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Pretreatment with Total Flavonoid Extract from Dracocephalum Moldavic L. Attenuates Ischemia Reperfusion-induced Apoptosis

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机构: [1]College of Pharmacy, Xinjiang Medical University, No. 393 Xinyi Road, Urumqi, 830054, China. [2]Xinjiang Institute of Materia Medica, No. 140 Xinhua South Road, Urumqi, China. [3]Department of Experimental Animal Center, Xuanwu Hospital of Capital Medical University, No. 45 Changchun Street, Beijing, China.
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We previously demonstrated the cardio-protection mediated by the total flavonoid extracted from Dracocephalum moldavica L. (TFDM) following myocardial ischemia reperfusion injury (MIRI). The present study assessed the presence and mechanism of TFDM-related cardio-protection on MIRI-induced apoptosis in vivo. Male Sprague-Dawley rats experienced 45-min ischemia with 12 h of reperfusion. Rats pretreated with TFDM (3, 10 or 30 mg/kg/day) were compared with Sham (no MIRI and no TFDM), MIRI (no TFDM), and Positive (trapidil tablets, 13.5 mg/kg/day) groups. In MIRI-treated rats, high dose-TFDM (H-TFDM) pre-treatment with apparently reduced release of LDH, CK-MB and MDA, enhanced the concentration of SOD in plasma, and greatly reduced the infarct size, apoptotic index and mitochondrial injury. H-TFDM pretreatment markedly promoted the phosphorylation of PI3K, Akt, GSK-3 beta and ERK1/2 in comparison with the MIRI model group. Western blot analysis after reperfusion also showed that H-TFDM decreased release of Bax, cleaved caspase-3, caspase-7 and caspase-9, and increased expression of BcI-2 as evident by the higher BcI-2/Bax ratio. TFDM cardio-protection was influenced by LY294002 (PI3K inhibitor) and PD98059 (ERK1/2 inhibitor). Taken together, these results provide convincing evidence of the benefit of TFDM pretreatment due to inhibited myocardial apoptosis as mediated by the Pl3K/Akt/GSK-3 beta and ERK1/2 signaling pathways.

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出版当年[2017]版:
大类 | 3 区 综合性期刊
小类 | 3 区 综合性期刊
最新[2023]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
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出版当年[2016]版:
Q1 MULTIDISCIPLINARY SCIENCES
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Q1 MULTIDISCIPLINARY SCIENCES

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第一作者机构: [1]College of Pharmacy, Xinjiang Medical University, No. 393 Xinyi Road, Urumqi, 830054, China. [2]Xinjiang Institute of Materia Medica, No. 140 Xinhua South Road, Urumqi, China. [3]Department of Experimental Animal Center, Xuanwu Hospital of Capital Medical University, No. 45 Changchun Street, Beijing, China.
通讯作者:
通讯机构: [1]College of Pharmacy, Xinjiang Medical University, No. 393 Xinyi Road, Urumqi, 830054, China. [2]Xinjiang Institute of Materia Medica, No. 140 Xinhua South Road, Urumqi, China. [3]Department of Experimental Animal Center, Xuanwu Hospital of Capital Medical University, No. 45 Changchun Street, Beijing, China.
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