are mediated by suppressing JNK activity through activation of the PI3K-Akt pathway.
WOS关键词	TUMOR-NECROSIS-FACTOR ; ISCHEMIA-REPERFUSION INJURY ; CARDIAC MYOCYTES ; B ACTIVATION ; MYOCARDIAL-INFARCTION ; ISCHEMIA/REPERFUSION INJURY ; TRANSCRIPTION FACTOR ; HEART-FAILURE ; CELL-DEATH ; AKT
WOS研究方向	Pharmacology & Pharmacy
语种	英语
出版者	WILEY-BLACKWELL
WOS记录号	WOS:000320270200010
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/277568]
专题	药理学第一研究室中科院受体结构与功能重点实验室新药研究国家重点实验室
通讯作者	Wang, Yi-Ping
作者单位	1.Univ Chinese Acad Sci, Beijing, Peoples R China 2.Chinese Acad Sci, State Key Lab Drug Res, Shanghai Inst Mat Med, Shanghai Inst Biol Sci, Shanghai 201203, Peoples R China; 3.Carefree Pharmaceut Co Ltd, Nanjing, Jiangsu, Peoples R China;
推荐引用方式 GB/T 7714	Wu, Wen-Yu,Wang, Wen-Yi,Ma, Yan-Ling,et al. Sodium tanshinone IIA silate inhibits oxygen-glucose deprivation/recovery-induced cardiomyocyte apoptosis via suppression of the NF-B/TNF- pathway[J]. BRITISH JOURNAL OF PHARMACOLOGY,2013,169(5):1058-1071.
APA	Wu, Wen-Yu.,Wang, Wen-Yi.,Ma, Yan-Ling.,Yan, Hong.,Wang, Xin-Bo.,...&Wang, Yi-Ping.(2013).Sodium tanshinone IIA silate inhibits oxygen-glucose deprivation/recovery-induced cardiomyocyte apoptosis via suppression of the NF-B/TNF- pathway.BRITISH JOURNAL OF PHARMACOLOGY,169(5),1058-1071.
MLA	Wu, Wen-Yu,et al."Sodium tanshinone IIA silate inhibits oxygen-glucose deprivation/recovery-induced cardiomyocyte apoptosis via suppression of the NF-B/TNF- pathway".BRITISH JOURNAL OF PHARMACOLOGY 169.5(2013):1058-1071.