Kim, Shin-Hee;Lee, Ki-Mu;Kim, Hyo-Shin;Lee, Gyu-Seung;Jeon, Byeong-Hwa;Kim, Kwang-Jin;Park, Jin-Bong
The Korean Journal of Physiology and Pharmacology
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v.7
no.6
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pp.311-316
/
2003
Endothelins secreted from keratinocytes are intrinsic mitogens and melanogens of human melanocytes in UVB-induced hyperpigmentation. To elucidate the cellular mechanism of antimelanogenic activity of bamboo extract, the effects of three ingredients of bamboo extract on endothelin 1 (ET-1)-induced $Ca^{2+}$ mobilization were investigated in cultured human melanocytes. ET-1 receptors in human melanocytes were characterized by using specific antagonist, and ET-1 was found to increase intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) by activating ET-B receptor. SM709 (1,2-O-diferulyl-glycerol), an ingredient of bamboo extract, inhibited ET-1-induced $[Ca^{2+}]_i$ increase in a concentration- and time-dependent manner, although another ingredients SM707 and SM708 had no effect on ET-1-induced $[Ca^{2+}]_i$ increase in human melanocytes. SM709 ($100{\mu}M$), however, did not affect $[Ca^{2+}]_i$ increase induced by thapsigargin and caffeine, suggesting that SM709 has no effect on the $Ca^{2+}$ store in melanocytes. Furthermore, SM709 did not affect $[Ca^{2+}]_i$ increase induced by LPA or ATP, known as G protein-mediated PLC activators like ET-1. Taken together, it is suggested that SM709 antagonizes ET-1-induced transmembrane signaling through ET-B receptor, which maybe a possible underlying mechanism of antimelanogenic activity of bamboo extract in human melanocytes.
This study was designed to evaluate the responses of cardiovascular system to endothelin (ET) and neuropeptide Y (NPY) in 12 week-old SHR treated with or without enalapril (ENP) for 6 weeks. The diastolic blood pressure and heart rate were lower in ENP-treated SHR than in control. The pressor response to intravenous, but not intracerebroventricular, ET or NPY was attenuated by ENP treatment. The chronotropic action induced by electrical stimulation was attenuated by ENP or ET. The negative chronotropic action of ET was blocked by yohimbine. The increase in aortic tension induced by electrical field stimulation (EFS) was depressed in ENP-treated group as compared with non-treated group, and enhanced by ET, but not NPY, in the non-treated group. The ET-induced increase in tension was enhanced by removal of endothelium in the control group but not in ENP-treated group. The plasma concentration of norepinephrine and ET-induced increase in concentration of norepinephrine and epinephrine in plasma were decreased in ENP-treated group. These results suggest that preventive effect of enalapril on the development of hypertension may result from depressing vasoactive action of endothelin and neuropeptide Y, and sympathetic neurotransmission at peripheral nervous system.
To elucidate a potential contribution of endotheline-1[ET-1] to the genesis of pulmonary hypertension and postoperative pulmonary hypertensive crisis in the patients with heart disease, we measured plasma levels of the ET-1 during perioperative period of open heart surgery. In addition, we examined changes of ET-1 during perioperative period and correlations between ET-1 levels and hemodynamic variables. 12 patients including 5 acquired heart disease and 7 congenital heart disease patients were selected randomly as a study group, Group A and B, respectively. 6 patients proved not having heart or hemodynamic problem were selected as a control, Group C. 110 blood samples from pulmonary artery[ET-P] and radial artery[ET-S] were taken and assayed by Sep-pak extraction and RIA. ET-1 levels of Group A were ET-P, 3.94$\pm$5.31pg /ml, ET-S, 3.10$\pm$2.90pg/ml[p>0.05], Group B were ET-P, 1.63$\pm$0.62pg/ml, ET-S, 1.99$\pm$2.45pg/ml[p>0.05], Group C were ET-P, 1.97$\pm$2.02pg/ml, ET-S, 1.72$\pm$0.77pg/ml[p>0.05]. There were no statistically significant differences of ET-1 levels among the Group A, B, C[p>0.05]. There was no correlation between pulmonary artery pressure[PAP] and ET-1 level[p>0.05], and ET-1 levels were not increased even in the cases of pulmonary hypertensive criwis or low cardiac output syndrome, whereas significant correlation between ET-S and pulmonary vascular res-istance[Rp] [r=0.36, p<0.05], and negative correlation between ET-S and OS saturation of pulmonary artery[OS-P][r= -0.49, p<0.01] were identified. Another significant finding was peak increase of ET-1 levels in the postoperative period 1 hour[p<0.05] and then gra-dualy decrease through the postoperative period. In conclusion, ET-1 has no correlation with PAP, whereas correlation with Rp, and inverse correlation with OS-P. It is suggested that ET-1 is neither the direct causative substance of pulmonary hypertension nor pulmonary vasospasm but there must be increased production of ET-1 in chronic pulmonary hypertensive state. Counter-regulatory mechanism to ET-1 is speculated during the pulmonary vasospasm.
Background: Endothelin(ET) is the most potent vasoconstrictor and bronchoconstrictor. The plasma ET-1 level is elevated in patients with acute pulmonary thromboembolism(APTE). This finding suggest that ET-1 may be an important mediator in the cardiopulmonary derangement of APTE. But whether ET-1 is a pathogenic mediator or a simple marker of APTE is not known. The role of ET-1 in the pathogenesis of cardiopulmonary dysfunction in APTE(delete) was investigated through an evaluation of the effects of $ET_A$-receptor antagonist on APTE. The increase in local levels of preproET-1 mRNA and ET-1 peptide in the embolized lung was also demonstrated. Methods: In a canine autologous blood clot pulmonary embolism model, $ET_A$-receptor antagonist(10 mg/kg intravenously, n=6) was administered one hour after the onset of the embolism. Hemodynamic measurements, blood gas tensions and plasma levels of ET-1 immunoreactivity in this treatment group were compared with those in the control group(n=5). After the experiment., preproET-1 mRNA expression(using Northern blot analysis) and the distribution of ET-1(by immunohistochemical analysis) in the lung tissues were examined. Results: The increases in pulmonary arterial pressure and pulmonary vascular resistance of the treatment group were less than those of the control group. Decrease in cardiac output was also less in the treatment group. Complications such as systemic arterial hypotension and hypoxemia did not occur with the administration of $ET_A$-receptor antagonist The plasma level of ET-1 like(ED: what does 'like' mean?) immunoreactivity was increased after embolization in both groups but was significantly higher in the treatment group. The preproET-1 mRNA and ET-1 peptide expressions were increased in the embolized lung. Conclusion: ET-1 synthesis increases with embolization in the lung and may plays play an important role in the pathophysiology of cardiopulmonary derangement of APTE. Furthermore, $ET_A$-receptor antagonist attenuates cardiopulmonary alterations seen in APTE, suggesting a potential benefit of this therapy.
Park, Sun-Hee;Lee, Bang-Yong;Han, Chang-Sung;Kim, Jin-Guk;Kim, Kyoung-Tae;Kim, Ki-Ho;Kim, Young-Heui
Journal of the Society of Cosmetic Scientists of Korea
/
v.34
no.2
/
pp.101-107
/
2008
In order to investigate the potential of a Angelica keiskei Koidzumi extract and its fractions as an active ingredient for whitening cosmetics, we prepared Angelica keiskei Koidzumi extract(70% ethanol), and the aqueous suspension was successively extracted with hexane, ethyl acetate(EA), and n-butanol fraction. We measured their inhibitory effects on mushroom tyrosinase and melanin synthesis in B16 melanoma cells and normal human kerationocytes in vitro. They did not show inhibitory activity against mushroom tyrosinase and the melanin synthesis except hexane and EA fractions. Hexane and EA fractions markedly inhibited cellular tyrosinase activity at a lower concentration(25 and 5 ${\mu}g/mL$, respectively) than arbutin(250 ${\mu}g/mL$). We also quantified the released amount of endothelin-1(ET-1), a mitogen of melanocyte, and interleukin-$1{\alpha}$(IL-$1{\alpha})$, a mediator of UVB-induced inflammation. Hexane and EA fractions did not affect IL-$1{\alpha}$ production, but they decreased UVB-induced ET-1 production in normal human keratinocytes in a dose dependant manner. As a result, hexane and EA fractions could inhibit the melanogenesis through the inhibition of UVB-induced ET-1 production in normal human keratinocytes. This result suggests that hexane and EA fractions of Angelica keiskei Koidzumi extract could be used as an active ingredient for cosmetics.
Background : The herbicide paraquat can cause severe lung injury and fibrosis in experimental animals. In this study we have investigated the changes in lung endothelin-1(Et-1) levels and immunohistochemical localization in relation to treatment with cyclophosphamide and methylprednisolone in paraquat induced pulmonary fibrosis in guinea pigs. Material and methods : 29 male Hartley guinea pigs were divided into 4 groups. Group I was normal control. Paraquat was instilled into the lung of guinea pig of group II, III and IV unilaterally. Group II was treated with cyclophosphamide and methylprednisolone. Group III was treated with methlprednisolone. Group IV was not treated. The degree of fibrosis was evaluated by H-E stains and Masson's trichrome stains and cell activity was assessed by Et-1 immunohistochemical stains. Statistical evaluation was performed using the Kruskawallis oneway analysis. Results : Paraquat induced an increase in numbers of fibroblasts and total amount of lung collagen in Group IV compared to the normal controls. There was no significant difference in total numbers of fibroblasts between any of paraquat instilled groups, but there was significant increase in total amount of collagen in Group IV compared to group II and III (p<0.05). The treatment of cyclophosphamide and methyprednisolone suppressed the growths of both fibroblasts and collagen, but this suppression was stastically significant only in the case of collagen Et-1 immunoreactivities of bronchial epithelium, type II pneumocytes, endothelial cells and fibroblast in group II and III were decreased compared to those in group IV. Conclusion : These results demonstrate that Et-1 is an important contributing factor in the pathogenesis of pulmonary fibrosis. Et-1 is synthesized and released by bronchial epithelium, Type II pneumocyte, endothelial cells, alveolar macrophages and fibroblasts. Especially they are associated with alveolar macrophage and fibroblasts. We conclude that combined therapy of cyclophosphamide and methylprednisolone are more effective in the control of Et-1 expression and collagen deposition.
Vascular diseases are significant complications of diabetes mellitus (DM), and the endothelial cells may play a pivotal role in the development of vascular disease in DM. Endothelin-1 (ET-1) released from endothelium is a potent vasoconstrictor peptide and circulating level of ET-1 is increased in a variety of disease states. The purpose of this study was to determine the changes of responsiveness to ET-1 in DM, and we experimented on the changes in the ET-1-induced contraction, levels of nitrite and lipid peroxidation, and ET-1 immunoreactivity in aorta from streptozotocin-induced DM rats. DM was induced by single injection of streptozotocin (55 mg/kg, i.p.). The immunoreactive ET-1 levels in endothelial layer of thoracic aorta were much higher in DM rats than control rats. Nitrite in tissue homogenate was decreased and plasma nitrite was increased in DM rats. Malondialdehyde (MDA) was significantly increased in DM rats and cGMP was not significantly different between control and DM rats. ET-1 produced concentration- dependent contractile responses that are significantly attenuated in DM rats compared to controls. In the presence of selective $ET_A$ receptor antagonist BQ610, the maximum contraction was decreased and the concentration ratios for BQ610 yielded $pA_2$ values of 7.3 (slope, 0.65) in control rats, whereas BQ610 had no antagonistic effect on ET-1-induced contraction in DM rats. However, pretreatment with BQ788, an $ET_B$ receptor antagonist, maximum response was decreased and the dose-response curves for ET-1 were shifted to the right in both groups and $pA_2$ values were 7.9 and 7.7 (slope, 1.05 in control and DM rats), respectively. IRL 1620 and sarafotoxin S6c, $ET_B$ agonists, induced relaxation in control rats but not in DM rats. These results indicate that endothelial cell dysfunction and enhanced immunoreactivity of ET-1 have been found in DM rat and ET-1-induced contraction was attenuated in DM rat. These attenuated responses might be at least in part caused by the alteration of $ET_A$ receptor properties (e.g. desensitization), and partly related with an alteration in intracellular mechanism for contraction to ET-1.
Kee, Hyung Min;Yi, Dae Yong;Yun, Ki Wook;Lim, In Seok;Ha, Tae-Seon
Childhood Kidney Diseases
/
v.18
no.1
/
pp.36-41
/
2014
Purpose: Urinary tract infections (UTIs) are the most common source of bacterial infections in infants and young children. Accurate diagnosis and treatment is important because of their association with renal scarring, which can lead to complications. Urine endothelin-1 (ET-1) is the major renal isoform produced and released by renal mesangial cells in response to glomerular injury. This study aimed to investigate whether urinary levels of ET-1 can be used as a biomarker for UTI diagnosis. Method: We conducted a prospective study using medical records of 70 patients below the age of 18 years, who visited Chung-Ang University Hospital from July 2012 to July 2013. We classified the patients into the UTI and control groups based on urine culture studies. The UTI group was further divided into upper and lower UTI groups using 99m-Technetium dimercaptosuccinic acid scintigraphy. Urine ET-1 was measured using enzyme linked immunosorbent assay with 0.3 mL urine. Results: The UTI and control groups were comprised of 45 and 25 patients, respectively. Mean urine ET-1 levels were significantly higher in the UTI group than in the control group ($1.41{\pm}0.35$ pg/mL vs. $0.33{\pm}0.07$ pg/mL, P =0.04). There was no significance difference in the quantitative value between the upper and lower UTI groups (P =0.552). There was no correlation between urine ET-1 and serum C-reactive protein (Pearson correlation [R]=0.24), urine ET-1 and serum white blood cell count (R=0.19). Conclusion: Our study suggests that urine ET-1 can be used for early diagnosis of UTI in children.
The aim of this study was to determine the roles of ET-1 and NO on uterine blood flow in pregnancy. Uterine arteries were isolated from 17 nonpregnant and 12 pregnant women. Nonpregnant group included patients with median age of $48.6{\pm}2.3$ years who underwent hysterectomy, because of myoma. Pregnant group included patients with median age of $31.3{\pm}1.4$ years undergoing cesarean delivery. ET-1 and ET-2 induced concentration-dependent contraction in isolated nonpregnant and pregnant uterine arteries. The contractile response and maximal contraction were increased in pregnant uterine arteries. In nonpregnant uterine arteries, there was no contraction in response to ET-3, whereas pregnancy induced concentration-dependent contraction by ET-3. Tissue nitrite/nitrate level and immunohistochemical staining of eNOS and iNOS were increased in pregnant uterine arteries, compared with nonpregnant uterine arteries. In addition, the expressions of eNOS and iNOS mRNA were significantly increased in pregnancy. Moreover, contractions by ET isopeptides, including ET-1, were enhanced, and immunohistochemical staining of ET-1 and ET-1 mRNA expression was increased in pregnant uterine arteries. These results suggest that NO production by increased NOS activity, especially eNOS activity, is related to placental and uterine blood flow. Furthermore, ET-1 appears to play a pathophysiological role in pregnant complications such as hypertension.
Proceedings of the Korean Biophysical Society Conference
/
2001.06a
/
pp.24-24
/
2001
The present study was undertaken to determine whether p38 mitogen-activated protein kinase participates in the regulation of vascular smooth muscle contraction by endothelin-I (ET-1) in rat thoracic aorta. ET-1 induced a sustained contraction. In contrast, both the intracellular Ca$\^$2+/ and myosin light chain (MLC) phosphorylations were not sustained.(omitted)
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