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Role of haem oxygenase-1 in microbial host defence
Chung, Su Wol,Hall, Sean R.,Perrella, Mark A. Blackwell Publishing Ltd 2009 Cellular microbiology Vol.11 No.2
<P>Summary</P><P>Haem oxygenase (HO)-1 is a cytoprotective enzyme that plays a critical role in defending the body against oxidant-induced injury during inflammatory processes. HO catalydes the degradation of haem to carbon monoxide (CO), biliverdin and ferrous iron. Biliverdin is converted to bilirubin, a potent endogenous antioxidant. CO has a number of biological functions, including anti-inflammatory properties. In various models of disease, HO-1 is known to play a critical role by ameliorating the pathological consequences of injury. In many of these models, the beneficial effects of HO-1 and its products of haem catabolism are by suppressing an inflammatory response. However, when investigating diseases due to microbial infections, inhibition of the inflammatory response could disrupt the ability of the immune system to eradicate an invading pathogen. Thus, questions remain regarding the role of HO-1 in microbial host defence. This microreview will address our present understanding of HO-1 and its functional significance in a variety of microbial infections.</P>
Kang, Bok Yun,Chung, Su Wol,Cho, Daeho,Kim, Tae Sung 전남대학교 약품개발연구소 2002 약품개발연구지 Vol.11 No.-
Interleukin (IL)-12 plays a pivotal role in the development of T helper type 1 (Th1)-immune response. which may have therapeutic effects on diseases associated with pathologic Th2 responses such as allergic disorders and asthma. In this study, we investigated the effects berberine, a benzodioxoloquinolizine alkaloid with anti-microbial and anti-tumor activities, on the production of IL-12 p40, an inducible subunit of IL-12, in mouse macrophages. Berberine-induced IL-12 p40 production and activation of p38 mitogen-activated protein kinase (MAPK) in dose-dependent manners, which were significantly inhibited by p38 MAPK inhibitors and yohimbine, indicating that p38 MAPK and α_2-adrenergic receptor were involved in the induction of IL-12 p40 production in mouse macrophages by berberine. Furthermore, berberine significantly enhanced IL-12 p40 production in mouse macrophages when combined with lipopolysaccharide, a well-known inducer of IL-12 production. These finding may explain some of the known biological effects of berberine and suggests berberine as an immunotherapeutic compound for induction of IL-12, which is potentially applicable for tumors. infectious disease, and airway inflammation.
Inhibition of interleukin-12 production in lipopolysaccharide-activated macrophages by curcumin
Kang, Bok Yun,Chung, Su Wol,Chung, Woon Jae,Im, Suhn Young,Hwang, Seung Yong,Kim, Tae Sung 전남대학교 약품개발연구소 1999 약품개발연구지 Vol.8 No.1
Pharmacological control of interleukin-12 production may be a key therapeutic strategy for modulating immunological diseases dominated by type-1 cytokine responses. In this study we investigated the effects of curcumin (1,7-bis[4-hydroxy-3-methoxyphenyl]-1,6-heptadiene-3,5-dione) on the production of interleukin-12 from mouse macrophages stimulated with lipopolysaccharide. Curcumin potently inhibited the production of interleukin-12 in a dose-dependent manner. The effect of curcumin on interleukin-12 p40 promoter activation was analyzed by transfecting RAW264.7 monocytic cells with p40 promoter/reporter constructs. The repressive effect mapped to a region in the p40 promoter containing a binding site for nuclear factor κB (p40-κB). Futhermore, activation of macrophages by lipopolysaccharide resulted in markedly enhanced binding activity to the κB site, which significantly upon addition of curcumin. These results suggest that curcumin-induced inhibition of interleukin-12 production in macrophages may explain some of the biological effects of curcumin including its anti-inflammatory activity.
Sulfasalazine attenuates tamoxifen-induced toxicity in human retinal pigment epithelial cells
Na Rae Hwang,Su Wol Chung 생화학분자생물학회 2020 BMB Reports Vol.53 No.5
Tamoxifen, a nonsteroidal estrogen receptor (ER) antagonist, is used routinely as a chemotherapeutic agent for ER-positive breast cancer. However, it is also causes side effects, including retinotoxicity. The retinal pigment epithelium (RPE) has been recognized as the primary target of tamoxifen-induced retinotoxicity. The RPE plays an essential physiological role in the normal functioning of the retina. Nonetheless, potential therapeutic agents to prevent tamoxifen-induced retinotoxicity in breast cancer patients have not been investigated. Here, we evaluated the action mechanisms of sulfasalazine against tamoxifen- induced RPE cell death. Tamoxifen induced reactive oxygen species (ROS)-mediated autophagic cell death and caspase-1- mediated pyroptosis in RPE cells. However, sulfasalazine reduced tamoxifen-induced total ROS and ROS-mediated autophagic RPE cell death. Also, mRNA levels of tamoxifen-induced pyroptosis-related genes, IL-1, NLRP3, and procaspase-1, also decreased in the presence of sulfasalazine in RPE cells. Additionally, the mRNA levels of tamoxifen-induced AMD-related genes, such as complement factor I (CFI), complement factor H (CFH), apolipoprotein E (APOE), apolipoprotein J (APOJ), toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4), were downregulated in RPE cells. Together, these data provide novel insight into the therapeutic effects of sulfasalazine against tamoxifen-induced RPE cell death.
Kang, Bok Yun,Chung, Su Wol,Kim, Tae Sung 전남대학교 약품개발연구소 2001 약품개발연구지 Vol.10 No.-
Hypericin, an active component of Hypericum perforatum, was evaluated for the regulation of interleukin-12 (IL-12) production in mouse macrophages. Hypericin significantly inhibited IL-12 production In lipopolysaccharide-activated macrophages In a dose-dependent manner (IC_50 = 1.45㎍/ml). Furthermore, hypericin potently Inhibited the activation of IL-12 gene promoter, suggesting that hypericin negatively regulated IL-12 production at the transcription level. These results may explain some known biological activities of hypericin including its anti-rheumatic effect.
Kang, Bok Yun,Chung, Su Wol,Kim, Seung Hyun,Ryu, Shi Yong,Kim, Tae Sung 전남대학교 약품개발연구소 2000 약품개발연구지 Vol.9 No.1
Pharmacological control of interleukin-12 (IL-12) and interferon-gamma (IFN-γ) production may be a key therapeutic strategy for modulating immunological diseases dominated by Th1-derived cytokine response. In this study, we investigated the effects of three different tanshinone pigments from Solvia miltiorrhiza (tanshinone I, dihydrotanshinone, and cryptotanshinone) on IL-12 production in mouse macrophages and on IFN-γ production in lymph node cells. All tested tanshinones significantly inhibited IL-12 production in lipopolysaccharide (LPS)-activated macrophages and also IFN-γ production in keyhole limpet hemocyanin (KLH)-primed lymph node cells in a dose-dependent manner. Dihydrotanshinone was more effective than tanshinone I or cryptotanshinone. Tanshinones significantly inhibited the expression of IL-12 p40 gene at the mRNA level. Furthermore, tanshinones potently inhibited the promoter activation of IL-12 p40 gene and nuclear factor (NF)-κB binding to the κB site, suggesting that tanshinones may negatively regulate IL-12 production at the transcription level. These results may explain some known biological activities of tanshinones including their anti-inflammatory effect, and suggest a possible use of tanshinones in the treatment of immunological diseases dominated by Th1-derived cytokine responses.
Disruption of Striated Preferentially Expressed Gene Locus Leads to Dilated Cardiomyopathy in Mice
Liu, Xiaoli,Ramjiganesh, Tripurasundari,Chen, Yen-Hsu,Chung, Su Wol,Hall, Sean R.,Schissel, Scott L.,Padera Jr, Robert F.,Liao, Ronglih,Ackerman, Kate G.,Kajstura, Jan,Leri, Annarosa,Anversa, Piero,Ye Ovid Technologies Wolters Kluwer -American Heart A 2009 CIRCULATION - Vol.119 No.2
<P>BACKGROUND: The striated preferentially expressed gene (Speg) generates 4 different isoforms through alternative promoter use and tissue-specific splicing. Depending on the cell type, Speg isoforms may serve as markers of striated or smooth muscle differentiation. METHODS AND RESULTS: To elucidate function of Speg gene isoforms, we disrupted the Speg gene locus in mice by replacing common exons 8, 9, and 10 with a lacZ gene. beta-Galactosidase activity was detected in cardiomyocytes of the developing heart starting at day 11.5 days post coitum (dpc). beta-Galactosidase activity in other cell types, including vascular smooth muscle cells, did not begin until 18.5 dpc. In the developing heart, protein expression of only Spegalpha and Spegbeta isoforms was present in cardiomyocytes. Homozygous Speg mutant hearts began to enlarge by 16.5 dpc, and by 18.5 dpc, they demonstrated dilation of right and left atria and ventricles. These cardiac abnormalities in the absence of Speg were associated with a cellular hypertrophic response, myofibril degeneration, and a marked decrease in cardiac function. Moreover, Speg mutant mice exhibited significant neonatal mortality, with increased death occurring by 2 days after birth. CONCLUSIONS: These findings demonstrate that mutation of the Speg locus leads to cardiac dysfunction and a phenotype consistent with a dilated cardiomyopathy.</P>