• 동의생리병리학회지
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• 제19권6호
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• pp.1594-1598
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• 2005

Scopoletin (6-methoxy-7-hydrorycournarin) is a phenolic coumarin and a member of the phytoalexins. In this study we investigated whether scopoletin causes apoptosis in human hepatoma HepG2 cells and, if so, by what mechanisms. We report that scopoletin induced apoptosis as confirmed by a chromatin condensation. The signal cascade acivated by scopoletin included the activation of caspase-3 as evidenced by increased pretense activity. Activation of caspase-3 resulted in the cleavage of 116 kDa poly(ADP-ribose) polymerase (PARP) to 85 kDa cleavage product in a dose-dependent fashion. Also, scopoletin-induced apoptotic mechanism of HepG2 cells involved the generation of hydrogen peroxide. Taken together, these results suggest that scopgletin induces hydrogen peroxide generation, which, in turn, causes activation of caspase-3, degradation of PARP, and eventually leads to apoptotic cell death in HepG2 cells.

• 동의생리병리학회지
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• 제19권3호
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• pp.640-646
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• 2005

This study was performed for the investigation of anticancer effects of Siegesbeckia glabrescens(SG) on HepG2 cells, a human hepatoma cell line. In the previous study, we examined the involvement of nitric oxide (NO) on anti-proliferative and apoptotic efficacy of SG in vascular smooth muscle cells. The possible mechanism of the apoptotic effects of SG was investigated in HepG2 cells. SG showed potent cytotoxic activity in HepG2 but not chang cells, liver normal cells. SG treatment caused morphological change such as cell shrinkage, nuclei condensation and cell blebbing in HepG2 cells. SG also increased the nitrite production of HepG2 cells in a dose-dependent manner. Furthermore, L-NNA treatment inhibited the anti-proliferative effect of SG. From RT-PCR, SG decreased Bcl-2 but no affected on Bax. Western blot for procaspase-3 and COX-2 showed that degradation of procaspase-3 protein level or inhibition of COX-2 protein expression by SG treatment. In addition, the apoptotic effect of SG was also demonstrated by DNA laddering. In conclusion, SG-induced HepG2 cells death can occur via apoptosis which was dose-dependent, and associated with apoptosis-related Bcl-2/Bax gene expressions, COX-2 inhibition, caspase-3 activation and NO pathway. These results suggest that SG is potentially useful as a chemotherapeutic/chemopreventive agent in hepatocellular carcinoma.

• 동의생리병리학회지
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• 제31권5호
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• pp.255-263
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• 2017

This article is for understanding relations between the classifications of gastritis and syndrome differentiation types of Korean Medicine through research on syndrome differentiations of clinically applied gastritis and literature of Korean Medicine. Clinical papers were searched in China Academic Journals(CAJ) of China National Knowledge Infrastructure(CNKI) from 1995 to 2015. Conclusions are as follows. First, disease mechanism of chronic gastritis are qi stagnation, damp stagnation, heat obstruction, blood stasis obstruction, yin damage, damage to collaterals with healthy qi deficiency and pathogenic qi. And qi movement stagnation is shown through the status of chronic gastritis. Second, chronic superficial gastritis belongs to qi aspect syndrome and mainly pathogen excess syndrome. And the key mechanisms are congestion and disharmony of stomach qi sometimes combined with liver depression, food accumulation and dampness-heat. Third, chronic atrophic gastritis belongs to qi-blood syndrome and deficiency-excess complex syndrome with the root of spleen qi deficiency and stomach yin deficiency and the tip of blood stasis, qi stagnation. And key mechanism is damage to collaterals with healthy qi deficiency and toxin-blood stasis. Forth, pathogen excess syndromes are shown at the early stage of chronic gastritis and healthy qi deficiency syndromes after the middle stage. Qi deficiency is shown at the beginning of the disease and yin deficiency at the late stage. And qi deficiency is related with superficial gastritis and yin deficiency with atrophic gastritis.

• 동의생리병리학회지
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• 제18권1호
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• pp.75-83
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• 2004

This experimental study was designed to investigate the effects of Sagunja-tang(SGJT), Ijin-tang(IJT), Yukgunja-tang(YGJT) on the change of cerebral hemodynamics [regional cerebral blood f1ow(rCBF), mean arterial blood pressure(MABP), and pial arterial diameter (PAD)] in normal rats, and further to determine the mechanism of action of YGJT. And, this Study was designed to investigate whether YGJT inhibit lactate dehydrogenase(LDH) activity in neuronal cells. The results were as follows ; 1. SGJT significantly increased rCBF but MABP was not changed comparing with normal MABP(l00 %). This results were suggested that SGJT significantly increased rCBF by dilating PAD. 2. IJT significantly decreased rCBF in a dose-dependent, but significantly increased MABP in a dose-dependent. This results were suggested that IJT significantly decreased rCBF by contracting PAD. 3. YGJT significantly increased rCBF and PAD in a dose-dependent, and YGJT increased MABP compared with normal MABP(100 %). This results were suggested that YGJT significantly increased rCBF by dilating PAD. 4. The YGJT-induced increase in rCBF was significantly accelerated by pretreatment with indomethacin (IDN, 1 mg/kg, i.p.), an inhibitor of cyclooxygenase but was significantly inhibited by methylene blue (MTB, 10 ㎍/㎏ i.p.), an inhibitor of guanylate cyclase. 5. The YGJT-induced increase in PAD and MABP were accelerated by pretreatment with IDN but was significantly inhibited by MTB. This results suggested that the mechanism of YGJT is mediated by guanylate cyclase. 6. YGJT inhibited significantly LDH activity in neuronal cells. This results were suggested that YGJT prevented the neuronal death. I thought that YGJT should have improvement of cerebral hemodynamics and inhibitive effect on the brain damage.

• 한국유기농업학회지
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• 제26권2호
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• pp.297-316
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• 2018

본 연구는 왕우렁이의 생리 생태적 특성 및 논 잡초방제를 위하여 투입된 왕우렁이들의 집단패사 원인을 구명하기 위하여 수행하였다. 1983년 국내에 도입되어 양식과 논 잡초방제를 위하여 활용되고 있는 왕우렁이의 종(species)은 연체동물문(Mollusca), 복족강(Gastropoda), 중복족목(Mesogastropoda), Ampulariidae과, Pomacea속에 속하는 Pomacea canaliculata Lamarck이다. 왕우렁이의 생리 생태적 특성조사 결과 왕우렁이 성체들이 국내에서 월동되고 있으나 왕우렁이 알로는 월동되지 못하고 있다. 수컷과 암컷의 비율은 1:1.99~2.33배로 암컷의 구성비가 높았다. 생장량은 1일에 87.7 mg이었으며, 껍질은 각고가 0.31 mm, 각경이 0.33 mm씩 자랐다. 왕우렁이의 생장은 먹이의 조건 등에 따라서 차이가 있을 수 있으며, 매우 빠른 생장량을 나타내었다. 한편, 건조에 대한 저항성은 매우 강하여 3개월까지 생존율이 약 80%에 달하였다. 왕우렁이 서식에 따른 수질에 미치는 영향을 평가한 결과 다량의 서식 밀도에서는 약간의 영향을 줄 수는 있겠으나, 잡초방제를 위하여 투입되는 밀도에서는 전혀 영향이 없었다. 논 잡초방제를 위하여 벼 이앙초기에 투입되는 왕우렁이가 2~3일 이내에 일시에 집단 패사되는 직접적인 원인은 미소생물인 패충류(참씨벌레)에 의하여 발생되지 않는 것으로 판명되었다. 다만 패충류 (참씨벌레)에 의하여 패사되는 비율은 밀도에 따라 2.86%와 5.71%로 매우 미미하였고, 통계적인 유의적인 차이가 없었다. 논 잡초방제를 위하여 투입된 왕우렁이들은 벼 이앙시기가 빨라지고, 일교차가 커지면서 추운 저온의 날씨로 인하여 논의 흙속으로 들어가서 죽거나 일부는 새의 먹이가 되어 사라지기 때문에 다량이 죽은 것으로 오해되었다.

• 동의생리병리학회지
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• 제17권4호
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• pp.914-922
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• 2003

Ailanthus altissima has been used to settle an upset stomach, to alleviate a fever, and as an insecticide. We reported that the water extract of A. altissima induced apoptotic cell death in HL-60 human leukemia cell line. Here, we showed the dose-dependent inhibitions of cell viability by the extract, as measured by cell morphology. The cell cycle control genes are considered to play important roles in tumorigenesis. The purpose of the present study is also to investigate the effect of A. altissima on cell cycle progression and its molecular mechanism in the cells. The level of p21 protein was increased after treatment of the extract, whereas both Bcl-2 and Bax protein levels were not changed. These results suggest that A. altissima induces apoptotic cell death via p21-dependent signaling pathway in HL-60 human leukemia cell line which delete wild type p53. G1 checkpoin related gene products tested (cyclin D3, cyclin dependent kinase 4, retinoblastoma, E2F1) were decreased in their protein levels in a dose-dependent manner after treatment of the extract. Taken together, these results indicate that the increase of apoptotic cell death by A. altissima may be due to the inhibition of cell cycle in HL-60 human leukemia cell line

• 동의생리병리학회지
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• 제36권6호
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• pp.209-212
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• 2022

We recently reported that Gastrodia elata extracts (GEE) had an effects to protect against lipopolysaccharide-induced cognitive impairment in vivo model. In this study, we investigated the neuroprotective effects and the mechanism of action of GEE in hydrogen peroxide (H₂O₂)-induced cell death of SH-SY5Y human neuroblastoma cell. The SH-SY5Y cells were divided into five groups, including control(non-treated group), 100 μM H₂O₂, 100, 200, 500 ㎍/㎖ GEE+ 100 μM H₂O₂ groups. Pre- and co-treatment with GEE prevented cell death induced by 100 μM H₂O₂ for 24 h in SH-SY5Y cells. Our findings also showed that anti-oxidants enzymes (Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase) were up-regulated by 100 μM H₂O₂. But GEE suppressed H₂O₂-induced anti-oxidants enzymes decrease in a dose-dependent manner. Treatment with GEE also inhibited phosphorylation of eukaryotic initiation factor-2α (eIF-2α) and p38 by H₂O₂. Taken together, the neuroprotective effects of GEE in terms of recovery of antioxidant enzymes expression, down-regulation of eIF-2α and p38 phosphorylation, and inhibition of cell death are associated with reduced oxidative stress in SH-SY5Y cells.

• 대한한의학방제학회지
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• 제11권1호
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• pp.57-90
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• 2003

The result of Bibliographic studies on the pathological mechanism of the sudden coma, we got the conclusion like this. 1. The sudden coma is an acute syndrome that refers to be a sudden fainting, an unconsciousness, an aphasia or a cold clammy limb, and immediately awakes or dies, and awakes in a short time, and if we awake, it doesn't leave over and above a sequela. 2. The clinical presentation of the sudden coma can be summarized as follows : The 1st is a disease raising the sudden death due to unconsciousness accompanied by wry mouth & sudden syncope with coma. The 2nd is simply the state of cold limbs. The 3rd is the meaning of the physique and symptomes of the six meridians. The last is the ancient method of expression in contrast of the beriberi. 3. The pathological mechanism of the sudden coma consists of the toxoid from outside, Qi and Xie, fatigue, damp phegm, the damage from seven emotions and the damage from five mental elements, especially the mental disorder due to the angry energy, causes the problems when the fleming-up of liver fire and the depressed of liver qi raise the physiological disorder. 4. Therapeutic methods of sudden coma are soothing the liver and remove stasis, soothing depression and circulating of the qi, calming the liver and suppressing yang. When that is early stage, at first, we must checking upward adverse flow of the qi after promoting the circulation of qi and awakening, and then, we must regulate excessive deficiency of yin yang by therapy that is based on differentiated in symptoms according to heat & cold, deficiency & excess, and use invigorating herb medicine for supporting vigour.

• 동의생리병리학회지
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• 제18권6호
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• pp.1733-1739
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• 2004

The water extract of Hwangryunhaedog-tang(HRHDT} has been traditionally used for treatment of ischemic heart and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of HRHDT rescues cells from these damages. This study was designed to investigate the protective mechanisms of HRHDT on hypoxia-induced cytotoxicity in H9c2 cardiomyoblast cells. Hypoxia, markedly decreased the viability of H9c2 cells, which was characterized with apparent apoptptic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. However, HRHDT significantly reduced hypoxia-induced cell death and apoptotic characteristics. Also, HRHDT prevented the mitochondrial dysfunction including the disruption of mitochondria membrane permeability transition (MPT) and an increase in expression of anti-apoptotic Bcl-2 proteins in hypoxia-H9c2 cells. Taken together, this study suggests that the protective effects of the water extract of HRHDT against hypoxic damages may be mediated by the modulation of Bcl-2 and Bak expression.

• Asian Pacific Journal of Cancer Prevention
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• 제16권15호
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• pp.6215-6223
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• 2015

Tyrosine phosphorylation plays an important role in regulating human physiological and pathological processes. Functional stabilization of tyrosine phosphorylation largely contributes to the balanced, coordinated regulation of protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs). Research has revealed PTPs play an important suppressive role in carcinogenesis and progression by reversing oncoprotein functions. Receptor-type protein tyrosine phosphatase O (PTPRO) as one member of the PTPs family has also been identified to have some roles in tumor development. Some reports have shown PTPRO over-expression in tumors can not only inhibit the frequency of tumor cell division and induce tumor cell death, but also suppress migration. However, the tumor-suppression mechanisms are very complex and understanding is incomplete, which in some degree blocks the further development of PTPRO. Hence, in order to resolve this problem, we here have summarized research findings to draw meaningful conclusions. We found tumor-suppression mechanisms of PTPRO to be diverse, such as controlling G0/G1 of the tumor cell proliferation cycle, inhibiting substrate phosphorylation, down-regulating transcription activators and other activities. In clinical anticancer efforts, expression level of PTPRO in tumors can not only serve as a biomarker to monitor the prognosis of patients, but act as an epigenetic biomarker for noninvasive diagnosis. In addition, the re-activation of PTPRO in tumor tissues, not only can induce tumor volume reduction, but also enhance the susceptibility to chemotherapy drugs. So, we can propose that these research findings of PTPRO will not only support new study ideas and directions for other tumor-suppressors, importantly, but also supply a theoretical basis for researching new molecular targeting agents in the future.