Tongxinluo Decreases Apoptosis of Mesenchymal Stem Cells Concentration-dependently Under Hypoxia and Serum Deprivation Conditions Through the AMPK/eNOS Pathway
Tongxinluo Decreases Apoptosis of Mesenchymal Stem Cells Concentration-dependently Under Hypoxia and Serum Deprivation Conditions Through the AMPK/eNOS Pathway
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通心络通过 AMPK/eNOS 途径减少缺氧和血清剥夺条件下浓度依赖性间充质干细胞的凋亡
DOI：
10.1097/fjc.0000000000000044
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发表时间：
2014-03
影响因子：
3
通讯作者：
Hao Zhang
中科院分区：
文献类型：
--
作者：
Chen Jin;Hai-Yan Qian;Qiu-Ting Dong;Hao Zhang
【摘要】：通心络(TXL)是一种中药,在我国被广泛用于治疗心血管疾病。我们之前的研究已经证明了 TXL 对体内间充质干细胞 (MSC) 的促生存作用。但TXL在体外是否能减少MSCs的凋亡，其机制尚不清楚。此外，AMPK/eNOS 通路在调节细胞凋亡中至关重要。因此，我们设计本研究来探讨TXL是否可以在缺氧和血清剥夺（H/SD）条件下减少MSCs凋亡，并确定AMPK/eNOS途径的作用。为了检验这一假设，在 H/SD 下用 TXL (50–400 µg/mL) 处理 MSC 6 小时。对于抑制剂研究，将细胞与 AMPK 抑制剂化合物 C 预孵育。结果表明，TXL 浓度依赖性地降低 MSC 凋亡，这通过减少膜联蛋白 V+/PI− 细胞和增加 JC-1 的红/绿比率来证明。此外，TXL 增强了 AMPK 和 eNOS 的磷酸化。然而，用化合物C治疗降低了AMPK和eNOS的磷酸化，并且伴随着TXL的抗凋亡作用减弱。总之，TXL至少部分通过AMPK/eNOS途径保护MSC免受H/SD诱导的损伤，这为TXL对心血管系统的多重作用提供了新的解释。
Abstract: Tongxinluo (TXL), a traditional Chinese medicine, is widely used to treat cardiovascular diseases in China. Our previous study has demonstrated the pro-survival role of TXL on mesenchymal stem cells (MSCs) in vivo. But whether TXL could decrease apoptosis of MSCs in vitro, and the underlying mechanism are still unknown. Moreover, AMPK/eNOS pathway is crucial in regulating cell apoptosis. Therefore, we designed the study to investigate whether TXL could decrease MSCs apoptosis under hypoxia and serum deprivation (H/SD) conditions and to determine the role of AMPK/eNOS pathway. To test the hypothesis, MSCs were treated with TXL (50–400 &mgr;g/mL) under H/SD for 6 hours. For inhibitor studies, the cells were preincubated with AMPK inhibitor compound C. Results indicated that TXL decreased MSCs apoptosis concentration-dependently evidenced by reduced Annexin V+/PI− cells and increased red/green ratio of JC-1. Further, TXL enhanced the phosphorylation of AMPK and eNOS. Whereas, treatment with compound C decreased the phosphorylation of AMPK and eNOS and was accompanied by attenuated anti-apoptotic effect of TXL. In conclusion, TXL protected MSCs against H/SD-induced injury at least in part through the AMPK/eNOS pathway, which provides a novel explanation for the multi-effect of TXL on cardiovascular system.
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影响因子：
3.7
作者：
Gojo, S;Gojo, N;Umezawa, A
通讯作者：
Umezawa, A
间充质干细胞和心脏修复。
影响因子：
5.3
作者：
Nesselmann C;Ma N;Bieback K;Wagner W;Ho A;Konttinen YT;Zhang H;Hinescu ME;Steinhoff G
通讯作者：
Steinhoff G
影响因子：
4
作者：
Rui-xia Xu;Jinghai Chen;X. Cong;Shengshou Hu;X. Chen
通讯作者：
Rui-xia Xu;Jinghai Chen;X. Cong;Shengshou Hu;X. Chen
DOI：
10.1016/j.biocel.2009.06.006
发表时间：
2009-10
期刊：
The international journal of biochemistry & cell biology
影响因子：
--
作者：
J. Wikstrom;G. Twig;O. Shirihai
通讯作者：
J. Wikstrom;G. Twig;O. Shirihai
影响因子：
5.4
作者：
Izumi, Yasukatsu;Shiota, Masayuki;Iwao, Hiroshi
通讯作者：
Iwao, Hiroshi