• Archives of Reconstructive Microsurgery
• /
• 제6권1호
• /
• 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 $PGE_1$.

• Asian Pacific Journal of Cancer Prevention
• /
• 제14권11호
• /
• pp.6761-6767
• /
• 2013

The nuclear receptor, peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$), is expressed in various cancer cells including breast, prostate, colorectal and cervical examples. An endogenous ligand of $PPAR{\gamma}$, 15-deoxy-${\Delta}^{12,14}$ prostaglandin $J_2$ (PGJ2), is emerging as a potent anticancer agent but the exact mechanism has not been fully elucidated, especially in breast cancer. The present study compared the anticancer effects of PGJ2 on estrogen receptor alpha ($ER{\alpha}$)-positive (MCF-7) and $ER{\alpha}$-negative (MDA-MB-231) human breast cancer cells. Based on the reported signalling cross-talk between $ER{\alpha}$ and $ER{\alpha}$, the effect of the $ER{\alpha}$ ligand, $17{\beta}$-estradiol (E2) on the anticancer activities of PGJ2 in both types of cells was also explored. Here we report that PGJ2 inhibited proliferation of both MCF-7 and MDA-MB-231 cells by inducing apoptotic cell death with active involvement of mitochondria. The presence of E2 potentiated PGJ2-induced apoptosis in MCF-7, but not in MDA-MB-231 cells. The $ER{\alpha}$ antagonist, GW9662, failed to block PGJ2-induced activities but potentiated its effects in MCF-7 cells, instead. Interestingly, GW9662 also proved capable of inducing apoptotic cell death. It can be concluded that E2 enhances $ER{\alpha}$-independent anticancer effects of PGJ2 in the presence of its receptor.

• 대한한방내과학회지
• /
• 제29권3호
• /
• pp.800-809
• /
• 2008

Objective : Although chronic prostatitis/chronic pelvic pain syndrcme(CP/CPPS) is a common disease, there is no consensus on the etiology or pathology and treatment. This was a double-blinded, placebo-controlled, randomized clinical trial, investigating the therapeutic effects of the traditional Korean medicine, Bosingunyang-tang(BSGYT). Method : Participants who met US National Institutes of Health (NIH) consensus criteria for CP/CPPS were entered after applying inclusion/exclusion criteria. They were randomized to the BSGYT or placebo group. and treated three times a day for 6 weeks. NIH-Chronic Prostatitis Symptom Index (NIH-CPSI) was used to estimate the clinical symptoms of CP/CPPS. Prostaglandin E2 and ${\beta}$-endorphin in prostatic fluid, collected by 2-glass pre-massage and post-massage test, were analyzed as factors associated with pain and inflammation. Result : The mean decrease in NIH-CPSI total score of the BSGYT group was 11.0 points, which is 5.7 points more than the placebo group. (Mann Whitney test P=0.038) Also the BSGYT group showed three times higher response rate than the placebo group in NIH-CPSI pain subscale score. (Fisher's exact test P=0.027) In those responders, prostaglandin E2 decreased significantly. (Wilcoxon's signed-ranks test P=0.037). No specific side effects were observed. Conclusion : After a 6-week treatment period, BSGYT improved clinical symptoms of CP/CPPS patients by decreasing PGE2 level in prostatic fluid.

• Journal of Chest Surgery
• /
• 제41권4호
• /
• pp.508-511
• /
• 2008

서구인에 비해 동양인, 특히 극동지방의 버거씨 발병률은 높으나 우회로술 단독만의 성적은 아직 만족할 만하지 못하다고 알려져 있다. 따라서 우회론수술과 함께 교감신경 차단술, 금연, 정맥 내 혈관 확장제 투여 등의 보다 적극적이고 다양한 치료법이 요구되고 있다. 본 논문은 49세의 버거씨병 환자에게 복제정맥을 이용한 대퇴동맥-슬와동맥간 우회로술 및 교감 신경 차단술과 함께 동맥 내(intra-arterial) 프로스타글란딘 투여를 시행한 증례이다.

• Nutrition Research and Practice
• /
• 제8권4호
• /
• pp.360-367
• /
• 2014

BACKGROUND/OBJECTIVES: The aim of this research was to study the different long term effects of consumption of dietary oil sources with varying omega-6/omega-3 (${\omega}-6/{\omega}-3$) polyunsaturated fatty acids (PUFAs) ratios on bone marrow fatty acid level, ex vivo prostaglandin $E_2$ ($PGE_2$) release, and mineral content of bone in rabbits. MATERIALS/METHODS: For this purpose, weaning and female New Zealand white rabbits were purchased and randomly divided into five groups and offered ad libitum diets containing 70 g/kg of added oil for 100 days. The dietary lipid treatments were formulated to provide the following ratios of ${\omega}-6/{\omega}-3$ fatty acids: 8.68 soy bean oil (SBO control), 21.75 sesame oil (SO), 0.39 fish oil (FO), 0.63 algae oil (DHA), and 0.68 algae oils (DHA/ARA). DHA and ARA are two types of marine microalgae of the genus Crypthecodinium cohnii. RESULTS: The dietary treatments had significant effects on the bone marrow fatty acids of rabbits. Rabbits fed the FO diet, containing the highest ${\omega}-3$ PUFA concentration, and those fed the SBO diet showed the highest ${\omega}-6$ PUFA. On the other hand, a positive correlation was observed between Ex vivo $PGE_2$ level and the ${\omega}-6/{\omega}-3$ dietary ratio. Significant effects of dietary treatment on femur Ca, P, Mg, and Zn contents were observed in both genders. CONCLUSIONS: Findings of the current study clearly demonstrated that dietary PUFA, particularly ${\omega}-6/{\omega}-3$ and ARA/EPA ratios are important factors in determining bone marrow fatty acid profile, and this in turn determines the capacity of bone for synthesis of $PGE_2$, thereby reducing bone resorption and improving bone mass during growth.

• 한국해양바이오학회지
• /
• 제2권2호
• /
• pp.86-93
• /
• 2007

만성염증은 치주염, 대장염, 간염 및 관절염과 밀접한 관련성이 있다고 알려져 있다. 최근에 항염증제가 해양자원으로부터 개발되고 있다. 본 연구에서는 감태 (EC)가 항염증효과가 있다는 것이 발견되었다. 갈조류에 속하는 감태의 에탄올 추출물이 RAW 264.7 세포에서 tumor necrosis factor-${\alpha}$ interleukin-$1{\beta}$, interleukin-6 and prostaglandin $E_2$와 같은 염증매개체의 생성에 탁월한 효과를 나타내었다. 더욱이 reporter gene assay 및 western blot 분석 에 서 감태추출물은 대식세포에서 염증매개체의 발현을 조절하는 NF-${\kappa}B$ 전사인자의 불활성화를 통하여 항염증효과를 나타내었다. 뿐만 아니라 감태추출물은 만성염증에 중요한 역할을 하는 기질금속단백질의 활성을 억제 하였다. 이러한 결과는 갑태추출물이 만성염증을 억제하는데 잠재적으로 이용될 수 있다는 것을 암시하고 있다.

• The Korean Journal of Pain
• /
• 제27권3호
• /
• pp.219-228
• /
• 2014

Background: A lipo-prostaglandin E1 agonist is effective for the treatment of neurological symptoms of spinal stenosis when administered by an oral or intravenous route. we would like to reveal the therapeutic effect of an epidural injection of lipo-prostaglandin E1 on hyperalgesia in foraminal stenosis. Methods: A total of 40 male Sprague-Dawley rats were included. A small stainless steel rod was inserted into the L5/L6 intervertebral foramen to produce intervertebral foraminal stenosis and chronic compression of the dorsal root ganglia (DRG). The rats were divided into three groups: epidural PGE1 (EP) (n = 15), saline (n = 15), and control (n = 10). In the EP group, $0.15{\mu}g{\cdot}kg-1$ of a lipo-PGE1 agonist was injected daily via an epidural catheter for 10 days from postoperative day 3. In the saline group, saline was injected. Behavioral tests for mechanical hyperalgesia were performed for 3 weeks. Then, the target DRG was analyzed for the degree of chromatolysis, chronic inflammation, and fibrosis in light microscopic images. Results: From the fifth day after lipo-PGE1 agonist injection, the EP group showed significant recovery from mechanical hyperalgesia, which was maintained for 3 weeks (P < 0.05). Microscopic analysis showed much less chromatolysis in the EP group than in the saline or control groups. Conclusions: An epidurally administered lipo-PGE1 agonist relieved neuropathic pain, such as mechanical hyperalgesia, in a rat foraminal stenosis model, with decreasing chromatolysis in target DRG. We suggest that epidurally administered lipo-PGE1 may be a useful therapeutic candidate for patients with spinal stenosis.

• Animal cells and systems
• /
• 제16권4호
• /
• pp.274-279
• /
• 2012

Thymoquinone (TQ), a drug extracted from the black seeds of Nigella sativa, has been shown to exhibit anti-inflammatory, anti-oxidant, and anti-neoplastic effects in numerous cancer cells. The effects of TQ on cyclooxygenase-2 (COX-2) expression and prostaglandin $E_2$ ($PGE_2$) production in MDA-MB-231, however, remain poorly understood. Western blot analysis and immunofluorescence staining were performed to study the expression levels of inflammation regulatory proteins in MDA-MB-231. $PGE_2$ assay was conducted to explore the TQ-induced production of $PGE_2$. In this study, we investigated the effects of TQ on COX-2 expression and $PGE_2$ production in MDA-MB-231. TQ significantly induced COX-2 expression and increased $PGE_2$ production in a dose-dependent manner, as determined by a Western blot analysis and $PGE_2$ assay. Furthermore, the activation of Akt and p38 kinase, respectively, was up-regulated in TQ treated cells. Inhibition of p38 kinase with SB203580 and PI3kinase (PI3K) with LY294002 abolished TQ-caused COX-2 expression and decreased $PGE_2$ production. These results collectively demonstrate that TQ effectively modulates COX-2 expression and $PGE_2$ production via PI3K and p38 kinase pathways in the human breast cancer cell line MDA-MB-231.

• The Korean Journal of Physiology
• /
• 제14권2호
• /
• pp.1-5
• /
• 1980

This study was undertaken to investigate the influence of prostaglandin $E_1(PGE_1)$ upon the activity of carbonic anhydrase and upon the inhibitory action of acetazolamide on carbonic anhydrase. The heparinized blood was sampled by cardiac puncture from Sprague-Dawley strain rats under ether anesthesia and was hemolysed by adding distilled water 1,000 times the amount of the blood. The activity of carbonic anhydrase of 0.1 ml of the hemolysate was measured by Maren's simplified micro-method. In the first experiment, the 7 rats were used, and the activity was measured by adding 0.1 ml of various concentrations of $PGE_1$(0.5, 1.25, 2.5, 5.0, 10 and $20\;{\mu}g/ml$). In the second experiment, the 6 rats were used and the activity was measured by adding 0.1 ml of $PGE_1(5\;{\mu}g/ml)$ and 0.1 ml of acetazolamide$(6{\times}10^{-7}M/l)$ respectively or simultaneously. Obtained results were as follows: 1) The activity of carbonic anhydrase was significantly inhibited by $PGE_1$ at doses of $0.5{\sim}10\;{\mu}g/ml$, maximally at a dose of $2.5\;{\mu}g/ml$, but inhibition was no more observed at a dose of $20\;{\mu}g/ml$. 2) The activity of the acetazolamide group was significantly less than that of the control group. 3) The activity of the $PGE_1+acetazolamide$ group was significantly less than those of the $PGE_1$ group and the acetazolamide group. It is inferred from the above results that the $PGE_1$ inhibits the activity of carbonic anhydrase dose-dependently and strengthens the inhibitory effect of acetazolamide on carbonic anhydrase.

• The Korean Journal of Physiology
• /
• 제14권2호
• /
• pp.17-20
• /
• 1980

This study was undertaken to investigate the effect of the acidosis on the gastric acid secretion in the isolated whole stomach of the rat and the effect of prostaglandin $E_1$ on the gastric acid secretion influenced by the acidosis. Twenty-two male albino rats(Sprague-Dawley strain) were used. The isolated whole stomach from each rat was introduced into the Kreb's solution which was continuously gassed with $95%O_2-5%CO_2$ for 1 hour, after irrigation of the lumen with cold physiological saline$(4^{\circ}C)$. Thereafter, each stomach was irrigated again with 5% dextrose solution (pH 7.4, $37^{\circ}C$), and filled with the dextrose solution. All the stomachs with the dextrose solution were divided into 4 groups according to the Kreb's solutions in which each stomach was incubated for 30 min: 1) control group, in the pH 7.4 solution, 2) $PGE_1$ group, in the pH 7.4 solution containing $5\;{\mu}g/ml$ of $PGE_1$, 3) acid group, in the pH 7.0 solution, and 4) $acid+PGE_1$ group, in the pH 7.0 solution containing $5\;{\mu}g/ml$ of $PGE_1$. After incubatory period, the contents of each stomach were collected and centrifuged(1,500 rpm, room temperature) for 15 min. The acid output in the supernatant was determined with 0.012 N NaOH by means of autotitrator(Dosimat, Metrohm Herisau Co.) at pH 7.4. Results obtained were as follows: 1) The acid output of the acid group increased significantly in comparison with the control value. 2) The acid output of the $acid+PGE_1$ group decreased significantly in comparison with the acid group. It is inferred from the above results that the acidosis facilitates the gastric acid secretion and $PGE_1$ inhibits the gastric acid secretion induced by the acidosis.