
http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Thaise Boeing,Francislaine Aparecida dos Reis Lívero,Priscila de Souza,Danielle Ayr Tavares de Almeida,Guilherme Donadel,Emerson Luiz Botelho Lourenço,Arquimedes Gasparotto Junior 한국식품영양과학회 2023 Journal of medicinal food Vol.26 No.5
The mitochondria have an important role in modulating cell cycle progression, cell survival, and apoptosis. In the adult heart, the cardiac mitochondria have a unique spatial arrangement and occupy nearly one-third the volume of a cardiomyocyte, being highly efficient for converting the products of glucose or fatty acid metabolism into adenosine triphosphate (ATP). In cardiomyocytes, the decline of mitochondrial function reduces ATP generation and increases the production of reactive oxygen species, which generates impaired heart function. This is because mitochondria play a key role in maintaining cytosolic calcium concentration and modulation of muscle contraction, as ATP is required to dissociate actin from myosin. Beyond that, mitochondria have a significant role in cardiomyocyte apoptosis because it is evident that patients who have cardiovascular diseases (CVDs) have increased mitochondrial DNA damage to the heart and aorta. Many studies have shown that natural products have mitochondria-modulating effects in cardiac diseases, determining them as potential candidates for new medicines. This review outlines the leading plant secondary metabolites and natural compounds derived from microorganisms as modulators of mitochondrial dysfunctions associated with CVDs.
Therapeutic Feasibility of the Natural Products in the Heart Complaints: An Overview
Priscila de Souza,Luísa Nathália Bolda Mariano,Rita de Cássia M. V. A. F. da Silva,Francielli Gasparotto,Emerson Luiz Botelho Lourenço,Guilherme Donadel,Thaise Boeing,Arquimedes Gasparotto Junior 한국식품영양과학회 2021 Journal of medicinal food Vol.24 No.12
Heart pain is the most frequent complaint leading patients to seek medical help. Functional heart symptoms, especially chest pain, are prevalent and, according to the International Classification of Diseases (ICD-10), are described as “somatoform autonomous functional disorders of the cardiovascular system.” The problem lies in the fact that pain does not always have a somatic background, that is, it may be related to crucial underlying heart disease. The population does not know how to differentiate somatic pain from significant ischemic symptoms, and based on the patient's complaints, traditional medicine ends up treating other underlying cardiac diseases. Many unsuccessful unconventional therapies have been proposed in recent years, including herbal medicines that seek to disrupt the disease's pathogenesis. The present review summarizes research carried out in the last 5 years on natural products' heart complaints, including myocardial ischemia, arrhythmia, and heart failure. Several herbal medicines may be used as a replacement or complementary treatment strategy. A total of 17 medicinal plants have shown promising results in preclinical studies. However, human clinical trials are scarce; only two have been presented. Generally, the data are bland, and many issues have been raised about herbal therapies' safety, efficacy, and mode of action. Besides, relevant clinical trials, future perspectives, and possible clinical applications are discussed.

痙攣性 腦-電氣衝擊에 의한 생쥐 視床下部 및 腦幹의 Monoamine 代謝의 變動에 관한 硏究
全普權,申炅浩,朴靑山,李明雅 大韓神經精神醫學會 1991 신경정신의학 Vol.30 No.4
Male ICR mice ranging from 15g to 20g were given a single ECS(1-ECS : 13mA, 1sec,100cps) daily or on alternate days for 10 days(5-ECS). The contents of monoamine metabolites in the hypothalamus and the brain stem(BS) were measured 10, 30. and 60 min after ECS-administration as well as before ECS. Contents of monoamine metabolites in the HT and the BS, such as 5-HIAA, MHPG, DOPAC and HVA increased rapidly after 1-ECS or 5ECS and then came down to the pre-ECS values. However, their increases induced by 5-ECS were significantly smaller than those by 1-ECS except the tedious increase of the hypothalamic HAV content. 5-HIAA and MHPG in the HT decrease significantly by the 4the administration of ECS in the course of the 5-ECS treatment. These results suggest that the repeated treatment of ECS may decrease the turnover rates of serotonin and noradrenaline in the hypothalamus.
Morphine의 血漿 Corticosterone增加作用에 미치는 Clonidine과 Alpha-Methyldopa의 抑制性 效果의 比較
洪基成,全普權,申萬鍊 고려대학교 의과대학 1986 고려대 의대 잡지 Vol.23 No.1
There is much disagreement on the role of adrenoceptor in the ACTH liberation from the adenohypophysis. In this paper, the influences of several adrenoceptor blockades on the inhibitory effect of clonidine and alpha-methyldopa on the morphine-induced increase of plasma corticosterone level in male mice were studied. The results obtained were summarized as follows; 1. Clonidine(100 and 500㎍/kg), alpha-methyldopa(30 and 230mg/kg) and naloxone(1 and 4mg/kg), respectively, showed the dose-dependent inhibitory effect on the morphine-induced increase of plasma corticosterone level. 2. Clonidine(500㎍/kg) did not affect the increase induced by- ACTH(5U/kg), picrotoxin (4mg/kg) or cold-swim stress of plasma corticosterone level. 3. Alpha-methyldopa( 250mg/kg) did not affect the ACTH-induced increase of plasma corticosterone level but significantly suppress the picrotoxin-induced increase, and it rather enhanced the increase induced by cold-swim of plasma corticosterone level. 4. The inhibitory effect of clonidine on the morphine-induced increase of plasma corticosterone level was not affected by prazosin(1mg/kg), propranolol(1mg/kg) and haloperidol (1mg/kg) but significantly suppressed by phenoxybenzamine(1mg/kg) and yohimbine(1mg/kg). 5. The inhibitory effect of alpha-methyldopa on the morphine-induced increase was not affected by prazosin and haloperidol but significantly suppressed by phenoxybenzamine, yohimbine and propranolol. These results suggest that the inhibitory effect of clonidine on the morphine-induced increase of plasma corticosterone level may be mainly mediated by its property as an alpha₂-adrenoceptor agonist, but the inhibitory effect of alpha-methyldopa may be somewhat different from that of clonidine and may be mediated by its action as alpha₂-adrenoceptor agonist and other nonselective actions.
Morphine에 依한 組織 Catecholamine含量의 變動에 미치는 Clonidine의 影響
李哲毅,全普權,申萬鍊 고려대학교 의과대학 1984 고려대 의대 잡지 Vol.21 No.1
It has been well known that noradrenaline neurons appear to be involved in both morphine and clonidine analgesia, and there are many evidences that the effects of the two drugs on brain noradrenaline-turnover are inhibitory. But the functional role of brain noradrenaline in the suppressive effect of clonidine on the development of opioid withdrawal signs has not yet been clarified. The present study was therefore undertaken in order to ascertain whether brain noradrenaline is responsible for clonidine-induced suppression of development of development of opioid withdrawal signs or cross-tolerance to morphine and clonidine, and so, seventeen hours after the last of 12 injections of increasing doses of both morphine and clonidine over 6 days according to the modified Paalzow’s and Weinstock’s and Weinstock’s methods of the development of tolerance to the two drugs of morphine and clonidine on brain and heart catecholamine contents were estimated in male mice. The results obtained were summarized as follows: 1. Morphine (20㎎/㎏ i.p.) slightly increased brain catecholamine content and significantly increased heart catecholamine content. The morphine-induced increase of brain catecholamine content was not altered all along the 7 day treatment of it, but the morphine-induced increase of heart catecholamine content was augmented after the 4 day treatment of it and the augmentation showed a moderate decline after the 7 day treatment. 2. Clonidine (500㎍/㎏ i.p.) significantly increased both brain and heart catecholamine contents. The clonidine-induced increase of brain catecholamine content was not altered all along the 7 day treatment of it, but the clonidine-induced increase of heart catecholamine content was slightly augmented after the 4 day treatment of it and then recovered to the initial level. 3. The combined effect of morphine and clonidine on the both brain and heart catecholamine contents was additive, and the additive combined-effect was not altered all along the 7 day treatment of the two drugs. The above results suggest that the tolerance development of morphine and the clonidineinduced suppression of opioid withdrawal signs may be mediated through other neuronal systems as well as noradrenergic system.