• Title, Summary, Keyword: $PGE_{2}$

Search Result 957, Processing Time 0.04 seconds

Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE2 production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity

  • Duan, Yuzhong;Chen, Fanglin;Zhang, Anmei;Zhu, Bo;Sun, Jianguo;Xie, Qichao;Chen, Zhengtang
    • BMB Reports
    • /
    • v.47 no.1
    • /
    • pp.45-50
    • /
    • 2014
  • Aspirin has been demonstrated to be effective in inhibiting COX-2 and $PGE_2$ in Alveolar macrophages (AMs). However, the mechanisms have not been fully understood. In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and$PGE_2$ upregulation, $I{\kappa}B{\alpha}$ degradation, NF-${\kappa}B$ activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity. The PKC inhibitor calphostin C dramatically reduced the COX-2 mRNA and $PGE_2$ levels, but the PTP inhibitor peroxovanadium (POV) significantly increased the COX-2 mRNA and$PGE_2$ levels. Furthermore, the PTP inhibitor mitigated the inhibitory effect of aspirin on COX-2 and$PGE_2$ upregulation and NF-${\kappa}B$ activation, whereas the PKC inhibitor enhanced the inhibitory effects of aspirin on the production of COX-2 and$PGE_2$. Our data indicate a novel mechanism by which aspirin acts as a potent anti-inflammatory agent in alveolus macrophages and ALI.

The Effects of Prostaglandin and Dibutyryl cAMP on Osteoblastic Cell Activity and Osteoclast Generation (Prostaglandin과 Dibutyryl cAMP가 조골세포의 활성과 파골세포 형성에 미치는 영향)

  • Mok, Sung-Kyu;You, Hyung-Keun;Shin, Hyung-Shik
    • Journal of Periodontal and Implant Science
    • /
    • v.26 no.2
    • /
    • pp.448-468
    • /
    • 1996
  • To maintain its functional integrity, bone is continuously remodelled by a process involving resorption by osteoeclasts and formation by osteoblasts, In order to respond to changes in the physical environment or to trauma with the relevant action, this process is strictly regulated by locally synthesized or systemic fators, Prostaglandin $E_2(PGE_2$) is perhaps one of the best studied factors, having been known to affect bone cell function for several decades.$PGE_2$ has both anabolic and catabolic activities. Excess of $PGE_2$ has been implicated in a number of pathological states associated with bone loss in a number of chronic inflammatory conditions such as periodontal disease and rheumatoid arthritis. $PGE_2$ and other arachidonic acid metabolites have been shown to be potent stimulators of osteoclastic bone resorption in organ culture. The anabolic effects of $PGE_2$ were first noticed when an increase in periosteal woven bone formation was seen after the infusion of $PGE_2$ into infants in order to prevent closure of the ductus arteriosus. The cellular basis for the catabolic actions of $PGE_2$ has been well characterized. $PGE_2$increases osteoclast recruitment in bone marrow cell cultures. Also $PGE_2$ has a direct action on osteoclast serving to inhibit activity and can also indirectly activate osteoclast via other cells in the vicinity, presumably osteoblast. The cellular mechanisms for the anabolic actions of $PGE_2$ are not nearly so well understood. The purpose of this paper was to study the effects of $PGE_2$ and dibutyl(DB)cAMP on osteoblastic clone MC3T3El cells and on the generation of osteoclasts from their precursor cells. The effect of $PGE_2$ and DBcAMP on the induction of alkaline phoaphatase(AlP) was investigated in osteoblastic clone MC3T3El cells cultured in medium containing 0.4% fetal bovine serum. $PGE_2$ and DBcAMP stimulated ALP activity and MTT assay in the cells in a dose-dependent manner at concentrations of lO-SOOng/ml. Cycloheximide, protein synthesis inhibitor, inhibited the stimulative effect of $PGE_2$ and DBcAMP on ALP activity in the cells. $PGE_2$also increased the intracellular cAMP content in a dose-dependent fashion with a maximal effect at 500ng/ml. The effect of $PGE_2$ on the generation of osteoclasts was investigated in a coculture system of mouse bone marrow cells with primary osteoblastic cells cultured in media containing 10% fetal bovine serum.After cultures, staining for tartrate-resistant acid phosphatase(TRAP)-marker enzyme of osteoclast was performed. The TRAP(+) multinucleated cells(MNCs), which have 3 or more nuclei, were counted. More TRAP(+) MNCs were formed in coculture system than in control group. $PGE_2(10^{-5}10^{-6}M)$ stimulated the formation of osteoclast cells from mouse bone marrow cells in culture. $PGE_2(10^{-6}M)$ stimulated the formation of osteoclast cells from mouse bone marrow cells in coculture of osteoblastic clone MC3T3E1 cells This results suggest that $PGE_2$ stimulates the differentiation of osteoblasts and generation of osteoclast, and are involved in bone formation, as well as in bone resorption.

  • PDF

Cure Kinetics of DGEBA/MDA/HQ-PGE System (DGEBA/MDA/HQ-PGE계의 경화 반응 속도론)

  • Song, Young-Wook;Shim, Mi-Ja;Kim, Sang-Wook
    • Applied Chemistry for Engineering
    • /
    • v.7 no.2
    • /
    • pp.356-361
    • /
    • 1996
  • Cure kinetics of diglycidyl ether of bisphenol A(DGEBA)/4,4'-methylene dianiline(MDA) with hydroquinone-phenyl glycidyl ether(HQ-PGE) as a reactive additive, which was preliminarily synthesized, was investigated by DSC and FT-IR analyses. Kissinger equation and Arrhenius' equation were used to calculate activation energy and pre-exponential factor. When HQ-PGE was added to DGEBA/MDA system, it reduced activation energy of system. When the 5 phr of HQ-PGE was added to DGEBA/MDA system, activation energy was 7.8 kcal/mol by FT-IR analysis and 11.3 kcal/mol by DSC, in comparison with the system without HQ-PGE, activation energy decreased about 30% and 9%, respectively. According to these results, HQ-PGE, introducing agent of this system, acted as a catalyst.

  • PDF

Identification of a Novel PGE2 Regulated Gene in SNU1 Gastric Cancer Cell

  • Park, Min-Seon;Kim, Hong-Tae;Min, Byung-Re;Kimm, Ku-Chan;Nam, Myeong-Jin
    • BMB Reports
    • /
    • v.33 no.2
    • /
    • pp.184-187
    • /
    • 2000
  • Prostaglandin $E_2$ ($PGE_2$) plays an important role in the regulation of various gastric functions, and the growth-inhibitory activities on tumor cells are studied in vitro and in vivo. Although the mechanisms have attracted many researchers in the past decade, the molecular mechanisms of cell cycle arrest, or induction of apoptosis by $PGE_2$, is unclear. We investigated the effects of $PGE_2$ on the growth of the human gastric carcinoma cell line SNU1 and genes that are regulated by $PGE_2$ and isolated them using differential display RT-PCR (DD RT-PCR). FACS analysis suggested that SNU1 cells were arrested at the G1 phase by $PGE_2$ treatment. This growth inhibitory effect was in a time- and dose-dependent manner. Treatment of SNU1 cells with $10\;{\mu}g/ml$ $PGE_2$, followed by DD RT-PCR analysis, revealed differently expressed bands patterns from the control. Among the differently expressed clones, we found an unidentified cDNA clone (HGP-27) overexpressed in $PGE_2$-treated cells. The full-length cDNA of HGP-27 was isolated using RACE, which consisted of a 30-nt 5'-noncoding region, a 891-nt ORF encoding the 296 amino acid protein, and a 738-nt 3'-noncoding region including a poly(a) signal. This gene was localized on the short arm of chromosome number 11. Using the Motif Finder program, a myb-DNA binding repeat signature was detected on the ORF region. The COOH-terminal half was shown to have similarity with the $NH_3$-terminal domain of thioredoxin (Trx). This relation between HGP-27 and Trx implied a potential role for HGP-27 in modulating the DNA binding function of a transcription factor, myb.

  • PDF

Cytoprotective Effects of Platycodon grandiflorus (Jacq.) A.DC on C6 Glioma Cell Apoptosis by Oxidative Stress (산화스트레스로 인한 C6 Glioma Cell Apoptosis에 대한 길경의 세포보호효과)

  • Jo, Jae Joon;Shin, Min Gu;Kim, Eui Su;Lee, Young Su;Shin, Yong Jin;Jeon, Sang Yun
    • Journal of Physiology & Pathology in Korean Medicine
    • /
    • v.28 no.4
    • /
    • pp.396-402
    • /
    • 2014
  • This study is designed to investigate cytoprotective effects of Platycodon grandiflorus (Jacq.) A.DC on C6 glioma cell apoptosis by oxidative stress. Experimental C6 glioma cells were classified into four groups as follows: normal group, PGE group, chemical groups, PGE+chemical groups. Oxidative stress that caused by chemicals in the C6 glioma cell, check the impact to Chemical group was administered normal group. Apoptotic effect protecting in order to observe the chemical group was administered PGE. We to observe effects of PGE on SOD inhibition, total glutathione production in C6 glioma cells were administered PGE. In case of administration PGE, apoptosis induced by Paraquat was significantly decreased. In case of administration PGE, apoptosis induced by SNP was significantly decreased. In case of administration PGE, apoptosis induced by $H_2O_2$ was significantly decreased. In case of administration PGE, apoptosis induced by Rotenone was decreased, but the statistical significance was not. In case of administration PGE, SOD inhibition activities significantly decreased. In case of administration PGE, Total glutathione did not affect the content. These results suggest that PGE is able to treat a disease caused by oxidative stress and prevent a aging. These results suggest that PGE is a disease caused by oxidative stress and aging, the prevention and treatment of food shall be able to be applied.

Study on therapeutic application of toxicity of Uranylnitrate in rats (천연 우라늄 독성에 관한 치료 연구)

  • Ryu, Yong-Wun;Lee, Jhin-Oh;Yun, Taik-Koo
    • Journal of Radiation Protection and Research
    • /
    • v.12 no.2
    • /
    • pp.9-18
    • /
    • 1987
  • The present study has determined BUN, createinine, c-AMP and $PGE_2$ activities as a clinical signs of radiation toxicity caused by uranylnitrate in rats. The significant increasing of $PGE_2$ concentration in plasma between the administration of uranylnitrate and lead nitrate were shown radiotoxic in nature on the effect of radiation energy. The reduction of PGE activities in plasma in uranylnitrate treated rats after furosemide, aldosterone and glucagone I.P. administration have observed the stimulating effect of uranium excretion into cells.

  • PDF

Simultaneous Determination of Prostaglandin E1 and Prostaglandin E1 Ethyl Ester in Hairless Mouse Skin Homogenate by High-Performance Liquid Chromatography

  • Choi, Han-Gon;Kim, Ji-Hyun;Li, Dong-Xun;Piao, Ming-Guan;Kwon, Tae-Hyub;Woo, Jong-Soo;Choi, Young-Wook;Yoo, Bang-Kyu;Yong, Chul-Soon
    • Journal of Pharmaceutical Investigation
    • /
    • v.35 no.5
    • /
    • pp.375-381
    • /
    • 2005
  • A rapid and specific high-performance liquid chromatographic method was developed and validated for the simultaneous determination of prostaglandin $E_{1}\;(PGE_{1})$ and prostaglandin $E_{1}$ ethyl ester $(PGE_{1}-EE)$ in hairless mouse skin homogenate. The sample treatment procedure involved deproteination and precipitation by acetonitrile. $PGE_{1}$ and $PGE_{1}-EE$ in supernatant were separated in a reversed-phase C18 column without being interfered by other components present in hairless mouse skin homogenate. 9-Anthracenecarboxylic acid was used as an internal standard. The retention times of $PGE_{1}$, 9-anthracenecarboxylic acid and $PGE_{1}-EE$ were, 4.5, 9.5 and 18.0 min, respectively. The assay showed linearity from 1 to $40\;{\mu}g/ml$ for both $PGE_{1}$ and $PGE_{1}-EE$. Precision expressed as RSD ranged from 2.3 to 14.1 % for $PGE_{1}$ and 1.6 to 11.0% for $PGE_{1}-EE$. Accuracy ranged from 100.5 to 119.6 % for $PGE_{1}$ and from 98.0 to 103.7% for $PGE_{1}-EE$. This method was employed successfully to follow the time course of concentrations of $PGE_{1}$ and $PGE_{1}-EE$ in hairless mouse skin homogenate for stability study.

Effect of Prostaglandin $E_1$ on Cutaneous Microcirculation of Flap or Replantation

  • Nakanishi, Hideki;Hashimoto, Ichiro;Tanaka, Shinji
    • Archives of Reconstructive Microsurgery
    • /
    • v.6 no.1
    • /
    • pp.1-8
    • /
    • 1997
  • Recently prostaglandin $E_1(PGE_1)$ has been shown to ensure flap survival by producing vasodilation of the peripheral vessels and platelet disaggreation. However, direct observation and detailed quantitative studies of the effects of $PGE_1$ on the cutaneous microcirculation have not been reported. In the present study, we investigated cutaneous microcirculatory changes in the rabbit ear chamber(REC) with an intravital microscope following intravenous administration of $PGE_1$. The results obtained in this study indicate that $PGE_1$ administered intravenously at a rate of 200ng/kg/min might act directly on the vessels and cause dilatation of metarterioles and capillaries without affecting vasomotion and systemic blood pressure. Clinically in order to evaluate the effect of an intravenous administration of $PGE_1$ on the cutaneous microcirculation, cutaneous blood flow, skin temperature and transcutaneous $Po_2$ in the pedicle or free flap of operated patients were evaluated by the combination of several measurements following the administration of $PGE_1$. The present study suggests that improvement of cutaneous microcirculation by $PGE_1$ may enhance the survival rate of flap or replantation. Both vessel arterial ischemia and venous congestion are main factors of tissue necrosis in the flap surgery. Vasodilatory or antithrombotic agents have been used in salvage of flap necrosis. However, the therapeutic effects of those drugs are still not well elucidated. Recently prostaglandin $E_1(PGE_1)$ has been shown to ensure flap survival by producing vasodilatation of the peripheral vessels and platelet disaggregation[1-3]. Emerson and sykes[4] have obtained significant improvement in the flap survival in the rat using $PGI_2$. Suzuki et al.[5] have reported prolonged flap survival length by using $PGE_1$ in the rabbit and concluded that $PGE_1$ improved the microcircuration in the flap. However, direct observation and detailed quantitative studies of the effects of $PGE_1$ on the cutaneous microcirculation have not been reported. In the present study, we investigated microcirculatory changes in the rabbit ear chamber[6,7] with an intravital microscope following intravenous administration of $PGE_1$.

  • PDF

Anti-oxidant Activities and Anti-atopic Dermatitis Effect of Combined Extract of Phellinus linteus and Glycyrrhiza uralensis (상황버섯, 감초 복합추출물의 항산화 및 인체적용 아토피 개선 효능 연구)

  • Kwon, OJun;Lee, AhReum;Do, KookBae
    • The Korea Journal of Herbology
    • /
    • v.32 no.2
    • /
    • pp.49-56
    • /
    • 2017
  • Objectives : This study investigated the anti-oxidant activities and improving effect of Phellinus linteus and Glycyrrhiza uralensis Extract (PGE) on Atopic Dermatitis. Methods : 2,2′-diphenyl-1-picrylhydrazyl (DPPH) radical, 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulphonic acid (ABTS) radical, Hydrogen peroxides scavenging activities and Superoxide dismutase (SOD)-like activities were used for the measurement of anti-oxidant ability. Cytotoxicity of PGE in Raw 264.7 cell was evaluated by MTT assay. To evaluate the anti-atopic dermatitis effect of PGE, a total of 33 patients with atopic dermatitis were observed trans epidermal water loss, skin moisture content, modified SCORAD index of atopic dermatitis and pruritic degree after applying the PGE for 4 weeks. Results : PGE scavenged DPPH ($IC_{50}=25ppm$) effectively, ABTS and Hydrogenperoxides scavenged similar to BHA. As for the SOD-like activity, it had lower effect than ascorbic acid, but it comparable activities in 500ppm. There was no cytotoxicity at PGE at concentrations of 10,000ppm. In clinical research about PGE on patients with atopic dermatitis, skin condition was improved. After 4 weeks, the application of PGE increased skin moisture content from 19.43 to 31.22. Moreover, it reduced the skin temperature (from 32.5 to 31.9), skin pH (from 5.39 to 5.22), trans epidermal water loss (from 39.03 to 24.46) and pruritus score (from 6.07 to 3.87). In addition, the Modified SCORAD index decreased from 31.28 to 20.3. Conclusions : In conclusion, PGE possesses anti-oxidant and anti-atopic dermatitis activities, thus it could be potentially valuable as anti-atopic dermatitis material.

Prostaglandin $E_1$ Increases cGMP Levels in Beating Rabbit Atria: Lack of Effects of $PGE_1$-induced Cyclic Nucleotides on Secretory and Contractile Functions

  • Jin, Xuan Shun;Quan, He Xiu;Kim, Sun-Young;Park, Sung-Hun;Kim, Sung-Zoo;Lee, Ho-Sub;Cho, Kyung-Woo
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.11 no.5
    • /
    • pp.175-182
    • /
    • 2007
  • Members of prostaglandin(PG) E-series elicit cellular effects mainly through adenylyl cyclase-cAMP signaling. The role of $PGE_2$-induced increase in cAMP has been shown to be compartmentalized in the cardiac myocytes: $PGE_2$-induced increase of cAMP is not involved in the control of cardiomyocytic contraction. The purpose of the present study was to define the effect of $PGE_1$ on the cGMP levels and the role of $PGE_1$ in the atrial secretory function. Experiments were performed in perfused beating rabbit atria and atrial contractile responses, cGMP and cAMP efflux, and atrial natriuretic peptide(ANP) secretion were measured. $PGE_1$ increased cGMP as well as cAMP efflux concentration in a concentration-dependent manner, however, no significant changes in atrial secretory responses were observed(with $1.0{\mu}M\;PGE_1$; for cGMP, $144.76{\pm}37.5%$, n=11 versus $-16.81{\pm}4.76%$, n=6, control, p<0.01; for cAMP, $187.60{\pm}41.52%$, n=11 versus $7.38{\pm}19.44%$, n=6, control, p<0.01). $PGE_1$ decreased atrial dynamics slightly but transiently, whereas $PGE_2$ showed similar effects but with lower potency. Isoproterenol increased atrial cAMP efflux(with 2.0 nM; $145.71{\pm}41.89$, n=5 versus $7.38{\pm}19.44%$, n=6, control, p<0.05) and mechanical dynamics and decreased ANP secretion. The $PGE_1$-induced increase in cGMP efflux showed a bell-shaped concentration-response curve. $PGE_1$-induced increase of cGMP efflux was not observed in the presence of L-NAME, an inhibitor of nitric oxide(NO) synthase, or ODQ, an inhibitor of NO-sensitive guanylyl cyclase. L-NAME and ODQ showed no significant effect on the $PGE_1$-induced transient decrease of atrial dynamics. These data indicate that $PGE_1$ increases cGMP levels via NO-soluble GC signaling in the cardiac atrium and also show that $PGE_1$-induced increases in cGMP and cAMP levels are not involved in the regulation of atrial secretory and contractile functions.