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남대철,김보건,이현재,신현대,이충재,황선철 대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.2
We investigated whether prunetin affects the proteolytic activity, secretion, and gene expression of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as in vivo production of MMP-3 in the rat knee joint to evaluate the potential chondroprotective effect of prunetin. Rabbit articular chondrocytes were cultured in a monolayer, and reverse transcriptionpolymerase chain reaction (RT-PCR) was used to measure interleukin-1β (IL-1β)- induced expression of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), and ADAMTS-5. In rabbit articular chondrocytes, the effects of prunetin on IL-1β-induced secretion and proteolytic activity of MMP-3 were investigated using western blot analysis and casein zymography, respectively. The effect of prunetin on MMP-3 protein production was also examined in vivo. The results were as follows: (1) prunetin inhibited the gene expression of MMP-3, MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5; (2) prunetin inhibited the secretion and proteolytic activity of MMP-3; (3) prunetin suppressed the production of MMP-3 protein in vivo. These results suggest that prunetin can regulate the gene expression, secretion, and proteolytic activity of MMP-3, by directly acting on articular chondrocytes.
Nam, Dae Cheol,Kim, Bo Kun,Lee, Hyun Jae,Shin, Hyun-Dae,Lee, Choong Jae,Hwang, Sun-Chul The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.2
We investigated whether prunetin affects the proteolytic activity, secretion, and gene expression of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as in vivo production of MMP-3 in the rat knee joint to evaluate the potential chondroprotective effect of prunetin. Rabbit articular chondrocytes were cultured in a monolayer, and reverse transcriptionpolymerase chain reaction (RT-PCR) was used to measure interleukin-$1{\beta}$ (IL-$1{\beta}$)-induced expression of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), and ADAMTS-5. In rabbit articular chondrocytes, the effects of prunetin on IL-$1{\beta}$-induced secretion and proteolytic activity of MMP-3 were investigated using western blot analysis and casein zymography, respectively. The effect of prunetin on MMP-3 protein production was also examined in vivo. The results were as follows: (1) prunetin inhibited the gene expression of MMP-3, MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5; (2) prunetin inhibited the secretion and proteolytic activity of MMP-3; (3) prunetin suppressed the production of MMP-3 protein in vivo. These results suggest that prunetin can regulate the gene expression, secretion, and proteolytic activity of MMP-3, by directly acting on articular chondrocytes.
Dae Cheol Nam,Bo Kun Kim,Hyun Jae Lee,Hyun-Dae Shin,Choong Jae Lee,Sun-Chul Hwang 대한생리학회-대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.2
We investigated whether prunetin affects the proteolytic activity, secretion, and gene expression of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as <i>in vivo</i> production of MMP-3 in the rat knee joint to evaluate the potential chondroprotective effect of prunetin. Rabbit articular chondrocytes were cultured in a monolayer, and reverse transcriptionpolymerase chain reaction (RT-PCR) was used to measure interleukin-1β (IL-1β)- induced expression of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), and ADAMTS-5. In rabbit articular chondrocytes, the effects of prunetin on IL-1β-induced secretion and proteolytic activity of MMP-3 were investigated using western blot analysis and casein zymography, respectively. The effect of prunetin on MMP-3 protein production was also examined<i> in vivo</i>. The results were as follows: (1) prunetin inhibited the gene expression of MMP-3, MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5; (2) prunetin inhibited the secretion and proteolytic activity of MMP-3; (3) prunetin suppressed the production of MMP-3 protein <i>in vivo</i>. These results suggest that prunetin can regulate the gene expression, secretion, and proteolytic activity of MMP-3, by directly acting on articular chondrocytes.
왕벚나무 껍질로부터 Naringenin, Sakuranetin, Prunetin의 분리 및 함량 분석
정길생,김은남,김성철 한국생약학회 2019 생약학회지 Vol.50 No.3
Prunus yedoensis Matsum. (Rosaceae) has been used for cough, urticaria, pruritus, dermatitis, asthma and relaxation in traditional Korean medicine. In this study, naringenin, sakuranetin and prunetin were isolated from the barks of P. yedoensis and quantification were performed by using high performance liquid chromatography (HPLC) method with diode array detector. The structures of naringenin and sakuranetin, prunetin were identified NMR spectroscopic data analysis. The content of each compound was analyzed by HPLC and the analytical method was validated through linearity, precision, accuracy and specificity test. The result showed that calibration curves of three compounds naringenin, sakuranetin and prunetin indicated great linearity with a correlation coefficient (R²) of 1.00, 1.00 and 0.99. Intra and inter day measurement accuracy of the three compounds ranged from 92.70 ~ 112.70%, and showed precision was less than 3%. Therefore, the content analysis showed that naringenin (0.132 ± 0.016%), sakuranetin (0.108 ± 0.023%), and prunetin (0.059 ± 0.014%).
이학주,이성숙,최돈하 한국목재공학회 2003 목재공학 Vol.31 No.4
전보에 이어 산벚나무(P. sargentii) 심재 에탄올 추출물로부터 4개의 페놀성 화합물을 단리하였으며 기기분석결과, isoflavone인 prunetin를 비롯하여 flavanone인 angophorol, sakuranetin 그리고 flavanone 배당체인 isosakuranin으로 각각 동정하였다. 그러나 이들의 항균 및 항산화 활성을 조사한 결과 활성이 낮아 산벚나무 에탄올 조추출물의 높은 항균 및 항산화 활성은 이들 단리물질과는 무관한 것으로 사료되었다. Four flavonoids were isolated from the heartwood of Prunus sargentii. The structures were identified by NMR spectroscopic analysis: prunetin as isoflavone, angophorol, and sakuranetin as flavanone, and isosakuranin as flavanone glycoside. However, these compounds indicated low antifungal and antioxidative activiteis. In this regard, it could suggest that high antifungal and antioxidative activities of extractives of P. sargentii have no relationship with these compounds.
( Jiho Ryu ),( Hyun Jae Lee ),( Su Hyun Park ),( Asaduzzaman Sikder ),( Ju Ock Kim ),( Jang Hee Hong ),( Jeong Ho Seok ),( Choong Jae Lee ) 대한결핵 및 호흡기학회 2013 Tuberculosis and Respiratory Diseases Vol.75 No.5
Background: We investigated whether prunetin significantly affects tumor necrosis factor-α (TNF-α)-induced MUC5AC mucin gene expression, production, inhibitory kappa B (IkB) degradation and nuclear factor kappa B (NF-kB) p65 translocation in human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-α for 24 hours or the indicated periods. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The effect of prunetin on TNF-α-induced degradation of IkB and translocation of NF-κB p65 was investigated by western blot analysis. Results: We found that incubation of NCI-H292 cells with prunetin significantly inhibited mucin production and down-regulated the MUC5AC gene expression induced by TNF-α. Prunetin inhibited TNF-α-induced degradation of IkB and translocation of NF-κB p65. Conclusion: This result suggests that prunetin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-κB signaling pathway.
Ryu, Jiho,Lee, Hyun Jae,Park, Su Hyun,Sikder, Md. Asaduzzaman,Kim, Ju-Ock,Hong, Jang-Hee,Seok, Jeong Ho,Lee, Choong Jae The Korean Academy of Tuberculosis and Respiratory 2013 Tuberculosis and Respiratory Diseases Vol.75 No.5
Background: We investigated whether prunetin significantly affects tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced MUC5AC mucin gene expression, production, inhibitory kappa B ($I{\kappa}B$) degradation and nuclear factor kappa B (NF-kB) p65 translocation in human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-${\alpha}$ for 24 hours or the indicated periods. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The effect of prunetin on TNF-${\alpha}$-induced degradation of $I{\kappa}B$ and translocation of NF-${\kappa}B$ p65 was investigated by western blot analysis. Results: We found that incubation of NCI-H292 cells with prunetin significantly inhibited mucin production and down-regulated the MUC5AC gene expression induced by TNF-${\alpha}$. Prunetin inhibited TNF-${\alpha}$-induced degradation of $I{\kappa}B$ and translocation of NF-${\kappa}B$ p65. Conclusion: This result suggests that prunetin inhibits the NF-${\kappa}B$ signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-${\kappa}B$ signaling pathway.
( 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.
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.