• 한국과학교육학회지
• /
• 제18권3호
• /
• pp.303-312
• /
• 1998

본 연구는 화학 평형 단원에 대한 멀티미디어 CAl를 제작하고, 고등학교 화학수업에 적용하여 성취도와 태도 면에서 전통적 수업과의 효과를 비교하였다. 이를 위하여 수업처치 전에 화학수업과 컴퓨터에 대한 태도 검사를 하였고, 중간고사 성적을 공변인으로, 중간고사의 과학성적을 구획변인으로 사용하였다. 화학 평형 단원을 대상으로 각각 전통적인 수업과 CAl를 수행한 후에 성취도 검사와 태도 검사를 실시하였다. 컴퓨터를 이용하여 화학수업을 받은 학생은 전통적인 수업을 받은 학생에 비하여 성취도는 유의미하게 향상 되었으나, 태도의 향상은 유의미하지 않았다. 또한 학습자의 사전 성취수준과 수업처치와의 상호작용은 관찰되지 않았다. 성별로 분석해 보니 여학생은 CAl에 의해 성취도가 향상되었으나, 남학생은 차이를 보이지 않았다. 이해와 적용의 하위범주 중 적용문제 영역에서 CAl에 의한 성취도의 향상이 있었으며, 화학 평형의 법칙, 화학 평형의 개념, 평형 이동의 적용 세 부분으로 나누었을 때 화학 평형의 개념에서 성취도의 향상이 가장 컸다. CAl가 컴퓨터에 대한 태도와 화학수업에 대한 태도에 긍정적인 변화를 주지 않았으며, 남학생은 CAl에 의해 화학수업에 대한 태도와 컴퓨터에 대한 태도 모두 긍정적으로 변했으나 여학생은 그렇지 못하였다. 이상의 결과에 대한 교육적 의미를 논의하였다.

• 한국식품영양과학회지
• /
• 제40권11호
• /
• pp.1507-1511
• /
• 2011

본 연구에서는 LPS에 의해 활성화된 RAW264.7 대식세포에서의 NO 생성 및 iNOS와 HO-1 단백질 발현의 변화를 측정하여 개망초(Erigeron annuus L.) 꽃(EAF) methanol 추출물의 항염증 효과를 확인하였다. RAW264.7 대식세포에 LPS를 처리한 결과 NO의 함량이 11.48 ${\mu}m$ 수준으로 증가하였다. 그러나 EAF methanol 추출물(25, 50, 100, 200 ${\mu}g$/mL)을 처리하였을 때 NO의 함량이 12.82, 9.61, 6.83, 2.52 ${\mu}m$로 농도 의존적으로 감소하였다. 또한 EAF methanol 추출물은 NO의 생성에 관여하는 iNOS 단백질의 발현을 농도 의존적으로 저해하였으며 HO-1 단백질의 발현을 유도하였다. EAF methanol 추출물에 의한 HO-1 발현이 NO 생성에 미치는 영향에 대해 확인하기 위해 HO-1의 inhibitor인 ZnPP를 사용하였다. 실험결과 ZnPP를 처리하여 HO-1의 발현을 저해하였을 때 추출물에 의해 감소된 NO의 함량이 다시 증가되었다. 본 연구 결과, EAF methanol 추출물은 염증을 유발하는 중요 인자인 NO를 저해하였고, iNOS의 발현을 억제시켰으며 산화적 손상으로부터 세포 보호 방어 기작에 관여하는 HO-1의 발현 등 항염증에 우수한 효과를 보였으며 항염증 연구의 기초 자료로 활용될 것으로 예상된다.

• 동의생리병리학회지
• /
• 제17권6호
• /
• pp.1500-1508
• /
• 2003

This study was performed to clarify the neurotoxic mechanism of nerve cells damage by brain ischemia. The cytotoxic effect of ischemia was determined by XTT assay, NR assay, superoxide dismutase(SOD) activity, amount of malondialdehyde(MDA), lactate dehydrogenase(LDH) activity, protein synthesis and tumor necrosis factor(TNF)-α activities after cerebral neurons derived from mouse were exposed to ischemia for 1∼30 minutes. In addition, the protective effect of extract of Daejo-whan(DJW) on ischemia-induced neurotoxicity was examined in these cultures. 1. Ischemia decreased cell number and viability by XTT assay or NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO₂ for 1∼20 minutes in these cultures. 2. Ischemia decreased SOD and protein syntheses, but it increased amount of MDA and, LDH and TNF-α activities in these cultures. 3. In the neuroprotective effect of DJW extracts on cerebral neurons damaged by ischemia, DJW extracts increased SOD activity and protein synthesis. While, it decreased amount of MDA and, LDH and TNF-α activities after cerebral neurons preincubated with herb extracts. It suggests that brain ischemia has neurotoxicity on cultured mouse cerebral neurons, and the herb extract such as DJW was very effective in blocking the neurotoxicity induced by ischemia in cultured mouse cerebral neurons.

• 대한약리학회지
• /
• 제30권1호
• /
• pp.101-109
• /
• 1994

Tetrahydroisoquinoline유도체인 GS 283의 약리학적 특성을 흰쥐 흉부대동맥, 기니픽 결장띠 및 토끼 장간막 동맥 및 흰쥐 뇌를 사용하여 조사하였다. 혈관 평활근에서 GS283은 고 $K^+$에 의한 수축을 농도 의존적으로 억제하여 $Ca^{2+}$ 길항작용을 보였다. 또한 ${alpha}_1$- 수용체 자극에 의한 수축도 억제하였다. GS 283의 혈관이완 작용은 propranolol영향을 받지 않으므로 ${\beta}$-수용체 자극작용에 의한 것이 아니었다. 세포내 칼슘이온과 근장력 변화를 동시에 측정하였을 때 GS 283의 억제효과는 조직내 형광의 증가를 수반했다. 이 증가는 fura 2형광에 의한것이 아니라 내인성 pyridine nucleotide에 의한 것이며 이는 GS 283이 미토콘드리아 기능을 억제하는 효과가 있음을 시사했다. 흰쥐 뇌의 cAMP와 cGMP 의존성 phosphodiesterase에 대한 GS 283의 $K_i$,값은 2.5와 6.7mM이었다. 이상의 결과에서 GS 283의 약리 작용은 $Ca^{2+}$ 길항작용, ${\alpha}_1$- 수용체억제 작용 및 cyclic nucleotide 의존성 phosphodiesterase 억제 등 다양한 작용이 있으며 평활근 수축 억제에 대한 GS283 작용에는 $Ca^{2+}$ 길항이 가장 중요한 요인이 될 것으로 생각된다.

• 대한한의학회지
• /
• 제27권3호
• /
• pp.107-131
• /
• 2006

Background and Aims: Dansamtongmek-tang (DSTMT) and Dansamsengmek-san (DSSMS) have been used for many years as therapeutic agents for the acute stage of cerebrovascular disease, hypertension and hyperlipidemia in Oriental medicine, but the effects of DSTMT and DSSMS on hyperlipidemia and safety for cell damage are not yet well-known. This study was done to investigate the effects of DSTMT and DSSMS on hyperlipidemia. Methods: In vivo test: after administering DSTMT and DSSMS to SHR and ICR occurred hyperlipidemia for 3 weeks, we analyzed body weight, cholesterol levels. TG, HDL-chol, LDL-chol, LDH in plasma, brain, liver and kidney tissue, and DNA by RT-PCR. In vitro test: after administering DSTMT and DSSMS to human hepatocellular carcinoma in hypoxia, we observed cell cohesion by light microscope, analyzed the inflow of Ca2+ by confocal laser scanning microscope and DNA by RT-PCR. Results: DSTMT significantly decreased the levels of triglyceride and increased the levels of HDL-cholesterol in SHR, and significantly decreased the levels of LDL-cholesterol and body weight and increased the levels of HDL-cholesterol in ICR. DSSMS significantly decreased body weight, total cholesterol levels, LDL-cholesterol, LDH and cardiac risk factor (CRE) in SHR and significantly decreased the levels of total cholesterol, triglyceride, LDL-cholesterol, LDH and CRF in ICR. DSTMT had an effect on protecting cells from damage by inhibiting production of p53 mRNA, and in DSSMS, by inhibiting production of p53 mRNA and p21 mRNA after hypoxia. DSTMT effectively blocked off Ca2+ at low density, but DSSMS effectively blocked off Ca2+ at high density. Both DSTMT and DSSMS had an effect on inhibiting lipid metabolism by blocking off production of apo B mRNA. Conclusions: These results suggest that DSTMT and DSSMS might be usefully applied for treatment of hyperlipidemia and suppression of brain damage.

• Journal of Ginseng Research
• /
• 제40권2호
• /
• pp.135-140
• /
• 2016

Background: Nephrotoxicity is a common side effect of medications. Panax ginseng is one of the best-known herbal medicines, and its individual constituents enhance renal function. Identification of its efficacy and mechanisms of action against drug-induced nephrotoxicity, as well as the specific constituents mediating this effect, have recently emerged as an interesting research area focusing on the kidney protective efficacy of P. ginseng. Methods: The present study investigated the kidney protective effect of fermented black ginseng (FBG) and its active component ginsenoside 20(S)-Rg3 against cisplatin (chemotherapy drug)-induced damage in pig kidney (LLC-PK1) cells. It focused on assessing the role of mitogen-activated protein kinases as important mechanistic elements in kidney protection. Results: The reduced cell viability induced by cisplatin was significantly recovered with FBG extract and ginsenoside 20(S)-Rg3 dose-dependently. The cisplatin-induced elevated protein levels of phosphorylated c-Jun N-terminal kinase (JNK), p53, and cleaved caspase-3 were decreased after cotreatment with FBG extract or ginsenoside 20(S)-Rg3. The elevated percentage of apoptotic LLC-PK1 cells induced by cisplatin treatment was significantly abrogated by cotreatment with FBG and the ginsenoside 20(S)-Rg3. Conclusion: FBG and its major ginsenoside 20(S)-Rg3, ameliorated cisplatin-induced nephrotoxicity in LLC-PK1 cells by blocking the JNKep53ecaspase-3 signaling cascade.

• 한국응용과학기술학회지
• /
• 제37권5호
• /
• pp.1138-1150
• /
• 2020

본 연구는 다양한 식물 추출물들이 가지고 있는 항산화 능력과 자외선 차단 능력을 동시에 조사하여 추후, 항산화 효과가 있는 자외선 차단제를 개발하고자 실험을 실시하였다. 먼저 33종의 식물 추출물들의 자외선 차단 능력을 조사하기 위하여 자외선 파장 280~400nm 사이의 흡광도 스펙트럼을 조사하고, 이로부터 우수한 자외선 차단능력을 갖는 것으로 보이는 식물 추출물로 황금, 홉, 녹차, 감초, 방풍, 칡, 그라비올라, 밀싹, 상백피, 가시박, 옻, 등 11종을 선별하였다. 선별된 식물추출물의 총 폴리페놀 함량, 총 플라보노이드 함량, DPPH radical 소거 활성을 측정하여 항산화 활성 정도를 살펴보고, 이로부터 다시 자외선 차단 능력과 항산화 활성이 동시에 우수한 식물 추출물로 황금, 홉, 감초추출물 3종을 선정하였다. 선정된 황금, 홉, 감초추출물을 1:1:1로 혼합하여 겔 형태의 크림을 제조하고, 이 크림이 가지는 자외선 차단 효과를 배양된 세포에 자외선을 조사하였을 때 보여주는 세포 손상 방어 효과를 측정하는 방법으로 결정하였다. 연구 결과, 선정된 식물 추출물의 혼합물은 자외선 흡수 능력에서 상호 보완적이며, 세포 손상 방어 효과도 증가하였음을 확인하였다. 이와 같은 결과를 통하여 다양한 식물 추출물들이 가지고 있는 항산화 능력과 자외선 차단 능력을 동시에 결정할 경우 항산화 효과가 있는 자외선 차단제 개발이 가능함을 확인하였다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제12권3호
• /
• pp.101-109
• /
• 2008

The aim of the present study was to examine the effects of ketamine, a dissociative anesthetics, on secretion of catecholamines (CA) secretion evoked by cholinergic stimulation from the perfused model of the isolated rat adrenal gland, and to establish its mechanism of action, and to compare ketamine effect with that of thiopental sodium, which is one of intravenous barbiturate anesthetics. Ketamine ($30{\sim}300{\mu}M$), perfused into an adrenal vein for 60 min, dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic NN receptor agonist, $100{\mu}M$) and McN-A-343 (a selective muscarinic M1 receptor agonist, $100{\mu}M$). Also, in the presence of ketamine ($100{\mu}M$), the CA secretory responses evoked by veratridine (a voltage-dependent $Na^+$ channel activator, $100{\mu}M$), Bay-K-8644 (an L-type dihydropyridine $Ca^{2+}$ channel activator, $10{\mu}M$), and cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, $10{\mu}M$) were significantly reduced, respectively. Interestingly, thiopental sodium ($100{\mu}M$) also caused the inhibitory effects on the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, veratridine, Bay-K-8644, and cyclopiazonic acid. Collectively, these experimental results demonstrate that ketamine inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization from the isolated perfused rat adrenal gland. It seems likely that the inhibitory effect of ketamine is mediated by blocking the influx of both $Ca^{2+}$ and $Na^+$ through voltage-dependent $Ca^{2+}$ and $Na^+$ channels into the rat adrenal medullary chromaffin cells as well as by inhibiting $Ca^{2+}$ release from the cytoplasmic calcium store, which are relevant to the blockade of cholinergic receptors. It is also thought that, on the basis of concentrations, ketamine causes similar inhibitory effect with thiopental in the CA secretion from the perfused rat adrenal medulla.

• 사상체질의학회지
• /
• 제15권1호
• /
• pp.72-89
• /
• 2003

To elucidate the neuroprotective effect of Yeoldahanso-tang(YHT) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT(SODIUM3,3'-{I-[(PHENYLAMINO) CARBONYL]-3,4-TETRAZOLIUM}- BIS (4-METHOXY-6-NITRO) BENZENE SULFONIC ACID HYDRATE), NR(Neutral red), MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and SRB(Sulforhodamin B) asssay. The activity of catalase and SOD(Superoxide dismutase) was measured by spectrophometry, and $TNF-{\alpha}$(Tumor cell necrosis $fector-{\alpha}$) and PKC(Protein kinase C) activity was measured after exposure to hypoxia and treatment of YHTWE. Also the neuroprotective effect of YHTWE was researched for the elucidatioion of neuroprotective mechanism. The results were as follows; 1. Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO2 for $2{\sim}26$ minutes in these cultures and YHTWE inhibited the decrease of cell viability. 2. H2O2 treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 ${\mu}M$ for 6 hours, but YHTWE inhibited the decrease of cell viability. 3. Hypoxia decreased catalase and SOD activity, and also $TNF-{\alpha}$ and PKC activity in these cultured cerebral neurons, but YHTWE inhibited the decrease of the catalase and SOD activity in these cultures. 4. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c forom mitochondria. YHTWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxicity on cultured mouse cerebral neurons, and the YHTWE has the neuroprotective effect in blocking the neurotoxicity induced by hypoxia in cultured mouse cerebral neurons.

• Journal of Ginseng Research
• /
• 제42권3호
• /
• pp.389-399
• /
• 2018

Background: The antioxidant effects of Panax ginseng have been reported in several articles; however, little is known about the antimelanogenesis effect, skin-protective effect, and cellular mechanism of Panax ginseng, especially of P. ginseng calyx. To understand how an ethanol extract of P. ginseng berry calyx (Pg-C-EE) exerts skin-protective effects, we studied its activities in activated melanocytes and reactive oxygen species (ROS)-induced keratinocytes. Methods: To confirm the antimelanogenesis effect of Pg-C-EE, we analyzed melanin synthesis and secretion and messenger RNA and protein expression levels of related genes. Ultraviolet B (UVB) and hydrogen peroxide ($H_2O_2$) were used to induce cell damage by ROS generation. To examine whether this damage is inhibited by Pg-C-EE, we performed cell viability assays and gene expression and transcriptional activation analyses. Results: Pg-C-EE inhibited melanin synthesis and secretion by blocking activator protein 1 regulatory enzymes such as p38, extracellular signal-regulated kinases (ERKs), and cyclic adenosine mono-phosphate response element-binding protein. Pg-C-EE also suppressed ROS generation induced by $H_2O_2$ and UVB. Treatment with Pg-C-EE decreased the expression of matrix metalloproteinases, mitogen-activated protein kinases, and hyaluronidases and increased the cell survival rate. Conclusion: These results suggest that Pg-C-EE may have antimelanogenesis properties and skin-protective properties through regulation of activator protein 1 and cyclic adenosine monophosphate response element-binding protein signaling. Pg-C-EE may be used as a skin-improving agent, with moisture retention and whitening effects.