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Prostaglandin A₂ (PGA₂)는 사람 골육종 세포인 U2OS 세포주에서 apoptosis와 heme oxygenase (HO)-1의 발현을 함께 유도하였다. PGA₂에 의한 apoptosis는 HO-1의 과도한 발현이나 HO-1에 대한 small interfering RNA에 의한 발현저하에 의하여 변동되지 않았으나 H₂O₂에 의한 세포사망은 HO-1의 발현 수준에 반비례하여 변동되었다. 또한 thiol antioxidant인 N-acetyl-L-cysteine (NAC)은 PGA₂에 의한 세포사망과 HO-1의 발현 증가를 모두 차단하였지만, non-thiol antioxidant인 butylated hydroxyanisole (BHA)과 ascorbic acid는 세포사망과 HO-1의 발현 유도를 차단하지 않았다. 이와 같은 결과들은 PGA₂는 산화성 손상에 의해서가 아니라 PGA₂의 thiol-reactivity에 의하여 apoptosis와 HO-1의 발현을 유도하며, HO-1의 발현은 PGA₂에 의한 apoptosis와는 독립적인 현상이거나 기능적으로 apoptosis 유도의 하부에 위치하고 apoptosis의 진행에는 기여하지 않을 것이라는 것을 시사해 준다. Prostaglandin A₂ (PGA₂), one of cyclopentenone PGs, induced both apoptosis and heme oxygenase (HO)-1 expression in U2OS cells. PGA₂-induced apoptosis was not perturbed by either over-expression or knock-down of HO-1, whereas H₂O₂-induced cell death was inversely modulated by the expression level of HO-1. In addition, N-acetyl-L-cysteine (NAC), a thiol antioxidant, blocked both apoptosis and HO-1 expression induced by PGA₂. But, non-thiol antioxidants like butylated hydorxyanisole (BHA) and ascorbic acid did not block either apoptosis or HO-1-induction. Taken together, these results suggest that PGA₂ induces both apoptosis and HO-1 expression, which are critically related to the thiol-reactivity of PGA₂, but not oxidative stress, and HO-1 expression may be independent or functionally located downstream of apoptosis by PGA₂ without contribution to apoptosis progression.
Prostaglandin $A_2$ ($PGA_2$)는 사람 골육종 세포인 U2OS 세포주에서 apoptosis와 heme oxygenase (HO)-1의 발현을 함께 유도하였다. $PGA_2$에 의한 apoptosis는 HO-1의 과도한 발현이나 HO-1에 대한 small interfering RNA에 의한 발현저하에 의하여 변동되지 않았으나 $H_2O_2$에 의한 세포사망은 HO-1의 발현 수준에 반비례하여 변동되었다. 또한 thiol antioxidant인 N-acetyl-L-cysteine (NAC)은 $PGA_2$에 의한 세포사망과 HO-1의 발현 증가를 모두 차단하였지만, non-thiol antioxidant인 butylated hydroxyanisole (BHA)과 ascorbic acid는 세포사망과 HO-1의 발현 유도를 차단하지 않았다. 이와 같은 결과들은 $PGA_2$는 산화성 손상에 의해서가 아니라 $PGA_2$의 thiol-reactivity에 의하여 apoptosis와 HO-1의 발현을 유도하며, HO-1의 발현은 $PGA_2$에 의한 apoptosis와는 독립적인 현상이거나 기능적으로 apoptosis 유도의 하부에 위치하고 apoptosis의 진행에는 기여하지 않을 것이라는 것을 시사해 준다. Prostaglandin $A_2$ ($PGA_2$), one of cyclopentenone PGs, induced both apoptosis and heme oxygenase (HO)-1 expression in U2OS cells. $PGA_2$-induced apoptosis was not perturbed by either over-expression or knock-down of HO-1, whereas $H_2O_2$-induced cell death was inversely modulated by the expression level of HO-1. In addition, N-acetyl-L-cysteine (NAC), a thiol antioxidant, blocked both apoptosis and HO-1 expression induced by $PGA_2$. But, non-thiol antioxidants like butylated hydorxyanisole (BHA) and ascorbic acid did not block either apoptosis or HO-1-induction. Taken together, these results suggest that $PGA_2$ induces both apoptosis and HO-1 expression, which are critically related to the thiol- reactivity of $PGA_2$, but not oxidative stress, and HO-1 expression may be independent or functionally located downstream of apoptosis by $PGA_2$ without contribution to apoptosis progression.
<P><B>Abstract</B></P> <P>Heme oxygenase-1 (HO-1) has an anti-inflammatory action in acute pancreatitis (AP). However, its mechanism of action and natural compounds/drugs to induce HO-1 in pancreas are not well understood. In this study, we investigated the regulatory mechanisms of HO-1 during AP using desoxo-narchinol-A (DN), the natural compound inducing HO-1 in the pancreas. Female C57/BL6 Mice were intraperitoneally injected with supramaximal concentrations of cerulein (50 μg/kg) hourly for 6 h to induce AP. DMSO or DN was administered intraperitoneally, then mice were sacrificed 6 h after the final cerulein injection. Administration of DN increased pancreatic HO-1 expression through activation of activating protein-1, mediated by mitogen-activated protein kinases. Furthermore, DN treatment reduced the pancreatic weight-to-body weight ratio as well as production of digestive enzymes and pro-inflammatory cytokines. Inhibition of HO-1 by tin protoporphyrin IX abolished the protective effects of DN on pancreatic damage. Additionally, DN treatment inhibited neutrophil infiltration into the pancreas via regulation of chemokine (C-X-C motif) ligand 2 (CXCL2) by HO-1. Our results suggest that DN is an effective inducer of HO-1 in the pancreas, and that HO-1 regulates neutrophil infiltration in AP via CXCL2 inhibition.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Desoxo-narchinol-A (DN) is a natural compound of HO-1 inducer in pancreas. </LI> <LI> Mechanism of DN-induced HO-1 is mediated by MAPK/Activator Protein-1/HO-1 signaling. </LI> <LI> DN-induced HO-1 blocks neutrophil infiltration into pancreas via inhibition of CXCL2. </LI> <LI> DN inhibits cerulein-induced acute pancreatitis (AP) and AP-associated lung injury. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
A recent study reported that p53 can induce HO-1 by directly binding to the putative p53 responsive element in the HO-1 promoter. In this study, we report that nutlin-3, a small molecule antagonist of HDM2, induces the transcription of HO-1 in a transcription-independent manner of p53. Nutlin-3 induced HO-1 expression at the level of transcription in human cancer cells such as U2OS and RKO cells. This induction of HO-1 did not occur in SAOS cells in which p53 was mutated and was prevented by knocking down the p53 protein using p53 siRNA transfection, but not by PFT-alpha, an inhibitor of the transcriptional activity of p53. Accompanying HO-1 expression, nutlin-3 stimulated the accumulation of ROS and the phosphorylation of MAPKs such as JNK, p38 MAPK and ERK1/2. Nutlin-3-induced HO-1 expression was suppressed by TEMPO, a ROS scavenger, and chemical inhibitors of JNK and p38 MAPK but not ERK1/2. In addition, nutlin-3-induced phosphorylation of JNK but not p38 MAPK was inhibited by TEMPO. Notably, the levels of nutlin-3-induced ROS were correlated with the mitochondrial translocation of p53 and this induction was prevented by PFT-beta, an inhibitor of the mitochondrial translocation of p53. Consistent with the effect of the ROS scavenger and MAPK inhibitors, PFT-beta reduced HO-1 expression and the phosphorylation of JNK induced by nutlin-3. In the experiments of analyzing cell death, the knockdown of HO-1 augmented nutlin-3-induced apoptosis. Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.
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이 논문은 조선후기 국내외에서 학문적인 역량이 탁월했을 뿐만 아니라 서예가로 높은 평가를 받았던 홍양호의 서화론에 관하여 고찰한 것이다. 그의 서화론은 크게 두 가지로 대별되는데, 하나는 홍양호의 서론 중 정신적으로 추구하고 있는 지향점이 무엇인가를 파악하는 ‘書論의 指向'이고, 다른 하나는 서예의 실천적이고 기법적인 면을 다룬 ‘書論의 實際'이다. 前者는 다시 象의 중요성을 밝힌 ‘象의 重視'와 글씨의 자연스러움을 추구한 ‘自然追求'로 나누었다. 후자는 개인의 성정을 드러낼 수 있는가를 다룬 ‘性情表出'과 감평의 기준을 다룬 ‘鑑評技法'으로 나누어 파악하였다. ‘象의 重視'에서 홍양호는 文字學과 『周易』의 象數學을 통해 ‘象'을 중요시 여긴 점이다. 홍양호보다 앞서 周易을 書論에 적용한 대표적인 인물로 玉洞李漵를 들 수 있는데, 그의 『筆訣』은 易理에만 너무 치우쳤다는 평가를 받고 있다. 다음으로 ‘自然追求'에서는 서화가 자연에서의 멋을 구해야 함을 인식하고 인위적인 기교를 배격하여 억지로 잘 쓰려고 했던 당대 서풍을 비판하였다. 이는 후대 서화가로 이름난 李三晩의 ‘順自然觀'에서 더욱 정치한 이론을 낳게 한다. ‘性情表出'에서는 부단한 노력과 바른 자세와 정신을 갖추지 않고는 도달할 수 없음을 밝혔다. 마지막으로 ‘鑑評技法'에서는 그는 한때 유행했던 ‘時體'를 부정하고 정통 서학의 맥이라 할 수 있는 북해 이옹의 서체를 익혀야 할 것을 역설하였고, 종국에는 왕희지를 추구할 것을 설파하고 있다. 대다수의 서예가들은 왕희지를 높이평가하고 있으나 홍양호는 서예감평의 기준을 ‘古意' 유무에 따라 판단하기에 이른다. 요컨대 그의 書論은 象→自然→硏鑽→古意로 요약된다. 홍양호는 ‘筆訣'이 있었으나 현존하지 않으므로 본 논고에서는 그의 문집에 남아있는 서론적인 부분만을 발췌 정리하여 사라진 필결의 내용도 추정해 보고자 했다. 뿐만 아니라 그는 당대 최고의 문장가라는 사실, 중국을 자주 사행한 일, 왕실과의 긴밀한 관계, 선대로부터 내려온 수장이 홍양호 후대까지 수장 정리되어온 일련의 관계에서 입증하기에 부족함이 없다. 또한 그의 서화에 대한 논의는 후대 서화 이론가에게 끼친 영향을 통해서도 재평가할 여지가 있음이 확인 되었다. 본고에서는 이론적인 면만을 다룬 한계점이 있으나, 이 연구를 통해 서화 비평과 서화수장 연구에 바탕으로 삼고자 한다. This study examined the calligraphic theory of Hong Yang-ho, who won fame at home and overseas in the late Chosun Dynasty not only for his outstanding academic competence but also as a calligrapher. His calligraphic theory can be discussed largely in two directions. One is ‘the goal of his calligraphic theory,' which is to find what Hong Yang-ho's calligraphic theory aims at, and the other is ‘the reality of calligraphic theory,' which deals with the practical and technical aspects of calligraphy. In this study, the former was again sub-divided into ‘emphasis on image,' which explains the importance of image, and ‘pursuit of nature', which pursued the being natural of characters. The latter was also subdivided into ‘expression of disposition,` which dealt with whether to be able to expression individuals' disposition, and ‘appreciation and evaluation technique,'which dealt with criteria for appreciation and evaluation. In ‘emphasis on image,' Hong Yang-ho attaches importance to ‘image' through graphonomy and Hsiang-shu-hsueh in I-Ching. In Korea, a representative person who applied I-Ching to calligraphic theory is Okdong Lee Seo, and it is believed that Hong Yang-ho might be influenced by him, and Lee Seo's Pilgyeol was criticized for its excessive inclination to the theory of I-Ching. Next, with regard to ‘pursuit of nature,' Hong Yang-ho maintainedthat calligraphy and art should find beauty in nature and artificial techniques should be excluded, and criticized the calligraphic style in his days, which sought invented beauty. Later, this position led to the birth of a further refined theory in Lee Sam-man's ‘view of pure nature.' With regard to ‘expression of disposition,' he suggested that one cannot attain the expression of disposition without unceasing efforts as well as right attitude and mind. Lastly in ‘appreciation and evaluation techniques,' he denied ‘temporary styles' that were popular for some time, and asserted learning Bukhae Li Yong's calligraphic style and ultimately pursuing Hui-Chih Wang. Most of calligraphers appreciated Hui-Chih Wanghigh, but Hong Yang-ho came to judge based on whether to have `intention' as a criterion for appreciation and evaluation. In short, his calligraphic theory is summarized into image, nature, hard pursuit, and intention. Among the four, intention was what Hong Yang-ho mentioned most frequently and attached the highest importance to. Hong Yang-ho wrote ‘Pilgyeol' but is not extant, so this studytried to estimate the contents of Pilgyeol by extracting parts related to calligraphic theory from his writings. Furthermore, the discussion of this study is supported by the fact that Hong Yang-ho was the supreme writer in his days, his frequent diplomatic missions to China, his close relationship with theroyal family, and materials transmitted from hisancestors and handed down to his descendents. Furthermore, it was confirmed that discussion on his calligraphy and art needs to be reevaluated through his influence on other calligraphic theorists. This study had a limitation as it coveredonly the theoretical aspect, but its results may provide a base for further research on calligraphy and art criticism and collection.
Backgrounds: Prostaglandin (PG) A2 reportedly stimulated expression of heme oxygenase (HO)-1 at the level of transcription via the activation of p38MAPK. Details of the mechanism, however, have not been provided, and this includes identification of the transcription factors responsible for PGA2-induced HO-1 expression. Herein is described an analysis of the role of nuclear factor erythroid 2 related factor 2 (Nrf2) and how PGA2 increases the activity of Nrf2 during PGA2-induced HO-1 expression. Methods: Expressions of HO-1 and Nrf2 were analyzed at the levels of both mRNA and protein. Nrf2 siRNA, SB203580, an inhibitor of p38MAPK, and scavengers of reactive oxygen species (ROS) were used to identify the effects of Nrf2, p38MAPK and ROS on PGA2-induced HO-1 expression. Results: Although SB203580 suppressed PGA2-induced HO-1 expression, genetic activation of p38MAPK could not stimulate the transcription of HO-1. Cycloheximide (CHX), an inhibitor of protein translation, almost completely prevented PGA2-induced increase of HO-1 transcription, but it did not prevent the phosphorylation of p38MAPK, which suggests that both de novo protein synthesis and p38MAPK activity are required to induce the transcription of HO-1 in response to PGA2 treatment. In addition, PGA2 increased the level of both Nrf2 mRNA and protein in a dose-dependent manner. Knockdown of Nrf2 using small interfering RNA (siRNA) suppressed PGA2-induced HO-1 expression. The PGA2-induced transcription of Nrf2 was prevented by ROS scavengers such as n-acetyl-l-cysteine and tempol but not CHX. Furthermore, siRNA against p38MAPK did not change the level of nuclear Nrf2 protein. Conclusion: These findings suggest that PGA2 induces HO-1 transcription via an increase in Nrf2 protein, the transcription of which is initiated by an accumulation of ROS that is independent of the p38MAPK activation pathway.
Prostaglandin (PG) A2 which is a cytotoxic PG, was reported to induce the expression of heme oxygenase (HO)-1 via activation of p38MAPK to keep U2OS cells from cell cycle arrest in G2M phase. The expression of HO-1 is primarily regulated at the level of transcription. But the transcription factors that are responsible for PGA2-induced HO-1 expression were not clarified yet. Here, we report that PGA2-induced transcription of HO-1 is mediated by p53, a tumor suppressive transcription factor. In HCT116 cells, PGA2 treatment led to the phosphorylation of p53 and an increase of p21WAF1 transcription as well as the activation of HO-1 transcription. Knocking p53 down via RNA interference or inhibiting the p53's transcriptional activity by pifithrin-α treatment led to suppression of the increase in the level of both HO-1 expression and activity of HO-1 promoter. Pretreatment of NU- 7441, a chemical inhibitor of DNA-activated protein kinase (DNA-PK), prevented both the PGA2-induced phosphorylation of p53 and an increase of HO-1 transcription. In addition, N-acetyl-l-cysteine, a scavenger of reactive oxygen species (ROS), also mimicked the effect of NU-7441 on the PGA2-induced activation of p53 and HO-1 transcription. Collectively, these results suggest that PGA2 induces the expression of HO-1 via activation of p53, which is mediated by the ROSDNA- PK pathway.
<P><B>Abstract</B></P> <P>Hydrothermal process was employed to synthesize the Yb<SUP>3+</SUP>/Tm<SUP>3+</SUP>, Yb<SUP>3+</SUP>/Ho<SUP>3+</SUP> and Yb<SUP>3+</SUP>/Tm<SUP>3+</SUP>/Ho<SUP>3+</SUP> doped BaMoO<SUB>4</SUB> octahedron microcrystals (0.50–5.0 µm). The synthesized phosphors have scheelite tetragonal structure. The elemental mapping suggests the uniform distribution of elements in the samples. The oxidation state of samples were investigated by X-ray photoelectron spectroscopy (XPS) which indicates the existence of Ba<SUP>2+</SUP>, Mo<SUP>6+</SUP>, O, Yb<SUP>3+</SUP>, Tm<SUP>3+</SUP> and Ho<SUP>3+</SUP> in samples. The presence of rare earth ions was also verified by observation of specific absorption peaks in diffuse reflectance spectra (DRS). The tunable multicolor upconversion (UC) emissions were successfully obtained under 980 nm NIR excitation by precisely adjusting the concentration of rare earth ions. The as prepared sample exhibits blue, green and red emission as a result of energy transfer from the Yb<SUP>3+</SUP> to Tm<SUP>3+</SUP> and Ho<SUP>3+</SUP> ions. The power dependent UC emission spectra show the two photonic processes. The energy transfer mechanism from Yb<SUP>3+</SUP> to Tm<SUP>3+</SUP> and Ho<SUP>3+</SUP> was explained <I>via</I> an energy level analysis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Synthesis of BaMoO<SUB>4</SUB>: Yb<SUP>3+</SUP>, Ln<SUP>3+</SUP> (Ln = Tm, Ho, Tm/Ho) by hydrothermal process. </LI> <LI> Investigation of upconversion luminescence of phosphors under 980 nm excitation. </LI> <LI> Obtaining the multicolor emission by adjusting doped rare-earth ions concentration. </LI> <LI> Explanation of photonic process and energy transfer mechanism. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>Multicolor upconversion emission properties of BaMoO<SUB>4</SUB>: Yb<SUP>3+</SUP>, Ln<SUP>3+</SUP> (Ln = Tm, Ho, Tm/Ho) octahedrons</P> <P>[DISPLAY OMISSION]</P>
Purpose: Tacrolimus (FK506) has been widely used as an immunosuppressant in organ transplanted recipients to suppress organ rejection phenomenon. We investigated the role of oxidative stress and heme oxygense-1 by FK506 on human Jurkat T cells. Methods: The cells viability was examined by DAPI stain, enzyme activity of caspase family proteins, and western blotting for Baks, PUMA, iNOS, HO-1. Cells were cultured in the absence or presence of CoPPIX or ZnPPIX and the fluorescence intensity was analyzed using a flow cytometry. Results: Treatment with FK506 increased the generation of reactive oxygen species (ROS), including hydrogen peroxide and superoxide anion, and NO in Jurkat cells in a dose-dependent manner. Immunohistochemistry and Western blot analysis data revealed the hemoxygenase-1 (HO-1) was induced by the addition of FK506 in Jurkat cells. Induction of CoPP, HO-1 inducer, resulted in decreased intracellular H₂O₂ and NO concentrations. Instead ZnPP, an HO-1 competitive inhibitor did it reversely. In addition, ZnPP regulates iNOS protein synthesis by inhibition of HO-1. Conclusion: Increase of HO-1 expression would induce to decrease the intracellular H₂O₂ and NO concentrations. Also, HO-1 would regulate iNOS protein synthesis. Consequently, we can expect the regulation of HO-1 expression with concomitants use of FK506 to suppress organ rejection phenomenon by enhancing apoptosis.