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Lee, Su-Yel,Lee, Hyun-Jae,Lee, Jae-Woo,Jeon, Byeong-Kyou,Kim, Ju-Ock,Lee, Choong-Jae The Korean Academy of Tuberculosis and Respiratory 2011 Tuberculosis and Respiratory Diseases Vol.70 No.3
Background: We investigated whether curcumin and genistein affect the MUC5AC mucin production from human airway epithelial cells that is induced by phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$). Methods: Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with PMA or TNF-${\alpha}$ for 24 hours. MUC5AC mucin production was measured by an ELISA. Results: (1) Curcumin dose-dependently inhibited the production of MUC5AC mucin that was induced by PMA or TNF-${\alpha}$; (2) Genistein inhibited PMA-induced MUC5AC mucin production. However, it did not decrease TNF-${\alpha}$-induced MUC5AC mucin production. Conclusion: These results suggest that curcumin and genistein inhibit the production of airway mucin induced by PMA.
( Su Yel Lee ),( Hyun Jae Lee ),( Jae Woo Lee ),( Byeong Kyou Jeon ),( Ju Ock Kim ),( Choong Jae Lee ) 대한결핵 및 호흡기학회 2011 Tuberculosis and Respiratory Diseases Vol.70 No.3
Background: We investigated whether curcumin and genistein affect the MUC5AC mucin production from human airway epithelial cells that is induced by phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-α (TNF-α). Methods: Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with PMA or TNF-α for 24 hours. MUC5AC mucin production was measured by an ELISA. Results: (1) Curcumin dose-dependently inhibited the production of MUC5AC mucin that was induced by PMA or TNF-α; (2) Genistein inhibited PMA-induced MUC5AC mucin production. However, it did not decrease TNF-α-induced MUC5AC mucin production. Conclusion: These results suggest that curcumin and genistein inhibit the production of airway mucin induced by PMA.
Lee, Hyun-Jae,Lee, Su-Yel,Jeon, Byeong-Kyou,Lee, Jae-Woo,Lee, Mi-Nam,Kim, Ju-Ock,Lee, Choong-Jae The Korean Academy of Tuberculosis and Respiratory 2010 Tuberculosis and Respiratory Diseases Vol.69 No.5
Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-${\alpha}$ for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-${\alpha}$; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-${\alpha}$. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-${\alpha}$, by directly acting on airway epithelial cells.
( Hyun Jae Lee ),( Su Yel Lee ),( Byeong Kyou Jeon ),( Jae Woo Lee ),( Mi Nam Lee ),( Ju Ock Kim ),( Choong Jae Lee ) 대한결핵 및 호흡기학회 2010 Tuberculosis and Respiratory Diseases Vol.69 No.5
Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-α- induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-α for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-α; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-α. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-α, by directly acting on airway epithelial cells.
( Jae Woo Lee ),( Hyun Jae Lee ),( Choong Jae Lee ),( Su Yel Lee ),( Byeong Kyou Jeon ),( Heung Seog Bae ),( Kyoung Rai Cho ) 한국응용약물학회 2011 Biomolecules & Therapeutics(구 응용약물학회지) Vol.19 No.1
In this study, we investigated whether ambroxol significantly affects secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min with ambroxol to assess the effect on mucin secretion using ELISA. Additionally, confluent NCI-H292 cells were pretreated with ambroxol for 30 min and then stimulated with EGF or PMA for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) ambroxol did not significantly affect ATP-induced mucin secretion from cultured RTSE cells; (2) ambroxol inhibited the production of MUC5AC mucin protein induced by EGF and PMA in NCI-H292 cells; (3) ambroxol also inhibited the expression of MUC5AC mucin gene induced by EGF and PMA in NCI-H292 cells. This result suggests that ambroxol can inhibit the production and gene expression of MUC5AC mucin, by directly acting on human airway epithelial cells.
에스트로겐성 물질에 의해 자극된 인간 유방암 세포 증식에 대한 다이드제인, 바이칼레인, 헤스페리딘 및 우르솔산의 억제 효과
이미남(Mi Nam Lee),이수열(Su Yel Lee),이현재(Hyun Jae Lee),석정호(Jeong Ho Seok),이충재(Choong Jae Lee) 대한약학회 2010 약학회지 Vol.54 No.3
We investigated whether three flavonoids including daidzein, baicalein, hesperidin and ursolic acid, a triterpene acid, affect proliferation of MCF-7 human breast cancer cells stimulated by estrogenic compounds. Ursolic acid and baicalein inhibited proliferation of MCF-7 cells induced by PhIP, a food-derived carcinogen with estrogenic activity. Daidzein and hesperidin inhibited estradiol-induced proliferation of MCF-7 cells. These compounds should be further investigated for the possible involvement in signaling pathway after estrogen receptor binding in breast cancer cells.
( Young Sik Kim ),( Jae Woo Lee ),( Hyun Jae Lee ),( Choong Jae Lee ),( Su Yel Lee ),( Byeong Kyou Jeon ),( Heung Seog Bae ) 한국응용약물학회 2010 Biomolecules & Therapeutics(구 응용약물학회지) Vol.18 No.4
We conducted this study to investigate whether baicalin, baicalein or schizandrin significantly affect MUC5AC mucin production induced by epidermal growth factor (EGF) or phorbol ester (PMA) in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of baicalin, baicalein or schizandrin for 30 min and then stimulated with EGF or PMA for 24 h, respectively. MUC5AC mucin protein production was measured by ELISA. The results were as follows: (1) Baicalin was found to inhibit the production of MUC5AC mucin protein induced by both EGF and PMA. (2) Baicalein, the aglycone of baicalin, also inhibited MUC5AC mucin production. (3) Schizandrin, derived from Schizandrae Fructus, inhibited MUC5AC mucin production by the same inducers. These results suggest that baicalin, baicalein and schizandrin can regulate the production of mucin protein by directly acting on human airway epithelial cells.
( Minhyeok Lee ),( Ji Woong Son ),( Chang Ryul Park ),( Daeun Kang ),( Su Yel Lee ),( Se Jin Park ),( Wan Jin Hwang ),( Gwan Woo Ku ),( Seong Lan Yu ),( In Beom Jeong ),( Sun Jung Kwon ),( Jaeku Kang 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Purpose Cancer stem cells (CSCs) identified in lung cancer exhibit resistance to chemotherapy, radiotherapy, and targeted therapy. Therefore, a technology to control of CSCs is needed to overcome such resistance to cancer therapy. Various evidences about the association between epithelial-mesenchymal transition related transcriptomic alteration and acquisition of CSC phenotype have been proposed recently. In our previous research, down-regulated miR-26a-5p is closely related to mesenchymal-like lung cancer cell lines. These findings suggest that miR-26a-5p might be involved in lung cancer stemness. Methods RNA polymerase III subunit G (POLR3G) was selected as a candidate target of miR-26a-5p related to cancer stemness. its quantitative relationship was investigated by polymerase chain reaction, western blot after transfection of miR-26a-5p. luciferase assay were done for investigating the direct regulation of miR-26a-5p on POLR3G expression. After transfection of miR-26a-5p, colony formation assay and sphere formation assay were performed to evaluate the effect on cancer stemness. By treating cancer cell by miR-26a-5p and paclitaxel, cell viability was checked by 3-(4,5-dimethylthiazol-2-yl)-5-(3- carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and Muse cell analyzer. Expression level of each gene and its impact on survival were revealed by the cancer genome atlas pancancer database. Results miR-26a-5p regulated the expression of POLR3G directly. Overexpression of miR-26a-5p induced down regulation of POLR3G and a marked reduction of colony formation and sphere formation. Co-treatment of miR-26a-5p with paclitaxel decreased cell growth, suggesting that miR-26a-5p might play a role as a chemotherapy sensitizer. In the cancer genome atlas data, downregulated miR-26a-5p and up-regulated POLR3G were shown compared to adjacent normal tissue. High miR-26a-5p and low POLR3G expression were also related to higher survival rate of patients with lung adenocarcinoma. Conclusions Overexpression of miR-26a-5p can suppress lung cancer stemness and make cancer cell become sensitive to chemotherapy. This finding provides a novel insight into a potential lung cancer treatment by regulating stemness.