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Park, Ji Young,Hong, Mei,Jia, Qi,Lee, Young-Chul,Yayeh, Taddesse,Hyun, Eujin,Kwak, Dong-Mi,Cho, Jae Youl,Rhee, Man Hee Hindawi Publishing Corporation 2012 Evidence-based Complementary and Alternative Medic Vol.2012 No.-
<P><I>Pistacia chinensis</I> (Chinese pistache) is a widely grown plant in southern China where the galls extract is a common practice in folk medicine. However, extracts from this plant have never been attempted for their cardiovascular protective effects in experimental setting. Here therefore we aimed to investigate the antiplatelet activity of <I>Pistacia chinensis</I> methanolic extract (PCME) in ADP stimulated rat platelets <I>in vitro</I>. PCME (2.5–20 <I>μ</I>g/mL) inhibited ADP-induced platelet aggregation. While PCME diminished [Ca<SUP>2+</SUP>]<I>i</I>, ATP, and TXA2 release in ADP-activated platelets, it enhanced cAMP production in resting platelets. Likewise, PCME inhibited fibrinogen binding to <I><I>α</I></I>IIb<I><I>β</I></I>3 and downregulated JNK, ERK, and Akt phosphorylations. Thus, PCME contains potential antiplatelet compounds that could be deployed for their therapeutic values in cardiovascular pathology.</P>
Park, Ji Young,Ji, Hyun Dong,Jeon, Bo Ra,Im, Eun Ju,Son, Young Min,Lee, Joo Young,Lee, Dong-Ha,Lee, Young-Chul,Hyun, Eujin,Jia, Qi,Hong, Mei,Park, Hwa-Jin,Rhee, Man Hee Hindawi Publishing Corporation 2013 Evidence-based Complementary and Alternative Medic Vol.2013 No.-
<P>A number of reagents that prevent thrombosis have been developed but were found to have serious side effects. Therefore, we sought to identify complementary and alternative medicinal materials that are safe and have long-term efficacy. In the present studies, we have assessed the ability of chlorine e6 (CE6) to inhibit ADP-induced aggregation of rat platelets and elucidated the underlying mechanism. CE6 inhibited platelet aggregation induced by 10 <I>µ</I>M ADP in a concentration-dependent manner and decreased intracellular calcium mobilization and granule secretion (i.e., ATP and serotonin release). Western blotting revealed that CE6 strongly inhibited the phosphorylations of PI3K, Akt, c-Jun N-terminal kinase (JNK), and different mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase 1/2 (ERK1/2) as well as p38-MAPK. Our study also demonstrated that CE6 significantly elevated intracellular cAMP levels and decreased thromboxane A<SUB>2</SUB> formation in a concentration-dependent manner. Furthermore, we determined that CE6 initiated the activation of PKA, an effector of cAMP. Taken together, our findings indicate that CE6 may inhibit ADP-induced platelet activation by elevating cAMP levels and suppressing PI3K/Akt activity. Finally, these results suggest that CE6 could be developed as therapeutic agent that helps prevent thrombosis and ischemia.</P>