• 대한본초학회지
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• 제34권1호
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• pp.43-50
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• 2019

Objectives : The purpose of this study was to proofread 'one ryang' in the Decoction of ${\ll}$Treatise on Cold Damage Diseases${\gg}$. Methods : I found out the ratio of maximum dose and minimum dose in this book. On the basis of the ratio, I corrected 'one ryang' in diverse decoctions. Results : In any decoction, maximum dose of medicinal medica in one decoction could not exceed four times minimum dose. Specifically, in the case that maximum dose in one decoction is sixteen ryang, it could not exceed eight times minimum dose in the same decoction. Any medicinal medica used in two decoctions or more, its maximum dose could not exceed four times minimum dose in other decoctions. On the basis of these results, it should be changed into three ryangs that are one ryang dose of 'Haematitum' of Seonbokdaeja Tang, 'Ginger' of Bujageongang Tang, Baektong Tang, Baektonggajeodamjep Tang and Senggangsasim Tang. Furthermore it should be changed into two ryangs that are one ryang dose of 'Coptidis Rhizoma' of Sohamhyung Tang, 'Ginger' of Dowha Tang, 'Ginseng Radix' of Whubaksenggangbanhagamchoinsam Tang, 'Polyporus, Poria Sclerotium, Alismatis Rhizoma, Talcum and Asini Corii Colla' of Jeoryeong Tang, 'Cimicifugae Rhizoma, Atractylodis Rhizoma Alba and Anemarrhenae Rhizoma' of Mahuangshengma Tang and 'Cassiae Cortex Interior' of Gyejigamchoryonggolmoryeo Tang. Conclusions : These results suggest that one ryang of thirteen medicinal medica such as Haematitum or Ginger of eleven decoctions such as Seonbokdaeja Tang or Bujageongang Tang should be changed into two or three ryangs.

• 동의신경정신과학회지
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• 제12권2호
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• pp.69-84
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• 2001

Objectives : We suggest the method of oriental neuropsychiatry treatment about amnesia through herb therapy. Methods : We investigate cause of disease, component of herbs about amnesia with classic current oriental medicine books. Results : Amnesia is due to simsinbulgyo(心腎不交), biwieyangher(脾胃陽虛), dammisimgyoo(痰迷心竅), emotional damage(七情所傷), extravasated blood(瘀血), deficiency of kidney (腎虛). There is 138 kind of herbs are used in our study that we find out that most frequently used herb is ginseng(人蔘). Heart meridian is the highest use in the all meridians. Sungon(性溫) is the highest use in the all kimi(氣味) Conclusions : We could confirm that herbs of amnesia treatment was related to the three vital organs(臟) named of spleen(脾), lung(肺), kidney(腎).

• Advances in Traditional Medicine
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• 제7권5호
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• pp.564-568
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• 2008

The root of Polygala tenuifolia Willd (PT) is known to have neuroprotective effects and as an antidementic herb in Chinese and Japanese traditional medicine. We examined potential neuroprotective effects of PT using the 4-vessel occlusion model in rats. In this study, the efficacy of PT for the prevention of neuronal damage and for the reduction of memory impairment was investigated. The results indicate that PT confers significant neuroprotection especially for ischemic hippocampal neurons.

• 한국식품영양과학회지
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• 제37권6호
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• pp.701-707
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• 2008

본 실험에서는 STZ로 당뇨를 유발시킨 흰쥐에 홍삼과 팽화홍삼의 항당뇨 효능에 대한 생리활성을 규명하고자 홍삼을 7주간 경구투여 후 체중, 혈당, 혈청 인슐린 및 아밀라아제, 지질관련 지수, OGTT, DNA의 산화적 손상정도 분석 및 췌장의 조직병리학적 변화를 관찰하였다. 체중증가는 실험 7주 후에 DM군과 비교 시 RG군에서 6.67배, PG군에서 5.25배 증가하였으나 DM군과 유의적인 차이는 없었다. 공복혈당은 DM군에 비해 RG군에서 11.54%, PG군에서 20.22%의 감소를 보였다. 구강내당능 검사결과 공복혈당, 포도당 투여 2시간 후 혈당은 DM군과 통계적 유의성은 없었다. 혈청 인슐린 농도는 PG군에서 가장 높게 나타났고, 혈청 아밀라아제 농도의 경우 RG군에서 높았으나 NC군보다는 낮게 나타났다. 혈청 총 콜레스테롤은 NC군을 제외한 모든 실험군 간에 유의적인 차이를 보이지 않았으나 혈청 중성지방의 경우 PG군에서 현저한 감소를 보였다(p<0.05). HDL-C는 NC군에 비해 당뇨유발군 모두에서 높게 나타났다. DNA 손상정도를 알아보기 위한 comet 분석에서는 PG군의 TL 및 TM은 NC군에서와 유사한 수준을 보였다. 췌장조직의 병리학적 관찰결과, 당뇨유발군 중 DM군의 췌장조직의 exocrine acinal cell 및 췌도세포에서는 focal 또는 multifocal cytoplasmic vacuolation과 췌장실질의 괴사 및 출혈성 병변이 관찰되었다. 이상의 결과로서 팽화홍삼의 투여가 홍삼에 비해 항당뇨 효과가 더 큰 경향을 보였으나 보다 확실한 결과를 위해 8주 이상의 홍삼 장기투여에 의한 항당뇨 효과 확인이 필요할 것으로 사료된다.

• Journal of Ginseng Research
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• 제30권3호
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• pp.112-116
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• 2006

본 연구는 TCDD로 급성독성을 유도한 자정 기니픽의 대퇴골 무게감소에 대한 홍삼사포닌의 효과를 조사하기 위해 수행하였다. 48 마리의 자성기니픽 ($820{\pm}25\;g$)을 6 군으로 나누어 정상군 (NC), TCDD 단독투여군 (TT), 사포닌 전투여 군 (PE10, 20), 사포닌후투여군 (CE10, 20)으로 나누었다. NC군은 vehicle과 saline 만을 투여하였고, TT군은 TCDD를 단회투여 ($5.0\;{\mu}g$, i.p) 하였다. PE10 및 20군은 TCDD 투여 1 주일 전부터 총 3 주동안 사포닌을 투여 (복강) 하였다. 반면 CE10 및 20군은 TCDD 투여한 직후부터 총 3 주동안 사포닌을 투여 (복강) 하였다. 사포닌 투여군의 체중변화를 살펴보면 TT군은 TCDD 투여후 유의적인 체중감소 현상이 관찰되었으나 PE10, 20 및 CE10, 20 등 사포닌 투여군에서는 TT군에 비해 체중이 모두 증가하는 경향을 보였다 . TCDD 투여는 지정기니픽의 대퇴골 무게를 유의적으로 감소시키는 반면 홍삼사포닌의 투여는 대퇴골 무게감소를 억제하는 경향을 보였다. 대퇴골 무게감소 억제현상은 PE20군에서 가장 높게 나타났다. 대퇴골의 $Ca^{2+}$도 TT군은 NC군 대비 약 20.4% 감소하는데 반해 사포닌 투여군은 TT군 대비 $Ca^{2+}$ 함량이 증가되는 경향을 나타내었다. 이러한 결과로부터 홍삼사포닌은 TCDD에 의해 억제된 기니픽의 대퇴골 내 $Ca^{2+}$ 함량을 증가시킴으로써 대퇴골의 무게감소를 회복시키는 것으로 추론할 수 있겠다.

• 한국식품영양과학회지
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• 제33권3호
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• pp.523-532
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• 2004

영양소의 섭취를 포함한 여러 식이성요인에 따라 일부 지역 남자 노인의 인체 임파구 SCE 빈도수가 어떤 영향을 받는지를 조사해 보고자하여 60세 이상의 노인 45명을 대상으로 설문조사를 실시한 후 채혈하여 임파구 SCE 시험을 실시하였다. 조사 대상자의 식이성 요인이 SCE 빈도수에 미치는 영향에 대해 분석한 결과는 다음과 같다. 1. 채혈 대상자를 흡연여부에 따라 흡연군(n=14), 담배를 피우다가 현재는 끊은 금연군(n=16), 비흡연군(n=15)으로 나눈 후 SCE 빈도수를 비교한 결과 흡연군의 SCE빈도수가 비흡연군에 비해 유의적으로 높았으며 노인의 나이가 많을수록 DNA 손상정도가 증가하였다. 대상 노인의 인구학적 요인 중 신장, 혹은 체중이 전 대상자군에서 SCE 빈도수와 각각 역의 상관관계를 보였으며 흡연군에서는 신장과 SCE빈도수가 역의 상관관계, 그리고 pack years로 본 흡연력과 SCE 빈도수가 정의 상관관계 를 보였다. 2. 전 대상자군에서는 24시간 회상법으로부터 구한 영양소의 섭취와 SCE빈도수 간에 상관관계가 없었으나 흡연군의 경우는 식이섬유질 섭취량, 금연군의 경우는 비타민 C 섭취량과 SCE 빈도수가 각각 정의 상관관계를 보였다. 그러나 비 흡연군에서는 지방, 인 혹은 비타민 A 섭취량과 SCE빈도수 간에 역의 상관관계를 보였다. 3. 흡연군에서 육어류 섭취빈도와 SCE빈도수 간에 정의 상관관계를 보였고, 비 흡연군에서 식 사균형도가 SCE 빈도수와 역의 상관관계를 보였다. 세 군을 모두 합한 전대상자군의 경우, 혈당수준과 SCE 빈도수 사이에 정의 상관관계가 나타났다. 금연군에서 감미료를 섭취하는 군의 SCE 빈도수가 섭취하지 않는 군보다 유의적으로 높았다. 나머지 식이성 요인들은 SCE 빈도수와 상관성을 보이지 않았다. 본 연구 결과는 앞으로 DNA손상도가 높은 노인 대상으로 이의 회복을 위하여 식이성 요인을 이용한 영양중재실험을 계획할 때, 혹은 노인 대상의 영양교육 시에 중요한 기초자료로 활용될 수 있을 것이다.

• Journal of Ginseng Research
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• 제41권4호
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• pp.503-512
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• 2017

Background: Chronic heavy alcohol consumption may raise the risk of developing type 2 diabetes mellitus. Saponins inhibit apoptosis of pancreatic islet cells and reduce lipid parameters. The present study was designed to investigate the effect of saponin on chronic ethanol-treated diabetic rats. Methods: Long-Evans Tokushima Fatty (LETO) and Otsuka Long-Evans Tokushima Fatty (OLETF) rats were pair-fed a Lieber-DeCarli diet with and without 5% ethanol for 12 wks. Two weeks after starting the pair-feeding with the Lieber-DeCarli diet, intraperitoneal injection of saponin was performed for 10 wks. To perform the experiments, rats were divided as follows: LETO-Control (LC), LETO-Ethanol (LE), LETO-Ethanol-Saponin (LES), OLETF-Control (OC), OLETF-Ethanol (OE), and OLETF-Ethanol-Saponin (OES). Results: The weights of epididymal and mesenteric fat tissue in LES and OES rats were the lightest from among the LETO and OLETF groups, respectively. The secretion of alanine aminotransferase and cholesterol in OES rats decreased significantly compared to their secretion in OC and OE rats, respectively. The islets of the pancreas in LE and OE rats showed clean, unclear, and smaller morphology compared to those of LC, LES, OC, and OES rats. In addition, the expression of insulin in the islets of the pancreas in LC, LES, OC, and OES rats was higher than in LE and OE rats. Conclusion: Saponin may not only be helpful in alleviating the rapid progress of diabetes due to chronic alcohol consumption in diabetic patients, but may also show potential as an antidiabetic drug candidate for diabetic patients who chronically consume alcohol.

• 약학회지
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• 제50권6호
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• pp.345-350
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• 2006

The pharmacological properties of ginseng are mainly attributed to ginsenosides, the active constituents that are found in the extracts of different species of ginseng. Lately; the studies on ginsenosides are mainly focused on IH-901, a major intestinal bacterial metabolite of ginsenosides. In this study; we examined the anti-diabetic activity of IH-901 in C57BU61 db/db mice model. IH-901 was administrated orally at a dose of 20 mg/kg for 5 weeks. During the experimental period, body weight and blood glucose levels were measured every week. After 5 weeks, db/db mice were sacrificed and diabetic parameters were analyzed. IH-901 treated group showed a significant decrease in fasting blood glucose levels (from 10.5 mM to 9.4 mM), insulin resistance index (from 163.6 to 100.2) and triglyceride levels (from 115.3 to 70.1) compared to the diabetic control. In Pancreatic islets morphology; IH-901 treated group revealed much less infltrated mononuclear cells, indicating that IH-901 recovered ${\beta}$-cell damage due to hyperglycemia. In addition, IH-901 upregulated expressions of glucose transporter 4 (GLUT4) and PPAR-${\gamma}$ in skeletal muscle and adipose tissue, respectively. Taken together IH-901might be a potential anti-hyperglycemic agent with insulin sensitizing effect.

• Journal of Ginseng Research
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• 제46권5호
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• pp.700-709
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• 2022

Background: Ginsenoside Rd is a natural compound with promising neuroprotective effects. However, the underlying mechanisms are still not well-understood. In this study, we explored whether ginsenoside Rd exerts protective effects on cerebral endothelial cells after oxygen-glucose deprivation/reoxygenation (OGD/R) treatment and its potential docking proteins related to the underlying regulations. Method: Commercially available primary human brain microvessel endothelial cells (HBMECs) were used for in vitro OGD/R studies. Cell viability, pyroptosis-associated protein expression and tight junction protein degradation were evaluated. Molecular docking proteins were predicted. Subsequent surface plasmon resonance (SPR) technology was utilized for validation. Flow cytometry was performed to quantify caspase-1 positive and PI positive (caspase-1+/PI+) pyroptotic cells. Results: Ginsenoside Rd treatment attenuated OGD/R-induced damage of blood-brain barrier (BBB) integrity in vitro. It suppressed NLRP3 inflammasome activation (increased expression of NLRP3, cleaved caspase-1, IL-1β and GSDMD-N terminal (NT)) and subsequent cellular pyroptosis (caspase-1+/PI + cells). Ginsenoside Rd interacted with SLC5A1 with a high affinity and reduced OGD/R-induced sodium influx and potassium efflux in HBMECs. Inhibiting SLC5A1 using phlorizin suppressed OGD/R-activated NLRP3 inflammasome and pyroptosis in HBMECs. Conclusion: Ginsenoside Rd protects HBMECs from OGD/R-induced injury partially via binding to SLC5A1, reducing OGD/R-induced sodium influx and potassium efflux, thereby alleviating NLRP3 inflammasome activation and pyroptosis.

• 동의생리병리학회지
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• 제23권2호
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• pp.397-404
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• 2009

For standardization of LMK02 quality, Ginsenoside Rg3 of Red Ginseng and Decursin of Angelica gigas Nakai in the constituents of LMK02 were estimated as indicative components. From LMK02 water extract, has been used in vitro test for its beneficial effects on neuronal survival and neuroprotective functions, particularly in connection with APP-related dementias and Alzheimer's disease (AD). $A{\beta}$ oligomer derived from proteolytic processing of the ${\beta}$-amyloid precursor protein (APP), including the amyloid-${\beta}$ peptide ($A{\beta}$), play a critical role in the pathogenesis of Alzheimer's dementia. We determined that oligomer amyloid-${\beta}$ ($A{\beta}$) have a profound attenuation in the increase in rat hippocampus H19-7 cells from. Experimental evidence indicates that LMK02 protects against neuronal damage from cells, but its cellular and molecular mechanisms remain unknown. Using a hippocampus cell line on $A{\beta}$ oligomer-induced neuronal cytotoxicity, we demonstrated that LMK02 inhibits formation of $A{\beta}$ oligomer, which are the behavior, and possibly causative, feature of AD. In the Red Ginseng, the average amounts of Ginsenoside Rg3 were $47.04{\mu}g/g$ and $42.3{\mu}g/g$, 90 % of its weight were set as a standard value. And, in the Angelica gigas Nakai, the average amounts of Decursin were 2.71 mg/g and 2.44mg/g, 90 % of its weight were also set as a standard value. The attenuated $A{\beta}$ oligomer in the presence of LMK02 was observed in the conditioned medium of this $A{\beta}$ oligomer-induced cells under in vitro. In the cells, LMK02 significantly activated antiapoptosis and decreased the production of ROS. These results suggest that neuronal damage in AD might be due to two factors: a direct $A{\beta}$ oligomer toxicity and multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of $A{\beta}$ oligomer, underlie the neuroprotective effects of LMK02 treatment.