In Vitro Phosphorylation of Purified Transketolase by Protein Kinase C

Soh, Yunjo,Jeong, Kyu-Shik Korean Society of Molecular Biology 1996 Molecules and cells Vol.6 No.6

Vitexin, an HIF-1α Inhibitor, Has Anti-metastatic Potential in PC12 Cells

Yunjo Soh,Hwa Jung Choi,Jae Soon Eun,Bang Geul Kim,김선여,Hoon Jeon 한국분자세포생물학회 2006 Molecules and cells Vol.22 No.3

Limonium tetragonum Reduces Osteoclast Formation and Resorption through Mitogen-activated Protein Kinase-c-Fos-NFATc1 Signaling Pathways

Yunjo Soh 한국생약학회 2023 Natural Product Sciences Vol.29 No.4

Osteoporosis is caused by an imbalance of osteoclasts and osteoblasts, and the major treatment technique for treating osteoporosis is to reduce the activity of osteoclastic bone resorption. Limonium tetragonum (LT) is a medicinal plant that contains bioactive molecules with anti-inflammatory and anti-cancer properties. Its effects on osteoclastogenesis, however, remain unclear. Limonium tetragonum extract (LTE) was examined for its inhibitory effect on osteoclastogenesis by TRAP and pit formation assay. As a result, LTE also significantly reduced TRAP formation, the capability to resorb calcium phosphate-coated plates, and F-actin ring formation. LTE reduced RANKL-induced activation of the MAPKs ERK, JNK, and p38 and the production of the transcription factors c-Fos and NFATc1 required for osteoclastogenesis. LTE also reduced the expression of osteoclastogenesis-related genes such as matrix metalloproteinase-9, tartrate-resistant acid phosphatase, and receptor activator of NF-κB. These findings suggest that LTE might be a promising treatment option for bone disorders caused by aberrant osteoclast production and function.

Vitexin Attenuates the Level of Hypoxia-Inducible Factor -la in PC12 Cells under Hypoxia

SOH Yunjo,KIM Sun Yeou,KIM Bang Geul,CHOI Hwa Jung 大韓藥學會 2005 大韓藥學會 總會 및 學術大會 Vol.2005 No.2

간효소에 의해 대사된 양격산화탕의 저산소/재관류로부터 PCl2 세포 보호효과

소윤조(Yunjo Soh) 大韓藥學會 2005 약학회지 Vol.49 No.1

The protective effect of Yangguksanwha-tang (YST) against hypoxia-reperfusion insult was investigated in PC12 cells. To elucidate the mechanism of the protective effect of YST, cell viability the changes in activities of superoxide dismutase, glutathione peroxidase, catalase, caspase 3 and the production of malondialdehyde were observed after treating PC12 cells with YST which was metabolized by rat liver homogenate. Pretreatment of YST with liver homogenate appeared to increase its protective effect against hypoxia-reperfusion insult. The result showed that YST had the highest protective effect against hypoxia/reperfusion at the dose of 2㎍/ml in PC12 cells, probably by recovering the redox enzyme activities and MDA to control level.

Recent Advances of Therapeutic Targets for the Treatment of Periodontal Disease

( Woo Jin Kim ),( Yunjo Soh ),( Seok-mo Heo ) 한국응용약물학회 2021 Biomolecules & Therapeutics(구 응용약물학회지) Vol.29 No.3

Periodontal disease is primarily associated with bacterial infection such as dental plaque. Dental plaque, an oral biofilm harboring a complex microbial community, can cause various inflammatory reactions in periodontal tissue. In many cases, the local bacterial invasion and host-mediated immune responses lead to severe alveolar bone destruction. To date, plaque control, non-surgical, and surgical interventions have been the conventional periodontal treatment modalities. Although adjuvant therapies including antibiotics or supplements have accompanied these procedures, their usage has been limited by antibiotic resistance, as well as their partial effectiveness. Therefore, new strategies are needed to control local inflammation in the periodontium and host immune responses. In recent years, target molecules that modulate microbial signaling mechanisms, host inflammatory substances, and bone immune responses have received considerable attention by researchers. In this review, we introduce three approaches that suggest a way forward for the development of new treatments for periodontal disease; (1) quorum quenching using quorum sensing inhibitors, (2) inflammasome targeting, and (3) use of FDA-approved anabolic agents, including Teriparatide and sclerostin antibody.

ROLES OF JNK-1 AND p38 IN SELECTIVE INDUCTION OF APOPTOSIS BY CAPSAICIN IN ras-TRANSFORMED HUMAN BREAST EPITHELIAL CELLS

KANG, Hye-Jung,SOH, Yunjo,KIM, Mi-Sung,LEE, Eun-Jung,SURH, Young-Joon,KIM Choi, Hyeong-Reh,KIM, Seung Hee,Moon, Aree 德成女子大學校 藥學硏究所 2002 藥學論文誌 Vol.13 No.1

Efforts have been made to develop a chemoprevention strategy that selectively triggers apoptosis in malignant cancer cells. Previous studies showed that capsaicin, the majorpungent ingredient of red pepper, had differential effect between normal and transformed cells. As an approach to unveil the molecular mechanism by which capsaicin selectively induces apoptosis in transformed cells, we investigated the effect of capsaicin in nontransformed and ras-transformed cells of a common origin: parental (MCF10A) and H-ras transformed (H-ras MCF10A) human breast epithelial cells. Here, we show that capsalcin selectively induces apoptosis in H-ras-transformed cells but not in their normal cell counterparts. The capsaich-induced apoptosis, which is dependent on ras transformation, involves the activity of DEVDase (caspase-3 like). In H-ras MCF10A cells, capsaicin treatment markedly activated c-Jun N-terminal protein kinase (JNK)-1 and p38 matigen-activated protein kinase (MAPK)while it deactivated extracellular signal-regulated protein kinases (ERKs). The use of kinase inhibitors and overexpression of dominant negative forms of MAPKs demonstrated a role of JNK-1 and p38, but not that of ERKs, in apoptosis induced by capsaicin in H-ras-transformed MCF10A cells. Based on the present study, we propose that capsaicin selectively induces apoptosis through modulation of ras-downstream signaling molecules in ras-activated MCF10A cells. Taken in conjunction with the fact that uncontrolled ras activation is probably the most common genetic defect in human cancer cells, our finding may be critical to the chemopreventive potential of capsaicin and for developing a strategy to induce tumor cell-specific apoptosis.

Protective Effect of HP08-0111 on Ligature-Induced Periodontitis

Young Ran Park,Hyoung Kwon Cho,Yunjo Soh KOREAN ACADAMY OF ORAL BIOLOGY 2010 International Journal of Oral Biology Vol.35 No.4

Periodontitis is an inflammatory disorder of the periodontium and is characterized by destruction of the tooth supporting tissues, mediated by the upregulation of synthesis and release of a variety of pro-inflammatory factors. Inflammatory cytokines and prostaglandins upregulate RANKL and its subsequent binding to RANK stimulates osteoclast formation, resorption activity, and survival. In our present study, we investigated the effects of HP08-0111, composed of Coptis japonica (Thunb.) Makino, vitamin C and vitamin E, upon inflammatory responses, osteoclastogenesis and alveolar bone loss. HP08-0111 decreased the expression of IL-1β and COX2 on LPS-induced RAW 264.7 cells and inhibited osteoclast-specific genes such as c-Fos, MMP-9, and TRAP. HP08-0111 also exhibited protective effects against alveolar bone loss in rats with ligature-induced periodontitis. Our results suggest that HP08-0111 is potentially an important therapeutic tool for the treatment of disorders associated with bone loss such as periodontitis.

Kalkitoxin attenuates calcification of vascular smooth muscle cells via RUNX-2 signaling pathways

Saroj K Shrestha,Se-Woong Kim,Yunjo Soh 대한수의학회 2023 Journal of Veterinary Science Vol.24 No.5

Background: Kalkitoxin (KT) is an active lipopeptide isolated from the cyanobacterium Lyngbya majuscula found in the bed of the coral reef. Although KT suppresses cell division and inflammation, KT’s mechanism of action in vascular smooth muscle cells (VSMCs) is unidentified. Therefore, our main aim was to investigate the impact of KT on vascular calcification for the treatment of cardiovascular disease. Objectives: Using diverse calcification media, we studied the effect of KT on VSMC calcification and the underlying mechanism of this effect. Methods: VSMC was isolated from the 6 weeks ICR mice. Then VSMCs were treated with different concentrations of KT to check the cell viability. Alizarin red and von Kossa staining were carried out to examine the calcium deposition on VSMC. Thoracic aorta of 6 weeks mice were taken and treated with different concentrations of KT, and H and E staining was performed. Real-time polymerase chain reaction and western blot were performed to examine KT’s effect on VSMC mineralization. Calcium deposition on VSMC was examined with a calcium deposition quantification kit. Results: Calcium deposition, Alizarin red, and von Kossa staining revealed that KT reduced inorganic phosphate-induced calcification phenotypes. KT also reduced Ca++-induced calcification by inhibiting genes that regulate osteoblast differentiation, such as runt-related transcription factor 2 (RUNX-2), SMAD family member 4, osterix, collagen 1α, and osteopontin. Also, KT repressed Ca2+-induced bone morphogenetic protein 2, RUNX-2, collagen 1α, osteoprotegerin, and smooth muscle actin protein expression. Likewise, Alizarin red and von Kossa staining showed that KT markedly decreased the calcification of ex vivo ring formation in the mouse thoracic aorta. Conclusions: This experiment demonstrated that KT decreases vascular calcification and may be developed as a new therapeutic treatment for vascular calcification and arteriosclerosis.

Protective Effect of HP08-0106 on Ligature-induced Periodontitis in Rats

Hwa Jung Choi,,Hyoung Kwon Cho,Yunjo Soh KOREAN ACADAMY OF ORAL BIOLOGY 2011 International Journal of Oral Biology Vol.36 No.4

Periodontitis is an inflammatory disorder of the periodontium, characterized by destruction of the tooth supporting tissues including alveolar bone and mediated by various pro-inflammatory mediators. Here, we demonstrated that HP08-0106, composed of four crude drugs-Gardenia jasminoides Grandiflora, Angelica gigas Nakai, Rehmannia glutinosa, and Schizonepeta tenuifolia in a weight ratio of 2:2:1:2, perturbs inflammatory responses, osteoclast formation in LPS-induced RAW 264.7 cells and alveolar bone resorption in ligature-induced periodontitis. HP08-0106 decreased the protein level of iNOS and COX2 as well as the secreted level of IL-1β, indicating that HP08-0106 has antiinflammatory effects. HP08-0106 also inhibited the expression of genes associated with osteoclastogenesis including c-Fos, MMP-9 and TRAP. Moreover, HP08-0106 exhibited a protective effect from alveolar bone loss in ligature-induced periodontitis animal models. Our results strongly suggest that HP08-0106 represent an important therapeutic tool to treat inflammatory disorders associated with bone loss such as periodontitis.