• BMB Reports
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• v.39 no.5
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• pp.479-491
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• 2006

Heme oxygenase (HO), the rate limiting enzyme in the breakdown of heme into carbon monoxide (CO), iron and bilirubin, has recently received overwhelming research attention. To date three mammalian HO isozymes have been identified, and the only inducible form is HO-1 while HO-2 and HO-3 are constitutively expressed. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-${\kappa}B$) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. The products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect against chemically-induced liver injury as well as hepatocarcinogenesis.

• Journal of Korean Neurosurgical Society
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• v.59 no.3
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• pp.259-268
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• 2016

Objective : Accumulation of advanced glycation end-products (AGE) and mitochondrial glycation is importantly implicated in the pathological changes of the brain associated with diabetic complications, Alzheimer disease, and aging. The present study was undertaken to determine whether sildenafil, a type 5 phosphodiesterase type (PDE-5) inhibitor, has beneficial effect on neuronal cells challenged with AGE-induced oxidative stress to preserve their mitochondrial functional integrity. Methods : HT-22 hippocampal neuronal cells were exposed to AGE and changes in the mitochondrial functional parameters were determined. Pretreatment of cells with sildenafil effectively ameliorated these AGE-induced deterioration of mitochondrial functional integrity. Results : AGE-treated cells lost their mitochondrial functional integrity which was estimated by their MTT reduction ability and intracellular ATP concentration. These cells exhibited stimulated generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential, induction of mitochondrial permeability transition, and release of the cytochrome C, activation of the caspase-3 accompanied by apoptosis. Western blot analyses and qRT-PCR demonstrated that sildenafil increased the expression level of the heme oxygenase-1 (HO-1). CoPP and bilirubin, an inducer of HO-1 and a metabolic product of HO-1, respectively, provided a similar protective effects. On the contrary, the HO-1 inhibitor ZnPP IX blocked the effect of sildenafil. Transfection with HO-1 siRNA significantly reduced the protective effect of sildenafil on the loss of MTT reduction ability and MPT induction in AGE-treated cells. Conclusion : Taken together, our results suggested that sildenafil provides beneficial effect to protect the HT-22 hippocampal neuronal cells against AGE-induced deterioration of mitochondrial integrity, and upregulation of HO-1 is involved in the underlying mechanism.

• Journal of Veterinary Clinics
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• v.24 no.2
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• pp.164-168
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• 2007

This study was performed to establish the recovery effect of So Si Ho Tang on hepatic injury in dogs. Clinically healthy eight dogs (1-3 yrs old, 3-5 kg) were divided into control group (n=3) and experimental group (50 mg/kg, n=5). Hepatic injury was induced by administration of $CCl_4$ in all groups. Control group was received no treatment after hepatic injury and experimental group was orally administered with So Si Ho Tang at a dose of 50 mg/kg. The change of serum ALT and AST activities was examined before hepatic injury and on day 0, day 5 and day 12 after administration of So Si Ho Tang. Histopathologic examinations were performed on day 12. As a result, significant changes in serum ALT were found on day 5(p<0.05) and day 12(p<0.05), compared with those of control group, respectively. In addition, significant change in serum AST was found on day 1 (p<0.05) and day 5 (p<0.05), compared with those of control group, respectively. In histopathologic examination, mild hemorrhage and fatty degeneration and vacuolization were observed in experimental group in contrast to those of control group. Accordingly, it was suggested that administration of So Si Ho Tang was effective for hepatic injury induced by $CCl_4$ in dogs.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2009.04b
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• pp.67-67
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• 2009

본 연구는 강유전체 박막의 buffer 층으로 사용되는 Yttrium oxide($Y_2O_3$) 박막에 대한 $BCl_3$/Ar 혼합가스 식각 특성에 대해 연구하였다. 식각 메카니즘을 해석하기 위해 QMS(Quadrupole Mass Spectrometer), OES(Optical Emission Spectroscopy)를 사용하여 플라즈마 특성을 추출하였다. 공정 조건(source power, bias power, pressure, total gas flow)을 동일하게 유지하고 $BCl_3$/Ar 혼합가스 비율을 변화시키며 실험을 진행 하였다. 혼합가스의 비율이 $BCl_3$(80%)/Ar(20%)일때 가장 높은 식각 속도을 나타냈고, 이후 점차 감소하였다. 이때의 식각 속도는 8.8 nm/min 였다. 이에 $Y_2O_3$는 이온 보조 화학식각 특성을 가짐을 확인하였다.

• Molecular & Cellular Toxicology
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• v.3 no.sup4
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• pp.33.3-33.3
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• 2007

• Bulletin of the Korean Chemical Society
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• v.21 no.11
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• pp.1069-1070
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• 2000

• Bulletin of the Korean Chemical Society
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• v.11 no.3
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• pp.187-188
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• 1990

• Journal of Plant Biology
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• v.34 no.4
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• pp.331-339
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• 1991

To elucidate the regulatory mechanism of virE operon from vir regions (virA, virB, virC, virD, virG, virE) of pTiA6 which have been known to be essential for efficient crown gall tumorigenesis in plants, the activity of the truncated virE, promoter was analyzed. pSM358cd, a recombinant plasmid in which virE :: Tn3-HoHo1 (Tn3-promoterless lacZ) was cloned into SalI site of pVK102, was digested with SalI, and virE :: Tn3-HoHo1 was seperated from pVK102. To construct the truncted virE recombinant plasmids (pJS031, pJS051, pJS102, pJS201, pJS301), 5'-end of vireE promoter was deleted with BAL31 and cloned into pVK102 and then transferred into a. tumefaciens A348(pTiA6). According to the activity of the truncated virE promoter in recombinant plasmids, they were classified into two groups, pJS031, pJS051, pJS101 and pJS201 belong to a functional group and pJS301 is a non-functional. The size of deleted nucleotides of pJS201 and pJS301 seemed to be about 130 nucleotides and about 250 nucleotides from 5'-end of virE promoter, respectively. Hence it was thought that the essential site of the virE promoter was located between about 130th nucleotide and 250th nucleotide from 5'-end of the virE promoter.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.10a
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• pp.65-65
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• 2019

In this study, we evaluated the anti-inflammatory effect of extracts of leaves (LCLE) and branches (LCBE) from L. caerulea in LPS-stimulated RAW264.7 cells. Inhibitory effect of LCLE and LCBE against LPS-induced overproduction of NO, iNOS and $IL-1{\beta}$ was higher than LCFE. Furthermore, LCLE and LCBE significantly inhibited the overexpression of COX-2, IL-6 and $TNF-{\alpha}$ in LPS-stimulated RAW264.7 cells. LCLE and LCBE did not inhibited LPS-induced degradation of $I{\kappa}B-{\alpha}$, but blocked the nuclear accumulation of p65. LCLE did not inhibited LPS-induced phosphorylation of ERK1/2 and p38, while LCBE significantly attenuated phosphorylation level of p38. LCLE and LCBE increased HO-1 protein level and decrease of iNOS and $IL-1{\beta}$ expression by LCLE and LCBE was inhibited by HO-1 knockdown. The inhibition of p38 by SB203580 and ROS by NAC blocked HO-1 expression by LCLE and LCBE. LCLE and LCBE increased p38 phosphorylation and the inhibition of ROS by NAC blocked p38 phosphorylation LCLE and LCBE. LCLE and LCBE induced nuclear accumulation of Nrf2, but this was significantly reversed by the inhibition of p38 and ROS. In addition, LCLE and LCBE increased ATF3 expression and decrease of iNOS and $IL-1{\beta}$ expression by LCLE and LCBE was inhibited by ATF3 knockdown. Collectively, LCLE and LCBE inhibited LPS-induced $NF-{\kappa}B$ activation by blocking p65 nuclear accumulation, increased HO-1 expression by ROS/p38/Nrf2 activation, and increased ATF3 expression. Furthermore, LCBE inhibited LPS-induced p38 phosphorylation.

• Geomechanics and Engineering
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• v.29 no.2
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• pp.183-192
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• 2022

Piled raft foundations are widely used and effective in supporting high-rise buildings around the world. In this study, a piled raft system was numerically simulated using PLAXIS 3D. The settlement comparison results between the actual building measurements and the three-dimensional (3D) numerical analysis, were in good agreement, indicating the usefulness of this approach for the evaluation of the feasibility of using a piled raft foundation in Ho Chi Minh City subsoil. The effects were investigated of the number of piles based on pile spacing, pile length, raft embedment on the settlement, load sharing, bending moments, and the shear force of the piled raft foundation in Ho Chi Minh City subsoil. The results indicated that with an increased number of piles, increased pile length, and embedding raft depth, the total and differential settlement decreased. The optimal design consisted of pile numbers of 60-70, corresponding to pile spacings is 5.5-6 times the pile diameter (D_p), in conjunction with a pile length-to-pile diameter ratio of 30. Furthermore, load sharing by the raft, by locating it in the second layer of stiff clay, could achieve 66% of the building load. The proposed model of piled raft foundations could reduce the total foundation cost by 49.61% compared to the conventional design. This research can assist practicing engineers in selecting pile and raft parameters in the design of piled raft foundations to produce an economical design for high-rise buildings in Ho Chi Minh City, Viet Nam, and around the world.