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Heo, Sook‐,Kyoung,Yun, Hyun‐,Jeong,Park, Won‐,Hwan,Park, Sun‐,Dong Wiley Subscription Services, Inc., A Wiley Company 2008 Journal of cellular biochemistry Vol.105 No.1
<P><B>Abstract</B></P><P>Vascular smooth‐muscle cell (VSMC) proliferation plays a vital role in hypertension, atherosclerosis and restenosis. It has been reported that emodin, an active component extracted from rhubarb, can stop the growth of cancer cells; however, it is not known if emodin exerts similar anti‐atherogenic effects in TNF‐α treated human aortic smooth‐muscle cells (HASMC). In this study, emodin treatment showed potent inhibitory effects in TNF‐α‐induced HASMC proliferation that were associated with induced apoptosis, including the cleavage of poly ADP‐ribose polymerase (PARP). Moreover, inhibitors of caspase‐3, ‐8 and ‐9 (Ac‐DEVD‐CHO, Z‐IETD‐FMK and Z‐LEHD‐FMK) efficiently blocked emodin‐induced apoptosis in TNF‐α treated HASMC. Therefore, emodin‐induced cell death occurred via caspase‐dependent apoptosis. Emodin treatment resulted in the release of cytochrome <I>c</I> into cytosol and a loss of mitochondrial membrane potential (ΔΨ<SUB>m</SUB>), as well as a decrease in the expression of an anti‐apoptotic protein (Bcl‐2) and an increase in the expression of an a pro‐apoptotic protein (Bax). Emodin‐mediated apoptosis was also blocked by a mitochondrial membrane depolarization inhibitor, which indicates that emodin‐induced apoptosis occurred via a mitochondrial pathway. Taken together, the results of this study showed that emodin inhibits TNF‐α‐induced HASMC proliferation via caspase‐ and a mitochondrial‐dependent apoptotic pathway. In addition, these results indicate that emodin has potential as an anti‐atherosclerosis agent. J. Cell. Biochem. 105: 70–80, 2008. © 2008 Wiley‐Liss, Inc.</P>
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Lee, Kyung‐,Won,Chung, Kyung‐,Sook,Seo, Ji‐,Hyung,Yim, Sung‐,Vin,Park, Hee‐,Jun,Choi, Jung‐,Hye,Lee, Kyung‐,Tae Wiley Subscription Services, Inc., A Wiley Company 2012 Journal of cellular biochemistry Vol.113 No.9
<P><B>Abstract</B></P><P>Sulfuretin, a flavonoid isolated from heartwood of <I>Rhus verniciflua</I>, has been reported to have anti‐cancer activities but the underlying molecular mechanism was not clear. In this study, sulfuretin induced apoptosis by activating caspases‐8, ‐9, and ‐3 as well as cleavage of poly(ADP‐ribose) polymerase. Furthermore, treatment with sulfuretin caused mitochondrial dysfunctions, including the loss of mitochondrial membrane potential (ΔΨ<SUB>m</SUB>), the release of cytochrome <I>c</I> to the cytosol, and the translocations of Bax and tBid. Sulfuretin also activated the extrinsic apoptosis pathway, that is, it increased the expressions of Fas and FasL, the activation of caspase‐8, and the cleavage of Bid. Furthermore, blocking the FasL–Fas interaction with NOK‐1 monoclonal antibody prevented the sulfuretin‐induced apoptosis. The therapeutical effect of sulfuretin in leukemia is due to its potent apoptotic activity through the extrinsic pathway driven by a Fas‐mediated caspase‐8‐dependent pathway. J. Cell. Biochem. 113: 2835–2844, 2012. © 2012 Wiley Periodicals, Inc.</P>
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Kanamycin activates caspase‐1 in NC/Nga mice
Han, Na‐,Ra,Kim, Hyung‐,Min,Jeong, Hyun‐,Ja Blackwell Publishing Ltd 2011 Experimental dermatology Vol.20 No.8
<P><B>Abstract: </B> Abuse of antibiotics to treat children has been associated with an increased risk of the development of inflammatory diseases. The underlying mechanism behind this association still remains to be clarified. Here, we examined the mechanisms behind kanamycin‐induced skin inflammation in NC/Nga mice. NC/Nga mice were orally administered kanamycin for 7 days consecutively. Blood, spleen and dorsal skin were taken 18 weeks after kanamycin treatment was stopped. Kanamycin significantly increased the allergic reaction. We also observed significant increases in caspase‐1 mRNA and protein expression in the dorsal skin of the kanamycin‐administered mice compared to the control mice. The increased enzymatic activity of caspase‐1 in the dorsal skin of the kanamycin‐administered mice increased the mRNA expressions of IL‐1β and IL‐18. The productions of IL‐1β and IL‐18 were also increased in the splenocytes obtained from kanamycin‐administered mice. Kanamycin upregulated the TNF‐α mRNA expression in the dorsal skin and the TNF‐α production in stimulated splenocytes. The activation of nuclear factor‐κB and degradation of IκBα were increased by kanamycin administration. Our findings suggest that the use of kanamycin during infancy may increase the potential for skin inflammatory reactions through the upregulation of caspase‐1.</P>
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