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Inhibition of Poly(I:C)-Induced Inflammation by Salvianolic Acid A in Skin Keratinocytes
( Qing-ling Zhang ),( Ri-hua Jiang ),( Xue Mei Li ),( Jung-woo Ko ),( Chang Deok Kim ),( Ming Ji Zhu ),( Jeung-hoon Lee ) 대한피부과학회 2019 Annals of Dermatology Vol.31 No.3
Background: Skin keratinocytes participate actively in inducing immune responses when external pathogens are introduced, thereby contributing to elimination of pathogens. However, in condition where the excessive inflammation is occurred, chronic skin disease such as psoriasis can be provoked. Objective: We tried to screen the putative therapeutics for inflammatory skin disease, and found that salvianolic acid A (SAA) has an inhibitory effect on keratinocyte inflammatory reaction. The aim of this study is to demonstrate the effects of SAA in poly(I:C)-induced inflammatory reaction in skin keratinocytes. Methods: We pre-treated keratinocytes with SAA then stimulated with poly(I:C). Inflammatory reaction of keratinocytes was verified using real-time polymerase chain reaction, enzyme-linked immunosorbent assay and Western blot. Results: When skin keratinocytes were pre-treated with SAA, it significantly inhibited poly (I:C)-induced expression of inflammatory cytokines including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α, and CCL20. SAA inhibited poly(I:C)-induced activation of nuclear factor-κB signaling. And SAA also inhibited inflammasome activation, evidenced by decrease of IL-1β secretion. Finally, SAA markedly inhibited poly(I:C)-induced NLRP3 expression. Conclusion: These results demonstrate that SAA has an inhibitory effect on poly(I:C)-induced inflammatory reaction of keratinocytes, suggesting that SAA can be developed for the treatment of inflammatory skin diseases such as psoriasis. (Ann Dermatol 31(3) 279∼285, 2019)
( Xiao Fen Jin ),( Bo Zhu ),( Ri He Peng ),( Hai Hua Jiang ),( Jian Min Chen ),( Jing Zhuang ),( Jian Zhang ),( Quan Hong Yao ),( Ai Sheng Xiong ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2010 BMB Reports Vol.43 No.8
In this study, we cloned the ERF-B3 subfamily transcription factor gene BnaERF-B3-hy15 from Brassica napus L. Huyou15. This 600 bp gene encodes a 199 amino acid classic ethylene responsive factor (ERF), which shown no binding or very weak binding GCC box-binding activity by the yeast one-hybrid assay. We used gene shuffling and the yeast one-hybrid system to obtain three mutated sequences that can bind to the GCC box. Sequence analysis indicated that two residues, Gly156 in the AP2 domain and Phe62 at the N-terminal domain were mutated to arginine and serine, respectively. Changes of Gly156 to arginine and Phe62 to serine increased the GCC- binding activity of BnaERF-B3-hy15 and the alter of Gly156 to arginine changed the AP2-domain structure of BnaERF-B3- hy15. [BMB reports 2010; 43(8): 567-572]
Nan, Ji-Xing,Jin, Xue-Jun,Lian, Li-Hua,Cai, Xing Fu,Jiang, Ying-Zi,Jin, Hong Ri,Lee, Jung Joon Pharmaceutical Society of Japan 2008 Biological & pharmaceutical bulletin Vol.31 No.4
<P>The hepatoprotective effects of a diterpenoid acanthoic acid isolated from <I>Acanthopanax koreanum</I> N<SMALL>AKAI </SMALL>were evaluated in a <SMALL>D</SMALL>-galactosamine/lipopolysaccharide-induced fulminant hepatic failure mouse model. Mice were pretreated orally with acanthoic acid 12 and 1 h before intraperitoneal injection of <SMALL>D</SMALL>-galactosamine and lipopolysaccharide. Pretreatment with the compound markedly reduced lethal liver injury in experimental animals. The effects were likely associated with a significant decrease in serum tumor necrosis factor (TNF)-α levels, which are correlated not only with those of alanine aminotransferase and aspartate aminotransferase but also with the reduced number of apoptotic hepatocytes in the liver as confirmed using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method and DNA fragmentation assay. These results suggest that acanthoic acid protects against <SMALL>D</SMALL>-galactosamine/lipopolysaccharide-induced fulminant liver failure at least in part by a mechanism associated with the down-regulation of TNF-α secretion.</P>
( Cong Wang ),( Yul-lye Hwang ),( Xue Mei Li ),( Soo Jung Kim ),( Ming Ji Zhu ),( Jeung-hoon Lee ),( Ri-hua Jiang ),( Chang Deok Kim ) 대한피부과학회 2019 Annals of Dermatology Vol.31 No.3
Background: Sebocytes are the major cells of sebaceous gland. The essential role of sebocytes is the production of sebum, a specific lipid mixture, that covers the body surface and provides the barrier function. At puberty, sebum production increases under the effects of various stimuli including androgens and insulin-like growth factor-1 (IGF-1). Excessive sebum production changes the microenvironment surrounding hair follicle, often leading to the onset of acne. Objective: We previously performed screening test using cultured human sebocytes, and found that bilobetin had a potential for inhibiting lipid production. The aim of this study is to demonstrate the effects of bilobetin on IGF-1-induced lipogenesis in sebocytes. Methods: We pretreated simian virus 40 T (SV40T)-transformed sebocytes with bilobetin then stimulated with IGF-1. Effects of bilobetin on lipogenesis of sebocytes were examined by thin layer chromatography and Western blot. Results: Bilobetin markedly inhibited IGF-1- induced lipid production in sebocytes, especially in terms of production of squalene and wax ester. Supporting these results, bilobetin showed significant inhibitory effect on squalene synthase promoter activity. In addition, bilobetin significantly down-regulated lipogenic transcription factors such as sterol response element binding protein (SREBP)-1 and SREBP-2. To delineate the possible action mechanism, we investigated the effect of bilobetin on intracellular signaling. As a result, bilobetin inhibited IGF-1-induced phosphorylation of AKT. Conclusion: Together, these results suggest that bilobetin has an inhibitory potential on sebum production in sebocytes, being applicable for acne treatment. (Ann Dermatol 31(3) 294∼299, 2019)