Anti-inflammatory effects of DA-9601, an extract of Artemisia asiatica, on aceclofenac-induced acute enteritis

DA-9601 is an extract obtained from Artemisia asiatica, which has been reported to have anti-inflammatory effects on gastrointestinal lesions; however, its possible anti-inflammatory effects on the small intestine have not been studied yet.Therefore, in this study, we investigated the protective effects of DA-9601 against the ACF-induced small intestinal inflammation. Inflammation of the small intestine was confirmed by histological studies and the changes in the CD4 + T cell fraction induced by the inflammation-related cytokines, and the inflammatory reactions were analyzed. Multifocal discrete small necrotic ulcers with intervening normal mucosa were frequently observed after treatment with ACF. The expression of IL-6, IL-17, and TNF-α genes was increased in the ACF group; however, it was found to have been significantly decreased in the DA-9601 treated group. In addition, DA-9601 significantly decreased the levels of proinflammatory mediators such as IL-1β, GMCSF, IFN-γ, and TNF-α; the anti-inflammatory cytokine IL-10, on the other hand, was observed to have increased. It is known that inflammatory mediators related to T cell imbalance and dysfunction continuously activate the inflammatory response, causing chronic tissue damage. The fractions of IFN-γ + Th1 cells, IL-4 + Th2 cells, IL-9 + Th9 cells, IL-17 + Th17 cells, and Foxp3 + Treg cells were significantly decreased upon DA-9601 treatment. These data suggest that the inflammatory response induced by ACF is reduced by DA-9601 via lowering of the expression of genes encoding the inflammatory cytokines and the concentration of inflammatory mediators. Furthermore, DA-9601 inhibited the acute inflammatory response mediated by T cells, resulting in an improvement in ACF-induced enteritis.

Anti-inflammatory effects of DA-9601, an extract of Artemisia asiatica, on aceclofenac-induced acute enteritis

DA-9601 is an extract obtained from Artemisia asiatica, which has been reported to have anti-inflammatory effects on gastrointestinal lesions; however, its possible anti-inflammatory effects on the small intestine have not been studied yet.Therefore, in this study, we investigated the protective effects of DA-9601 against the ACF-induced small intestinal inflammation. Inflammation of the small intestine was confirmed by histological studies and the changes in the CD4 + T cell fraction induced by the inflammation-related cytokines, and the inflammatory reactions were analyzed. Multifocal discrete small necrotic ulcers with intervening normal mucosa were frequently observed after treatment with ACF. The expression of IL-6, IL-17, and TNF-α genes was increased in the ACF group; however, it was found to have been significantly decreased in the DA-9601 treated group. In addition, DA-9601 significantly decreased the levels of proinflammatory mediators such as IL-1β, GMCSF, IFN-γ, and TNF-α; the anti-inflammatory cytokine IL-10, on the other hand, was observed to have increased. It is known that inflammatory mediators related to T cell imbalance and dysfunction continuously activate the inflammatory response, causing chronic tissue damage. The fractions of IFN-γ + Th1 cells, IL-4 + Th2 cells, IL-9 + Th9 cells, IL-17 + Th17 cells, and Foxp3 + Treg cells were significantly decreased upon DA-9601 treatment. These data suggest that the inflammatory response induced by ACF is reduced by DA-9601 via lowering of the expression of genes encoding the inflammatory cytokines and the concentration of inflammatory mediators. Furthermore, DA-9601 inhibited the acute inflammatory response mediated by T cells, resulting in an improvement in ACF-induced enteritis.

Regulation of Diabetes: a Therapeutic Strategy for Alzheimer's Disease?

Accumulated evidence suggests that sporadic cases of Alzheimer's disease (AD) make up more than 95% of total AD patients, and diabetes has been implicated as a strong risk factor for the development of AD. Diabetes shares pathological features of AD, such as impaired insulin signaling, increased oxidative stress, increased amyloid-beta (Aβ) production, tauopathy and cerebrovascular complication. Due to shared pathologies between the two diseases, anti-diabetic drugs may be a suitable therapeutic option for AD treatment. In this article, we will discuss the well-known pathologies of AD, including Aβ plaques and tau tangles, as well as other mechanisms shared in AD and diabetes including reactive glia and the breakdown of blood brain barrier in order to evaluate the presence of any potential, indirect or direct links of pre-diabetic conditions to AD pathology. In addition, clinical evidence of high incidence of diabetic patients to the development of AD are described together with application of anti-diabetic medications to AD patients.

Possible Effects of Radiofrequency Electromagnetic Field Exposure on Central Nerve System

Technological advances of mankind, through the development of electrical and communication technologies, have resulted in the exposure to artificial electromagnetic fields (EMF). Technological growth is expected to continue; as such, the amount of EMF exposure will continue to increase steadily. In particular, the use-time of smart phones, that have become a necessity for modern people, is steadily increasing. Social concerns and interest in the impact on the cranial nervous system are increased when considering the area where the mobile phone is used. However, before discussing possible effects of radiofrequency-electromagnetic field (RF-EMF) on the human body, several factors must be investigated about the influence of EMFs at the level of research using in vitro or animal models. Scientific studies on the mechanism of biological effects are also required. It has been found that RF-EMF can induce changes in central nervous system nerve cells, including neuronal cell apoptosis, changes in the function of the nerve myelin and ion channels; furthermore, RF-EMF act as a stress source in living creatures. The possible biological effects of RF-EMF exposure have not yet been proven, and there are insufficient data on biological hazards to provide a clear answer to possible health risks. Therefore, it is necessary to study the biological response to RF-EMF in consideration of the comprehensive exposure with regard to the use of various devices by individuals. In this review, we summarize the possible biological effects of RF-EMF exposure.

Exposure to 835 MHz RF-EMF decreases the expression of calcium channels, inhibits apoptosis, but induces autophagy in the mouse hippocampus

The exponential increase in the use of mobile communication has triggered public concerns about the potential adverse effects of radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones on the central nervous system (CNS). In this study, we explored the relationship between calcium channels and apoptosis or autophagy in the hippocampus of C57BL/6 mice after RF-EMF exposure with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Firstly, the expression level of voltage-gated calcium channels (VGCCs), a key regulator of the entry of calcium ions into the cell, was confirmed by immunoblots. We investigated and confirmed that pan-calcium channel expression in hippocampal neurons were significantly decreased after exposure to RF-EMF. With the observed accumulation of autolysosomes in hippocampal neurons via TEM, the expressions of autophagy-related genes and proteins (e.g., LC3B-II) had significantly increased. However, down-regulation of the apoptotic pathway may contribute to the decrease in calcium channel expression, and thus lower levels of calcium in hippocampal neurons. These results suggested that exposure of RF-EMF could alter intracellular calcium homeostasis by decreasing calcium channel expression in the hippocampus; presumably by activating the autophagy pathway, while inhibiting apoptotic regulation as an adaptation process for 835 MHz RF-EMF exposure.

LRRK2 Kinase Activity Induces Mitochondrial Fission in Microglia via Drp1 and Modulates Neuroinflammation

Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease (PD). LRRK2 contains a functional kinase domain and G2019S, the most prevalent LRRK2 pathogenic mutation, increases its kinase activity. LRRK2 regulates mitochondria morphology and autophagy in neurons. LPS treatment increases LRRK2 protein level and mitochondrial fission in microglia, and down-regulation of LRRK2 expression or inhibition of its kinase activity attenuates microglia activation. Here, we evaluated the direct role of LRRK2 G2019S in mitochondrial dynamics in microglia. Initial observation of microglia in G2019S transgenic mice revealed a decrease in mitochondrial area and shortage of microglial processes compared with their littermates. Next, we elucidated the molecular mechanisms of these phenotypes. Treatment of BV2 cells and primary microglia with LPS enhanced mitochondrial fission and increased Drp1, a mitochondrial fission marker, as previously reported. Importantly, both phenotypes were rescued by treatment with GSK2578215A, a LRRK2 kinase inhibitor. Finally, the protein levels of CD68, an active microglia marker, Drp1 and TNF-α were significantly higher in brain lysates of G2019S transgenic mice compared with the levels in their littermates. Taken together, our data suggest that LRRK2 could promote microglial mitochondrial alteration via Drp1 in a kinase-dependent manner, resulting in stimulation of pro-inflammatory responses. This mechanism in microglia might be a potential target to develop PD therapy since neuroinflammation by active microglia is a major symptom of PD.

Alteration of Striatal Tetrahydrobiopterin in Iron-Induced Unilateral Model of Parkinson's Disease

It has been suggested that transition metal ions such as iron can produce an oxidative injuries to nigrostriatal dopaminergic neurons, like Parkinson's disease (PD) and subsequent compensative increase of tetrahydrobiopterin (BH4) during the disease progression induces the aggravation of dopaminergic neurodegeneration in striatum. It had been established that the direct administration of BH4 into neuron would induce the neuronal toxicity in vitro. To elucidate a role of BH4 in pathogenesis in the PD in vivo, we assessed the changes of dopamine (DA) and BH4 at striatum in unilateral intranigral iron infused PD rat model. The ipsistriatal DA and BH4 levels were significantly increased at 0.5 to 1 d and were continually depleting during 2 to 7 d after intranigral iron infusion. The turnover rate of BH4 was higher than that of DA in early phase. However, the expression level of GTP-cyclohydrolase I mRNA in striatum was steadily increased after iron administration. These results suggest that the accumulation of intranigral iron leads to generation of oxidative stress which damage to dopaminergic neurons and causes increased release of BH4 in the dopaminergic neuron. The degenerating dopaminergic neurons decrease the synthesis and release of both BH4 and DA in vivo that are relevance to the progression of PD. Based on these data, we propose that the increase of BH4 can deteriorate the disease progression in early phase of PD, and the inhibition of BH4 increase could be a strategy for PD treatment.

Differential Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on Motor Behavior and Dopamine Levels at Brain Regions in Three Different Mouse Strains

Developing an animal model for a specific disease is very important in the understanding of the underlying mechanism of the disease and allows testing of newly developed new drugs before human application. However, which of the plethora of experimental animal species to use in model development can be perplexing. Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a very well known method to induce the symptoms of Parkinson's disease in mice. But, there is very limited information about the different sensitivities to MPTP among mouse strains. Here, we tested three different mouse strains (C57BL/6, Balb-C, and ICR) as a Parkinsonian model by repeated MPTP injections. In addition to behavioral analysis, endogenous levels of dopamine and tetrahydrobiopterin in mice brain regions, such as striatum, substantia nigra, and hippocampus were directly quantified by liquid chromatography-tandem mass spectrometry. Repeated administrations of MPTP significantly affected the moving distances and rearing frequencies in all three mouse strains. The endogenous dopamine concentrations and expression levels of tyrosine hydroxylase were significantly decreased after the repeated injections, but tetrahydrobiopterin did not change in analyzed brain regions. However, susceptibilities of the mice to MPTP were differed based on the degree of behavioral change, dopamine concentration in brain regions, and expression levels of tyrosine hydroxylase, with C57BL/6 and Balb-C mice being more sensitive to the dopaminergic neuronal toxicity of MPTP than ICR mice.

Acute compartment syndrome of the forearm and hand in a patient of spine surgery: A case report / 대한마취과학회지

A 38-year-old woman underwent a 4-hour operation in the prone position for a laminectomy at C4-7 and posterior cervical decompressive fusion at C7-T1 under general anesthesia. After undraping at the end of surgery, considerable swelling with many blisters of the left forearm and hand was observed. The chest roll at the left side had moved cephalad into the axilla and compressed the axillary structures. An emergency fasciotomy to decompress the compartments of the forearm and dorsal surface of the hand was performed. In the post anesthesia care unit, the radial pulse of the left hand was palpable and the level of oxygen saturation was normal. Forearm and hand edema subsided gradually over several days and the patient was discharged with full function of her left arm. This compartment syndrome suggests careful attention should be paid to the position of the chest roll when the prone position is established for a long duration.

Effects of AIF on Knee Osteoarthritis Patients: Double-blind, Randomized Placebo-controlled Study

Anti-inflammatory factor (AIF) is a water soluble extract of three herbs, Panax notoginseng (Burk.) F. H. Chen, Rehmannia glutinosa Libosch and Eleutherococcus senticosus. The present study aimed to investigate the safety and efficacy of herb extracts, AIF, on Korean knee osteoarthritis patients for six weeks. Fifty seven patients with knee osteoarthritis, ranging from 43 to 73 years of age, who fulfilled the "American College of Rheumatology" (ACR) classification of idiopathic osteoarthritis of knee and radiographic criteria were randomly selected and enrolled for the study. After initial screening and resting period, two capsules each of AIF (Each capsule contains; 400 mg) and similar identical placebo were administered twice a day to both groups. Pain intensity at second, fourth, and sixth weeks of study as well as one week after discontinuation of drugs was assessed by using 100 mm visual analogue scale (VAS). Changes in the Korean version of the Western Ontario and McMaster Universities (K-WOMAC) index score were compared at the initiation and completion of the study. VAS assessed by patients were significantly reduced (at visit 2; 54.64+/-14.72, at visit 4, 37.32+/-16.58, p<0.001) after AIF administration. Results showed an improvement in the physical function of K-WOMAC scale which was significantly higher (p=0.013) in AIF than placebo group, and decreases of total K-WOMAC score were also significantly higher (p=0.030) in AIF groups than placebo group. No serious adverse effect was observed, and there was no difference in incidence of adverse effect between AIF and placebo groups. In this population of Korean patients with knee osteoarthritis, AIF was found to be safe, tolerable and effective for symptomatic improvement of pain and physical function.

Effects of R. Glutinosa and E. Senticosus on Postmenopausal Osteoporosis

In this study, we investigated the therapeutic effects of a novel formulation of low-dose calcium and vitamin D3, blended with Rehmannia glutinosa Libosch and Eleutherococcus senticosus Max (RE+), in postmenopausal women. The controls were given either a placebo or high dose calcium and vitamin D3 (Ca+D). Bone mineral density (BMD) in the L2-3 lumber spines and femur regions was assessed, and serum osteocalcin, bone-specific alkaline phosphatase (BALP), and cross-linked N-telopeptide of type I collagen (NTx) were used as markers of osteoblast and osteoclast activity. Furthermore, all variables were measured before and after 6 and 12 months of treatment. The osteocalcin level was higher in the RE+ group, and BALP was almost the same in all groups. Serum NTx was significantly decreased in the RE+ group after 12 months (p<0.05). The NTx in the Ca+D and placebo groups showed no significant change. The decrease of femur BMD was further demonstrated in the placebo group, but significantly increased in the RE+ group after 6 and 12 months of treatment (p<0.05). There were significant differences in the percent changes of femur BMD between the placebo and RE+ groups (p<0.01) and Ca+D and RE+ groups (p<0.05). The decrease of spine BMD in the placebo group was inhibited both in the Ca+D and RE+ groups, however, there was significant difference only between the placebo and RE+ groups (p<0.05). These findings suggest that continuous oral therapy of the RE+ formulation reduces rapidly decreasing bone mineral density in postmenopausal women more effectively than high doses of calcium and vitamin D3 alone by inhibiting osteoclastic activity. Therefore, it seems that the RE+ has its own antiosteoporotic effects. We suggest larger clinical studies to determine the most efficacious dosage and benefits of this novel treatment.

Oxidatvive Stress in Rat Model of Preeclampsia and Clinical Correlates

There are growing evidences suggesting a pivotal role of oxidative stress in the pathophysiology of preeclampsia. We investigated oxidative stress in the rat model of preeclampsia, and in clinical cases. Pregnant female rats were injected intraperitoneally with deoxycorticosterone acetate (DOCA) and given 0.9% saline as drinking water during their pregnancy. We assessed plasma F2-isoprostane (8-iso-PGF2alpha) and malondialdehyde (MDA) in a rat model, and the same markers in the plasma of maternal blood and fetal cord blood in pregnant women with preclampsia. Blood samples from the umbilical arteries and veins were collected separately. The concentrations of MDA were increased in the preeclampsia groups of animal and humans, compared with the control group; it was significantly increased in the umbilical artery and vein of the preeclampsia group. The concentrations of F2-isoprostane were elevated in the preeclampsia groups of animal and humans, compared with the control group, and the increase in F2-isoprostane concentration was prominent in the umbilical vein than umbilical artery of the preeclampsia group. Therefore, it appears that the placenta has an important role in the pathophysiology of preeclampsia, and the F2-isoprostanes of the umbilical vein may serve as a relatively reliable marker for ischemic/hypoxic injury to the fetus during the perinatal period.

Traumatic Hip Dislocation in Children: Case Report

From August 1998 to June 2005, we treated 5 children (7 cases) who suffered with traumatic dislocation of hip. The mean follow-up period was 4.1 years (range: 1~8 years). Acceptable reduction was achieved in all cases by first closed reduction. The complications were 2 redislocations in 2 patients, respectively. Closed reduction is an effective method for treating traumatic dislocation of the hip in children and long term follow-up should be performed for detecting late-onset complications such as avascular necrosis, growth disturbance and traumatic osteoarthritis.

Hydroxyl Radical Production after Intrastriatal Injection of Dopamine and the Effect of Growth Hormone on the Apoptosis of Striatal Neurons Injured by Hypoxia-ischemia in Newborn Rat Brain / 대한소아내분비학회지

PURPOSE:We investigated the production of oxygen hydroxyl radicals in the striatum of neonatal rat brain after intrastriatal injection of dopamine (DA) and the effect of growth hormone (GH) on the apoptosis of striatal neurons injured by hypoxia-ischemia. METHODS:The extracellular striatal levels of 2,3-dihydroxybenzoic acid (DHBA) and 2,5-DHBA as indicators of hydroxyl radical(OH-) production were measured by in vivo microdialysis in the striatums of 7 day-old newborn rats (n=10) after direct intrastriatal infusion of dopamine hydrochloride (1.0 micromol/microL). The samples of perfused artificial cerebrospinal fluid (CSF) were collected every 10 minutes interval. The levels of DA, 2,3-DHBA and 2,5-DHBA of CSF were analysed by HPLC (high performance liquid chromatography). Also, the brains were removed at 24 hour after hypoxic-ischemic injury by Rice-Vannucci method. The coronal sections (12 micrometer) of paraffin-fixed brains were stained by TUNEL (terminal transferase-mediated dUTP nick-end-labelling) technique, and the neuronal cells undergoing apoptosis in the striatum were observed by fluorescent microscopy and compared between GH-treated (50 mg/kg, Dong-Ah Pharmacy Co.) and saline-treated rats. RESULTS:The extracellualr striatal levels of 2,3-DHBA and 2,5-DHBA increased abruptly in the first 10 minutes samples after intrastriatal injection of DA. After then, the levels declined slowely. The levels of striatal extracelluar 2.3-DHBA increased up to 621.8+/-508.7% of basal levels (P<0.05), and the levels of 2.5-DHBA increased up to 262.8+/-198.1% of basal levels (P<0.05). GH reduced markedly the number of apoptotic neuronal cells in the striatum after hypoxic-ischemic brain injury. CONCLUSION: The level of hydroxyl radicals increased abruptly after intrastriatal injection of DA and GH reduced markedly the number of apoptotic neuronal cells in the striatum after hypoxic-ischemic brain injury.

Monoaminergic Activity by Drugs Acting on Adrenergic alpha2-receptors in Rat Hippocampus and Primary Visual Cortex / 대한정신약물학회지

OBJECTIVE: The aim of the this study was to compare the effects of clonidine (a alpha2-adrenoceptor and imidazoline receptor agonist), yohimbine (a selective alpha2-adrenoceptor antagonist) and idazoxan (a alpha2-adrenoceptor and imidazoline receptor antagonist) on extracellular monoamines and their metabolites by using the awakening animal microdialysis and high-performance liquid chromatography with electrochemical detection (HPLC-ECD) in brain regions, which are suggested to have regulatory role in depression. METHODS: We used intracerebral microdialysis in awakening rats by inserting probe through the dorsal hippocampus and occipital cortex especially in primary visual cortex, We studied respective effects of 2.0 mg/kg of clonidine, 5.0 mg/kg of yohimbine, and 5.0 mg/kg of idazoxan on the release of MHPG (a major metabolite of norepinephrine), norepinephrine (NE), DOPAC (a major metabolite of dopamine), and 5-HIAA (a main metabolite of serotonin) by intraperitoneal administration. RESULTS: Clonidine decreased the release of MHPG, NE, DOPAC, and 5-HIAA in both dorsal hippocampus and occipital cortex regions, and there were no significant differences in releasing pattern of all monoamines and their metabolites. Both yohimbine and idazoxan enhanced the release of MHPG, NE, DOPAC, and 5-HIAA in both brain regions, but there were significant differences in releasing pattern of NE and 5-HIAA. Idazoxan induced the delayed and higher efflux of NE and 5-HIAA in the primary visual cortex than yohimbine, but not in the hippocampus. CONCLUSION: This study shows that the selective alpha2-adrenoceptor antagonists increase basal monoamine output and enhance the metabolism of them in the hippocampus and primary visual cortex, and the imidazoline receptor has modulatory role in the regulation of monoamine release in primary visual cortex than hippocampus. It also suggests that high turnover rate of serotonin and norepinephrine in primary visual cortex may contribute to the pathophysiological role in depression.

Surgical Treatment of Post-traumatic Elbow Stiffness / 대한정형외과학회잡지

PURPOSE: We analyzed the clinical results of surgical treatment in patients with post-traumatic stiff elbow. MATERIALS AND METHODS: We performed surgical release in 22 elbows with posttraumatic stiffness of extraarticular origin. The average preoperative arc was 48.3 degrees, with an average flexion contracture of 39.5 degrees and an average further flexion of 87.2 degrees. Depending on their radiographic findings, cases were divided on the basis of whether ectopic ossification was present (16 cases) or not (6 cases); and as to whether the articular surface was involved (11 cases) or not (11 cases). The postoperative final arc and ratio of desired gain were compared between the groups. RESULTS: The average final arc was 108.9 degrees in the ectopic ossification group and 85.7 degrees in the non-ectopic ossification group, and showed a significantly higher arc in the ectopic ossification group. The ratios of desired gain were 89.3% and 62.6%, respectively, being significantly higher in the ectopic ossification group. In terms of articular surface involvement, no significant difference was observed between the two groups. CONCLUSION: When performing operative treatment for post-traumatic stiff elbow, assessment of the cause plays an important role. In case of ectopic ossification, satisfactory results can be expected with operative treatment after the ectopic bone has matured.

Effect of Hypoxia-Ischemia on Striatal Monoamine Metabolism in Neonatal Rat Brains

PURPOSE: We intended to evaluate the effect of hypoxia-ischemia on extracellular striatal monoamine metabolism in neonatal rat brains by in vivo microdialysis. METHODS: The right common carotid arteries of five or six-day old rats were surgically ligated, and the probes for microdialysis were inserted into the right striatum with stereotaxic instrument. After stabilization for two hours, artificial cerebrospinal fluid was infused via the probe for microdialysis and samples were collected during hypoxia-ischemia and recovery periods at 20 minute intervals. The concentrations of DA(dopamine), DOPAC(3,4-di-hydroxyphenyl acetic acid), HVA(homovanillic acid), NE(norepinephrine), and 5-HIAA(5-hydroxy indoleacetic acid) were measured by HPLC(high performance liquid chromatography) and the changes were analysed. RESULTS: The striatal levels of dopamine metabolites such as DOPAC and HVA, were significantly decreased during hypoxia-ischemia, and increased to their basal level during reoxygenation(P0.05). DOPAC showed the most remarkable decrease(23.0+/-4.2%, P<0.05), during hypoxia-ischemia and increase to the basal levels during reoxygenation(120.8+/-54.9%, P<0.05), and HVA showed the same pattern of changes as those of DOPAC during hypoxia-ischemia(35.3+/-7.6% of basal level, P<0.05) and reoxygenation (105.8+/-32.3%). However, the level of NE did not show significant changes during hypoxia-ischemia and reoxygenation. The levels of 5-HIAA decreased(74.9+/-3.1%) and increased(118.1+/-7.8%) during hypoxia-ischemia and reoxygenation, respectively(P<0.005). CONCLUSION: Hypoxia-ischemia had a significant influence on the metabolism of striatal monoamine in neonatal rat brains. These findings suggest that monoamine, especially dopamine, and its metabolites could have a significant role in the pathogenesis of hypoxic-ischemic injury of neonatal rat brains.

Effects of Ylang-Ylang Essential Oil on the Relaxation of Rat Bladder Muscle in vitro and White Rabbit Bladder in vivo

Current and primary treatment modality in overactive bladder includes the administration of anticholinergics. The demand for new agents has been rising since anticholinergics have proven to come with many side effects. This study was designed to investigate the effects of ylang-ylang essential oil (YYEO) on the relaxation of urinary bladder muscle in vitro and in vivo. Effects of YYEO were assessed on resting tension, and electrical field stimulation- and various drug-induced contraction in vitro by checking the isometric tension changes of muscle strips and same procedures were repeated in the presence of methylene blue, Nw-Nitro-L-arginine methyl ester hydrochloride (L-NAME), or N-ethylmaleimide, and in vivo. YYEO decreased significantly the contractility of strips. There was no statistically significant difference between the treated group only with YYEO and the pretreated group with YYEO and methylene blue or L-NAME. When N-ethylmaleimide was employed, there was a statistically significant decrease in the rate of contraction. In vivo studies showed the same results compared with in vitro study. The results of this study indicate that YYEO has a relaxing effect on the bladder, and such mechanism is thought to be brought about by a pathway mediated by c-AMP.

Is Peak Penile Blood Flow Volume Velocity with Electromagnetic Blood Flowmeter Suitable for the Index of Penile Erection Evaluation in a Rat as Intracavernous Pressure? / 대한비뇨기과학회지

PURPOSE: The development of a new series drugs for treating erectile dysfunction presents the a need for an easy and inexpensive animal experimental models for evaluating the drug effects on penile erectile function. The intracavernous pressure (ICP) is a suitable index for evaluating a penile erection. However, the continuous monitoring of the changes in the penile blood flow volume with an electromagnetic blood flowmeter may provide a new model for measuring the peak penile blood flow volume velocity (PBFVV) as a new index for a penile erection in a rat. MATERIALS AND METHODS: To establish a new suitable index for evaluating a penile erection in rats, measuring both the PBFVV with an electromagnetic blood flowmeter and the ICP with a polygraph were performed and compared. Fifty male adult Sprague-Dawley rats (250 gm) were divided into ICP and PBFVV measurement groups. The rats were anesthetized with 50mg/kg of pentobarbital sodium by an intraperitoneal injection. The left carotid artery was cannulated to measure the systemic blood pressure. Saline or papaverine were injected intracavernously. The ICP was measured with a pressure transducer and a polygraph. The PBFVV was measured after the penile shaft was placed in the ring of a electromagnetic blood flowmeter probe. RESULTS: Both the ICP and peak PBFVV following the intracavernous injection of papaverine were higher compared to both the ICP and peak PBFVV following the saline injection. Both the ICP and PBFVV after an intracavernous papaverine injection increased up to a peak value and then decreased. There was no significant concomitant changes in the systemic blood pressure. CONCLUSIONS: The PBFVV in rats were higher and reflected the veno-occlusive response following the intracavernous papaverine injection as well as the ICP. It is suggested that the peak PBFVV with the electromagnetic blood flowmeter as well as the ICP represents a suitable index for evaluating a penile erection in a rats.

The Change of Histologic Features and Eicosanoids Level in Rat Testicular Ischemia-Reperfusion Injury / 대한비뇨기과학회지

PURPOSE: It has been suggested that prostaglandins (PGs) play an important role in ischemia-reperfusion (IR) organ injury. However, the significance of PGs is not well documented for a testicular IR injury. The purpose of this study was to assess the potential role of PGs in rat testicular ischemia and IR injury MATERIALS AND METHODS: Sprague-Dawley male rats were divided into 7 groups, each containing 7 rats. The right spermatic cord was clamped with vascular clamps for 30 minute (group B, C), 90 minute (D, E) and 240 minute (F, G). Groups B, D, and F were ischemia groups and the group C, E, and G were reperfusion groups. Reperfusion was carried out after ischemia lasting 30, 90 and 240 min. The levels of thromboxane B2 (TxB2), 6-keto-PGF1alpha and prostaglandins E2 (PGE2) were measured using High-Performance Liquid Chromatography (HPLC). RESULTS: The levels of TxB2 were significantly elevated in groups D, E, F, and G than in the controls (p<0.05, each group). The TxB2 levels in the ischemia group F were significantly decreased compared to that of group D (p<0.05). The histological features shown in groups D, and F were typical ischemic changes, but atypical in groups B, and C. The most severe damage was noted in group G. These features were well matched with the changes of TxB2 in testicular ischemia and IR injury. The levels of 6-keto-PGF1alpha were significantly elevated in all the ischemia and IR groups compared to that of the controls (p<0.05). CONCLUSIONS: These results suggested that TxB2 might have an active role in testicular IR injury, although PGE2 and 6-keto-PGF1alpha seemed not to have an active role.