• Nutrition Research and Practice
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• v.9 no.6
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• pp.579-585
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• 2015

BACKGROUND/OBJECTIVES: Sonchus asper is used extensively as an herbal anti-inflammatory for treatment of bronchitis, asthma, wounds, burns, and cough; however, further investigation is needed in order to understand the underlying mechanism. To determine its mechanism of action, we examined the effects of an ethyl acetate fraction (EAF) of S. asper on nitric oxide (NO) production and prostaglandin-E2 levels in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. MATERIALS/METHODS: An in vitro culture of RAW264.7 macrophages was treated with LPS to induce inflammation. RESULTS: Treatment with EAF resulted in significant suppression of oxidative stress in RAW264.7 macrophages as demonstrated by increased endogenous superoxide dismutase (SOD) activity and intracellular glutathione levels, decreased generation of reactive oxygen species and lipid peroxidation, and restoration of the mitochondrial membrane potential. To confirm its anti-inflammatory effects, analysis of expression of inducible NO synthase, cyclooxygenase-2, tumor necrosis factor-${\alpha}$, and the anti-inflammatory cytokines IL-$1{\beta}$ and IL-6 was performed using semi-quantitative RT-PCR. EAF treatment resulted in significantly reduced dose-dependent expression of all of these factors, and enhanced expression of the antioxidants MnSOD and heme oxygenase-1. In addition, HPLC fingerprint results suggest that rutin, caffeic acid, and quercetin may be the active ingredients in EAF. CONCLUSIONS: Taken together, findings of this study imply that the anti-inflammatory effect of EAF on LPS-stimulated RAW264.7 cells is mediated by suppression of oxidative stress.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.20 no.12
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• pp.2395-2400
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• 2016

Conventional drug carriers such as liposomes, nanoparticles, polymer micelles, polymeric conjugate and lipid microemulsion for cancer chemotherapy shield normal tissues from toxic drugs to treat cancer cells in tumors. However, inaccurate tumor targeting uncontrolled drug release from the carriers and unwanted accumulation in healthy sites can limit treatment efficacy with current conventional drug carriers with insufficient concentrations of drugs in the tumors and unexpected side effects as a result. Sickle red blood cells show natural tumor preferential accumulation without any manipulation due to the adhesive interaction between molecular receptors on the membrane surface and counter-receptor on endothelial cells. In addition, structural changes of microvascular in tumor sites enhances polymerization of sickle red blood cells. In this research, we examined the use of sickle red blood cells as a new drug carrier with novel tumor targeting and controlled release properties to quantify its therapeutic effects.

• Journal of Environmental Science International
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• v.20 no.12
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• pp.1509-1519
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• 2011

The protective effect of nitric oxide (NO) on the antioxidant system under paraquat(PQ) stress was investigated in leaves of 8-week-old lettuce (Lactuca sativa L.) plants. PQ stress caused a decrease of leaf growth including leaf length, width and weight. Application of NO donor, sodium nitroprusside (SNP), significantly alleviated PQ stress induced growth suppression. SNP permitted the survival of more green leaf tissue preventing chlorophyll content reduction and of higher quantum yield for photosystem II than in non-treated controls under PQ exposure, suggesting that NO has protective effect on chloroplast membrane in lettuce leaves. Flavonoids and anthocyanin were significantly accumulated in the leaves upon PQ exposure. However, the rapid increase of these compounds was alleviated in the SNP treated leaves. PQ treatment resulted in lipid peroxidation and induced accumulation of hydrogen peroxide ($H_2O_2$) in the leaves, while SNP prevented PQ induced increase in malondialdehyde (MDA) and $H_2O_2$. These results demonstrate that SNP serves as an antioxidant agent able to scavenge $H_2O_2$ to protect plant cells from oxidative damage. The activities of two antioxidant enzymes that scavenge reactive oxygen species, superoxide dismutase (SOD) and catalase (CAT) in lettuce leaves in the presence of NO donor under PQ stress were higher than those under PQ stress alone. Application of 2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), a specific NO scavenger, to the lettuce leaves arrested SNP mediated protective effect on leaf growth, photosynthetic pigment and antioxidant systems. However, PTIO had little effect on lettuce leaves under PQ stress compared with that of PQ stress alone. The obtained data suggest that the damage caused by PQ stress is in part due to increased generation of active oxygen by maintaining increased antioxidant enzyme activities and SNP protects plants from oxidative stress. From these results it is suggested that NO might act as a signal in activating active oxygen scavenging system that protects plants from oxidative damage induced by PQ stress and thus confer PQ tolerance.

• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.18 no.1
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• pp.31-45
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• 1988

The author studied the histopathologic changes according to a single or a split dose and the time after irradiation on the acinar cells of rat parotid gland. 99 Sprague Dawley rats, weighing about l20gm, were divided into control and 3 experimental groups. In experimental groups, GroupⅠ and Ⅱ were delivered a single dose of l5Gy, 18Gy and Group Ⅲ and Ⅳ were delivered two equal split doses of 9Gy, 10.5Gy for a 4 hours interval, respectively. The experimental groups were delivered by a cobalt-60 teletherapy unit with a dose rate of 222cGy/min, source-skin distance of 50㎝, depth of l㎝ and a field size of l2×5㎝. The animals were sacrificed at 1, 2, 3, 6, 12 hours, 1, 3, 7 days after irradiation and examined by light and electron microscopy. The results were as follows: 1. As the radiation dose increased and the acinar cells delivered a single dose exposure were more damaged, and the change of acinar cells appeared faster than those of a split dose exposure. 2. The histopathologic change of acinar cells appeared at 1 hour after irradiation. The recovery from damaged acinar cells appeared at 1 day after irradiation and there was a tendency that the recovery from damage of a split dose exposure was somewhat later than that of a single dose exposure. 3. Light microscope showed atrophic change of acinar cells and nucleus, degeneration and vesicle formation of cytoplasm, widening of intercellular space and interlobular space. 4. Electron microscope showed loss of nuclear membrane, degeneration of nucleus and nucleoli, clumping of cytoplasm, widening and degeneration of rough endoplasmic reticulum, loss of cristae of mitochondria, lysosome, autophagosome and lipid droplet. 5. Electron microscopically, the change of rough endoplasmic reticulum was the most prominent and this appeared at 1 hour after irradiation as early changes of acinar cells. The nuclear change appeared at 2 hours after irradiation and the loss of cristae of mitochondria was observed at 2 hours after irradiation in all experimental groups.

• Molecules and Cells
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• v.37 no.7
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• pp.554-561
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• 2014

Lysophosphatidic acid (LPA) is a lipid growth factor that exerts diverse biological effects through its cognate receptors ($LPA_1-LPA_6$). $LPA_1$, which is predominantly expressed in the brain, plays a pivotal role in brain development. However, the role of $LPA_1$ in neuronal migration has not yet been fully elucidated. Here, we delivered $LPA_1$ to mouse cerebral cortex using in utero electroporation. We demonstrated that neuronal migration in the cerebral cortex was not affected by the overexpression of $LPA_1$. Moreover, these results can be applied to the identification of the localization of $LPA_1$. The subcellular localization of $LPA_1$ was endogenously present in the perinuclear area, and overexpressed $LPA_1$ was located in the plasma membrane. Furthermore, $LPA_1$ in developing mouse cerebral cortex was mainly expressed in the ventricular zone and the cortical plate. In summary, the overexpression of $LPA_1$ did not affect neuronal migration, and the protein expression of $LPA_1$ was mainly located in the ventricular zone and cortical plate within the developing mouse cerebral cortex. These studies have provided information on the role of $LPA_1$ in brain development and on the technical advantages of in utero electroporation.

• Molecules and Cells
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• v.40 no.9
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• pp.643-654
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• 2017

Autophagy is a degradation pathway in eukaryotic cells in which aging proteins and organelles are sequestered into double-membrane vesicles, termed autophagosomes, which fuse with vacuoles to hydrolyze cargo. The key step in autophagy is the formation of autophagosomes, which requires different kinds of vesicles, including COPII vesicles and Atg9-containing vesicles, to transport lipid double-membranes to the phagophore assembly site (PAS). In yeast, the cis-Golgi localized t-SNARE protein Sed5 plays a role in endoplasmic reticulum (ER)-Golgi and intra-Golgi vesicular transport. We report that during autophagy, sed5-1 mutant cells could not properly transport Atg8 to the PAS, resulting in multiple Atg8 dots being dispersed into the cytoplasm. Some dots were trapped in the Golgi apparatus. Sed5 regulates the anterograde trafficking of Atg9-containing vesicles to the PAS by participating in the localization of Atg23 and Atg27 to the Golgi apparatus. Furthermore, we found that overexpression of SFT1 or SFT2 (suppressor of sed5 ts) rescued the autophagy defects in sed5-1 mutant cells. Our data suggest that Sed5 plays a novel role in autophagy, by regulating the formation of Atg9-containing vesicles in the Golgi apparatus, and the genetic interaction between Sft1/2 and Sed5 is essential for autophagy.

• BMB Reports
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• v.39 no.5
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• pp.626-635
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• 2006

Lysophosphatidic acid acyltransferase (LPAAT) is an intrinsic membrane protein that catalyzes the synthesis of phosphatidic acid (PA) from lysophosphatidic acid (LPA). It is well known that LPAAT is involved in lipid biosynthesis, while its role in tumour progression has been of emerging interest in the last few years. To date, seven members of the LPAAT gene family have been found in human. Here we report a novel LPAAT member, designated as LPAAT-theta, which was 2728 base pairs in length and contained an open reading frame (ORF) encoding 434 amino acids. The LPAAT-theta gene consisted of 12 exons and 11 introns, and mapped to chromosome 4q21.23. LPAAT-theta was ubiquitously expressed in 18 human tissues by RT-PCR analysis. Subcellular localization of LPAAT-theta-EGFP fusion protein revealed that LPAAT-theta was distributed primarily in the endoplasmic reticulum (ER) of COS-7 cells. Furthermore, we found that the overexpression of LPAAT-theta can induce mTOR-dependent p70S6K phosphorylation on Thr389 and 4EBP1 phosphorylation on Ser65 in HEK293T cells.

• BMB Reports
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• v.45 no.1
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• pp.26-31
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• 2012

TRIM72 is known to play a critical role in skeletal muscle membrane repair. To better understand the molecular mechanisms of this protein, we carried out an in vitro binding study with TRIM72. Our study proved that TRIM72 binds various lipids with dissociation constants ($K_d$) ranging from 88.2 ${\pm}$ 9.9 nM to 550.5 ${\pm}$ 134.5 nM. In addition, the intrinsic fluorescence of TRIM72 exponentially decreased when the protein was diluted with stirring. The time-resolved fluorescence decay occurred in a concentration-independent manner. The fluorescence-decayed TRIM72 remained in its secondary structure, but its binding properties were significantly reduced. The dissociation constants ($K_d$) of fluorescence-decayed TRIM72 for palmitate and stearate were 159.1 ${\pm}$ 39.9 nM and 355.4 ${\pm}$ 106.0 nM, respectively. This study suggests that TRIM72 can be dynamically converted by various stimuli. The results of this study also provide insight into the role of TRIM72 in the repair of sarcolemma damage.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.1025-1034
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• 2009

This study was carried out to examine the protective effect of Cultured Wild Ginseng(CWG) on the acute and subacute toxicities induced by doxorubicin(Doxo) in mice. Heart and liver weight was decreased following Doxo administration. In contrast, such a decrease was significantly attenuated by CWG administration. The value of serum CPK in Doxo group was increased compared with normal group. But the value of CWG group were decreased significantly compared with the values of Doxo group in the liver of the Doxo group, cloudy swelling of hepatic cells and narrowing of sinusoids were observed. Whereas in the CWG group, well oriented hepatic cell cords and sinusoids were observed. In the testis of the Doxo group, necrotic and degenerative changes of the seminiferous tubules, especially beneath testicular membrane were observed. But those lesions were alleviated in CWG group. Cross sectional area of testis and diameter of semineferous tubule were significantly increased in CWG group compared with Doxo group. Body weight was reduced in Doxo group compared with normal group. In contrast, such a decrease was significantly attenuated by CWG administration atwa5th day. Spermatogenetic cells in seminiferous tubules were necrotic and desquamated and the cellularity of seminiferous epithelia was reduced in Doxo group. But those lesions were attenuated by CWG administration. Cross sectional area of testis and diameter of seminiferous tubule were significantly increased in CWG group compared with Doxo group. In addition, the increase in lipid peroxidation(LPO) in testis was inaddition, the, iout such a increased was significantly inhibited in CWG group. BrdU labelled cells in the seminiferous tubules were remarkably decreased in Doxo group. Whereas the number of seminiferous tubules labelled with BrdU in spermatogonia was increased by CWG administration. The obtained results suggest that CWG has protective effect on doxorubicin-induced toxicity. This effect might be mediated through the supplementation of vital energy.

• Toxicological Research
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• v.11 no.2
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• pp.215-221
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• 1995

This paper examines the effects of dietary polyunsaturated fatty acid/saturated fatty acid (p/s) ratios and butylated hydroxytoluene (BHT) on the hepatic microsomaI mixed-function oxidase sy. stem in 2~acetylaminofiuorene (2-AAF) treated rats. Sprague-Dawley male rats were fed the diet of beef tallow (p/s 0.08), beef tallow plus soybean oil (p/s 1.0), and soybean oil (p/s 4.0) at the level of 15%fat and with or without 0.3% BHT. After 2-AAF was injected twice at the ages of 23 and 27 weeks, cholesterol/phospholipid molar ratio, thiobarbituric acid reactive substances (TBARS) level, cytochrome P450, cytochrome $b_5$, NADPH-cytochrome $b_5$, and NADPH-cytochrome c reductase activity were measured from isolated hepatic microsomal fractions. In the beef tallow (p/s 0.08) and beef tallow plus soybean oil (p/s 1.0) groups, cholesterol/phospholipid molar ratio showed decreasing tendency by 2-AAF and BHT. Cytochrome P-450 content was decreased in the group of soybean oil (p/s 4.0) and NADPH-cytochrome c reductase activity was increased by 2-AAF and BHT in all the dietary groups. While TBARS levels were increased by 2-AAF in all the dietary groups, they were reduced by BHT in the soybean oil (p/s 4.0) group. These results suggest that long term intake of soybean oil (p/s 4.0) diet induced changes in the nature of microsomal membrane and induced less cytochrome P-450, low level feeding of BHT increased cytochrome c reductase activity and lowered microsomal lipid peroxidation levels, which were increased by 2-AAF treatment.