Oh, You Na;Jin, Soojung;Park, Hyun-jin;Kim, Byung Woo;Kwon, Hyun Ju
Journal of Life Science
/
v.25
no.5
/
pp.515-522
/
2015
Treculia africana Decne, a breadfruit species, is native to many parts of West and Tropical Africa. The breadfruit belongs to the family Moraceae and is one of the four members of the genera Treculia. The crude extract of T. africana has been used in folk medicine as an anti-inflammatory agent for various ailments, such as whooping cough. In this study, we evaluated the anti-oxidative and anti-cancer activities of the methanol extract of T. africana Decne (META) and the molecular mechanisms of its anti-cancer effects in human colon carcinoma HT29 cells. The META exhibited anti-oxidative activity through a DPPH radical scavenging capacity and inhibited cell growth in a dose-dependent manner in HT29 cells. META treatment induced apoptosis of HT29 cells, showing an increase in the percentage of both SubG1 cells and Annexin V-positive cells and the formation of apoptotic bodies in a dose-dependent manner. META-mediated apoptosis was associated with the up-regulation of the death receptor FAS and Bax and a decrease in the Bcl-2 expression. META-treated HT29 cells also showed the release of cytochrome c from the mitochondria into the cytosol, activation of caspase-3, caspase-8, and caspase-9, and proteolytic cleavage of poly ADP-ribose polymerase (PARP). These findings suggest META may exert an anti-cancer effect in HT29 cells by inducing apoptosis through both intrinsic and extrinsic pathways.
Kim, Hyun-Ji;Bae, In-Seon;Seo, Kang-Seok;Kim, Sang Hoon
Journal of Life Science
/
v.24
no.7
/
pp.798-803
/
2014
Cathepsin D (CtsD), an aspartyl peptidase, is involved in apoptosis, resulting in the release of cytochrome C from mitochondria in cells. Here, we investigated microRNA regulation of CtsD expression in 3T3-L1 cells First, we observed the expression of CtsD in cells in response to doxorubicin (Dox). As expected, the level of CtsD mRNA was increased in 3T3-L1 cells exposed to Dox in a dose-dependent manner. Cellular viability of ectopically expressed CtsD cells was also decreased. Next, we used the miRanda program to search for particular microRNA targeting CtsD. MiR-145 was selected as a putative controller for CtsD because miR-145 had a high mirSVR score. In a reporter assay, the luciferase activity of cells containing the CtsD 3'-UTR region was decreased in cells transfected with miR-145 mimic compared to that of a control. The level of CtsD expression was down-regulated in preadipocytes ectopically expressing miR-145 and up-regulated by an miR-145 inhibitor. Cells also suppressed miR-145 expression when exposed to Dox. The miR-145 inhibitor reduced the cellular viability of 3T3-L1 cells. Taken together, these data suggest that miR-145 regulates CtsD-mediated cell death in adipocytes. These findings may have valuable implications concerning the molecular mechanism of CtsD-mediated cell death in obesity, suggesting that CtaD could be a useful therapeutic tool for the prevention and treatment of obesity by regulating fat cell numbers.
The objective of this study was to evaluate the anti-inflammation effect of extract of Carthamus tinctorious seed, on skin obtained from Gyeong buk, Korea. Regulatory mechanisms of cytokines and nitric oxide (NO) involved in immunological activity of Raw 264.7 cells. Tested cells were pretreated with 70% ethanol extracted of Carthamus tinctorious seed and further cultured for an appropriated time after the addition of lipopolyssacharide (LPS). During the entire experimental period, 5, 10, 25 and 50 ${\mu}g/ml$ of Carthamus tinctorious seed showed no cytotoxicity. In these concentrations, ethyl acetate layer of ethanol extracted Carthamus tinctorius seed (CT-E/E) inhibited the production of NO and prostaglandin $E_2$ ($PGE_2$), tumor necorsis factor-a (TNF-${\alpha}$), interleukin-$1{\beta}$ (IL-$1{\beta}$), interleukin-6 (IL-6) expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2). At a 50 ${\mu}g/ml$ level of CT-E/E, $PGE_2$, iNOS and COX-2 inhibition activity were shown 60%, 38%, and 42%, respectively. In addition, CT-E/E reduced the release of inflammatory cytokines including TNF-${\alpha}$, IL-$1{\beta}$ and IL-6. These results suggest that Carthamus tinctorious seed extracts may be a potential anti-inflammatory therapeutic agent due to the significant effects on inflammatory factors.
Kim, Hyeon-Jeong;Kim, Dong-Hee;Lee, Jin-Young;Hwang, Jae-Sam;Lee, Joon-Ha;Lee, Seul-Gi;Jeong, Hyeon-Guk;An, Bong-Jeun
Journal of Life Science
/
v.23
no.1
/
pp.38-43
/
2013
The objective of this study was to evaluate the effect of the synthetic CopA3 peptide of Copris tripartitus on skin inflammation. Regulatory mechanisms of cytokines and nitric oxide (NO) are involved in the immunological activity of RAW 264.7 cells. Tested cells were treated with different concentrations of CopA3 and further cultured for an appropriate time after lipopolyssacharide (LPS) addition. During the entire experimental period, 5, 25, 50, and 100 ${\mu}g/ml$ of CopA3 had no cytotoxicity. At these concentrations, CopA3 inhibited tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-$1{\beta}$ (IL-$1{\beta}$), and interleukin-6 (IL-6). CopA3 also inhibited the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). CopA3 inhibited the activity of iNOS and COX-2 by 41% and 59%, respectively, at 100 ${\mu}g/ml$. In addition, CopA3 reduced the release of inflammatory cytokines including TNF-${\alpha}$, IL-$1{\beta}$, and IL-6. These results suggest that CopA3 may have significant effects on inflammatory factors and that it may be a potential anti-inflammatory therapeutic agent.
Journal of the korean academy of Pediatric Dentistry
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v.34
no.1
/
pp.73-80
/
2007
Compomer that release fluoride could be used on proximal caries of child effectively. But oral cavity is always wet, so saliva inhibits bonding of tooth and compomer. When the saliva exist on bonding, it can be occured microleakages. The purpose of this study was to evaluate the influence of salivary contamination on compomer restoration and degree of microleakage according to restoration methods. Dyract $AP^{(R)}$ and prime and $bond^{(R)}$ NT was applied by the manufacture s instructions. Elipar Trilight was applied for light curing. Saliva pool was made for reconstruction of oral cavity. Two premolar was embedded in acrylic resin. After class II cavity preperation, Dyract $AP^{(R)}$ was restored under several condition, the specimen was thermocycled 500 times with 30 second dwell time. 0.5% methylene blue was used for microleakage test. Micoleakage was measured by the ratio of the infiltration length to occlusal and gingival side interface. Data were analyzed statistically using Kruskal Wallis Test, Mann-Whitney Test. The Result were as follows ; 1. In occlusal side, there were no statistical differences. 2. In gingival side, there were no statistical differences in Group III ($ContactMatrix^{TM}$, Rubber dam, $Oraseal^{(R)}$), Group IV (No saliva contamination). 3. In gingival side, there were no statistical differences in Group I$(ContactMatrix^{TM})$, II($ContactMatrix^{TM}$, Rubber dam). 4. In gingival side, there were statistical differences in Group I$(ContactMatrix^{TM})$, II($ContactMatrix^{TM}$, Rubber dam).
Chung, Joon-Ki;Hong, Sung-Cheul;Choi, Su-Kyung;Kang, Maeng-Hee;Ku, Mi-Geong;Park, Sang-Il;Yun, Il
YAKHAK HOEJI
/
v.34
no.3
/
pp.180-191
/
1990
A comparison was made of the effects of selective ${\alpha_1}-adrenoceptor$ agonist phenylephrine and selective ${\alpha_2}-adrenoceptor$ agonist clonidine on endothelium-containing and endothelium-denuded rings of the rat aorta. In the case of phenylephrine, removal of endothelium increased sensitivity 2.5 fold at $EC_{50}$ level and maximum contractive response 1.4 fold. In the case of clonidine, which gave only 15% of maximum contractive response given to phenylephrine on endothelium-containing rings, removal of the endothelium increased sensitivity 5.6 fold at $EC_{50}$ level and maximum contractive response 5 fold, which was about 55% of that given by phenylephrine. In endothelium-denuded ring, phenylephrine-induced contraction tended to be more increased in tonic contraction than in phasic contraction as compared to that in endothelium-containing ring, while clonidine-induced contraction was monophasic and was increased only in tonic contraction. In the calcium-free solution or in the presence, of verapamil, contraction stimulated by clonidine was almost abolished while that stimulated by phenylephrine produced only phasic contraction. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium derived relaxing factor (EDRF), because hemoglobin, a specific blocking agent of EDRF, abolished this depression. It is unlikely that the endothelium-dependent relaxation was due to stimulation of release of EDRF, because clonidine did not produce endothelium-dependent relaxation in 5-hydroxytryptamine-precontracted ring even when its contractile action was blocked by the ${\alpha_1}-adrenoceptor$ antagonist, prazosin. When the efficacy of phenylephrine was reduced to about the initial efficacy of clonidine by pretreatment with dibenamine, the contraction-response curves for phenylephrine became very similar to the corresponding curves obtained for clonidine before receptor inactivation. In the dibenamine-treated rings, contraction of phenylephrine was abolished in calcium-free solution or in the presence of verapamil like that obtained for clonidine before receptor inactivation. These results suggest that EDRF spontaneously released from endothelium depress contraction more profoundly in a case of an agonist with low efficacy and the phenylephrine-induced contraction was totally dependent on extracellular calcium as was that obtained for clonidine when the efficacy of phenylephrine was reduced to that of clonidine by irreversible inactivation of ${\alpha_1}-adrenoceptor$ with dibenamine.
Background: The prevalence of allergic inflammatory diseases such as atopic dermatitis (AD), asthma, and allergic rhinitis worldwide has increased and complete recovery is difficult. Korean Red Ginseng, which is the heat-processed root of Panax ginseng Meyer, is widely and frequently used as a traditional medicine in East Asia. In this study, we investigated whether Korean Red Ginseng water extract (RGE) regulates the expression of proinflammatory cytokines and chemokines via the mitogen-activated protein kinases (MAPKs)/nuclear factor kappa B ($NF-{\kappa}B$) pathway in allergic inflammation. Methods: Compound 48/80-induced anaphylactic shock and 1-fluoro-2,4-dinitrobenzene (DNFB)-induced AD-like skin lesion mice models were used to investigate the antiallergic effects of RGE. Human keratinocytes (HaCaT cells) and human mast cells (HMC-1) were also used to clarify the effects of RGE on the expression of proinflammatory cytokines and chemokines. Results: Anaphylactic shock and DNFB-induced AD-like skin lesions were attenuated by RGE administration through reduction of serum immunoglobulin E (IgE) and interleukin (IL)-6 levels in mouse models. RGE also reduced the production of proinflammatory cytokines including $IL-1{\beta}$, IL-6, and IL-8, and expression of chemokines such as IL-8, thymus and activation-regulated chemokine (TARC), and macrophage-derived chemokine (MDC) in HaCaT cells. Additionally, RGE decreased the release of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), $IL-1{\beta}$, IL-6, and IL-8 as well as expressions of chemokines including macro-phage inflammatory protein $(MIP)-1{\alpha}$, $MIP-1{\beta}$, regulated on activation, normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein (MCP)-1, and IL-8 in HMC-1 cells. Furthermore, our data demonstrated that these inhibitory effects occurred through blockage of the MAPK and $NF-{\kappa}B$ pathway. Conclusion: RGE may be a useful therapeutic agent for the treatment of allergic inflammatory diseases such as AD-like dermatitis.
Clonidine, a centrally-acting antihypertensive agent known to reduce central sympathetic outflow and modulate presynaptic transmitter's release, has shown to suppress central noradrenergic hyperactivity induced by immobilization stress in animals, by decreasing the MAC of halothane and the dose of narcotics required to prevent reflex cardiovascular response to noxious stimuli, and to have potent analgesic properties in humans. These characteristics suggest that clonidine might be a useful adjunct to the anesthetic management of patients with preexisting hypertension. Accordingly, we determined the clinical efficacy and safety on analgesia, sedation and hemodynamic stability in the perioperative period. Thirty patients(ASA physical status II-III) with a history of arterial hypertension, scheduled for elective orthopedic surgery were randomly assigned to two groups. We applied CPA-clonidine patch($6.9\;mg/cm^2$, 0.2 mg delivered daily) or placebo patch to each groups, 48 hours prior to induction of anesthesia. Antihypertensive medication was continued until the morning of the scheduled surgery. All patients received premedication of atropine and lorazepam, and induced anesthesia with thiopental and succinylcholine, and maintained with enflurane and 50% nitrous oxide, while sustaining the BP and pulse rate at acceptable range. For the relief of pain postoperatively, diclofenac and fentanyl were administered intramuscularly on demand. The results were as follows: 1) The change of hemodynamic responses in clonidine group was less compared to the placebo group. 2) Intraoperative anesthetic requirement for enflurane in clonidine group were significantly lower than placebo group. 3) Postoperative analgetic requirement in clonidine group were significantly lower than placebo group. In clonidine group, 5 cases out of 15 cases were required no analgetics, and the incidence of administration of additional fentanyl was decreased to 5 cases, comparing with 10 cases in placebo group.
Kim, Se-Mi;Shin, Sae-Byeok;Kim, Ju-Hwan;Kwon, In-Ho;Kim, Yong-Hee;Lee, Sang-No;Cho, Hea-Young;Lee, Yong-Bok
Journal of Pharmaceutical Investigation
/
v.38
no.6
/
pp.413-419
/
2008
Carvedilol, is a nonselective $\beta$-blocking agent and it also has vasodilating properties that are attributed mainly to its blocking activity at ${\alpha}_1$-receptors. The purpose of the present study was to evaluate the bioequivalence of two carvedilol tablets, $Dilatrend^{(R)}$ tablet 12.5 mg (Chong Kun Dang Pharmaceutical Co., Ltd.) and Cadilan tablet 12.5 mg (KyungDong Pharmaceutical. Co., Ltd.), according to the guidelines of the Korea Food and Drug Administration (KFDA). The release of carvedilol from the two carvedilol formulations in vitro was tested using KP VIII Apparatus II method with pH 4.5 dissolution medium. Thirty two healthy male subjects, $25.00{\pm}3.09$ years in age and $70.71{\pm}11.35\;kg$ in body weight, were divided into two groups and a randomized $2{\times}2$ cross-over study was employed. After a single tablet containing 12.5 mg as carvedilol was orally administered, blood samples were taken at predetermined time intervals and the concentrations of carvedilol in serum were determined using HPLC with fluorescence detector. The dissolution profiles of two formulations were similar in the tested dissolution medium. The pharmacokinetic parameters such as $AUC_t$, $C_{max}$ and $T_{max}$ were calculated and ANOVA test was utilized for the statistical analysis of the parameters using logarithmically transformed $AUC_t$, $C_{max}$ and untransformed $T_{max}$. The results showed that the differences between two formulations based on the reference drug, $Dilatrend^{(R)}$ tablet 12.5 mg, were 4.66%, 8.33% and -7.45% for $AUC_t$, $C_{max}$ and $T_{max}$, respectively. There were no sequence effects between two formulations in these parameters. The 90% confidence intervals using logarithmically transformed data were within the acceptance range of log 0.8 to log 1.25 (e.g., $\log\;0.9823{\sim}\log\;1.1042$ and $\log\;1.0132{\sim}\log\;1.1875$ for $AUC_t$ and $C_{max}$, respectively). Thus, the criteria of the KFDA bioequivalence guideline were satisfied, indicating Cadilan tablet 12.5 mg was bioequivalent to $Dilatrend^{(R)}$ tablet 12.5 mg.
Kim, Sok-Ho;Na, Ji-Young;Song, Ki-Bbeum;Choi, Dea-Seung;Kim, Jong-Hoon;Kwon, Young-Bae;Kwon, Jung-Kee
Journal of Ginseng Research
/
v.36
no.2
/
pp.161-168
/
2012
The abnormal maturation and ossification of articular chondrocytes play a central role in the pathogenesis of osteoarthritis (OA). Inhibiting the enzymatic degradation of the extracellular matrix and maintaining the cellular phenotype are two of the major goals of interest in managing OA. Ginseng is frequently taken orally, as a crude substance, as a traditional medicine in Asian countries. Ginsenoside $Rb_1$, a major component of ginseng that contains an aglycone with a dammarane skeleton, has been reported to exhibit various biological activities, including anti-inflammatory and anti-tumor effects. However, a chondroprotective effect of ginsenoside $Rb_1$ related to OA has not yet been reported. The purpose of this study was to demonstrate the chondroprotective effect of ginsenoside $Rb_1$ on the regulation of pro-inflammatory factors and chondrogenic genes. Cultured rat articular chondrocytes were treated with 100 ${\mu}M$ ginsenoside $Rb_1$ and/or 500 ${\mu}M$ hydrogen peroxide ($H_2O_2$) and assessed for viability, reactive oxygen species production, nitric oxide (NO) release, and chondrogenic gene expression. Ginsenoside $Rb_1$ treatment resulted in reductions in the levels of pro-inflammatory cytokine and NO in $H_2O_2$-treated chondrocytes. The expression levels of chondrogenic genes, such as type II collagen and SOX9, were increased in the presence of ginsenoside $Rb_1$, whereas the expression levels of inflammatory genes related to chondrocytes, such as MMP1 and MMP13, were reduced by approximately 50%. These results suggest that ginsenoside $Rb_1$ has potential for use as a therapeutic agent in OA patients.
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