• 대한한의학회지
• /
• 제28권3호통권71호
• /
• pp.216-231
• /
• 2007

Objectives : Chengsimyeunja-eum and Sunghyangjungi-san are prescriptions used for cerebral infarction clinically; it is known that these formulas reduce ischemic damage. According to previous research data, controlling certain types of glucose is considered to decrease the risk of cerebral infarction. Based on this fact, we investigated the effects of Chengsimyeunja-eum and Sunghyangjungi-san extracts on reperfusion following ischemic damage to diabetic rats, the change of c-FOS and Bax positive neurons in the hippocampus and cerebral cortex and protein through immunohistochemical methods, changes of serum glucose level, serum triglyceride level, and hepatic glucokinase activity. Methods : We induced ischemic damaged in diabetic rats, and the rats were administered Chengsimyeunja-eum and Sunghyangjungi-san extracts. Results : Chengsimyeunja-eum demonstrated significant decrease of c-Fos positive neurons in both hippocampus and cerebral cortex as well as a significant decrease of Bax positive neurons in hippocampus after ischemic damage on diabetic rats and decrease of serum glucose level after ischemic damage on diabetic rats. Sunghyangjungi-san demonstrated significant decreases of c-Fos and Bax positive neurons in both hippocampus and cerebral cortex after ischemic damage on diabetic rats. Conclusions : Chengsimyeunja-eum, effect on glucose level control, has a remarkable effect of protection of neurons not effective on glucose level. Sunghyangjungi-san showed neuroprotective effect through preventing neuronal cell death.

• 대한한의학방제학회지
• /
• 제8권1호
• /
• pp.147-167
• /
• 2000

Reactive oxygen species (ROS) play an important role in the pathogenesis of a variety of life threatening conditions such as atherosclerosis, myocardial infarction and cerebral stroke. In this study, the effect of Sunghyangchungisan (SHCS) as a cytoproctant against ROS-induced cell injury was studied by investigating its effect on $H_{2}O_2-induced$ cell injury in cultured endothelial cells derived from the human umbilical vein. SHCS effectively proteced the cells against $H_{2}O_2-induced$ injury determined by trypan blue exclusion ability and lactate dehydrogenase (LDH) release. The effect of SHCS was concentration-dependent and the concentrations to inhibit by 50% the cell death and LDH release were $0.9{\pm}0.1$ and $1.2{\pm}0.1\;mg/ml$, respectively. In addition, SHCS effectively protected the cells against t-butylhydroperoside- and menadione-Induced injury as well. SHCS inhibited lipid peroxidation determined by malondialdehyde production. SHCS exerted as an effective scavenger of ROS produced by exposing the cells to $H_{2}O_2$ The activities of the intracellular ROS scavenging enzymes such as superoxide dismutase, catalase and glutathione peroxidase were not Influenced by SHCS.These results indicate that SHCS might exert as an effective cytoprotectant against ROS-induced cell injury. Further intensive studies would provide us insights into mechanisms of the pharmacological actions of SHCS.

• 대한한의학회지
• /
• 제21권4호
• /
• pp.193-203
• /
• 2000

Objectives : Hindered barrier function of vascular endothelium has been implicated in the initiation and progression of degenerative vascular diseases such as atherosclerosis. In this study, the effect of Sunghyangchungisan(SHCS) as a protectant against oxidant-induced destruction of endothelial barrier function was assessed. Methods : Toward this end, endothelial cells derived from the human umbilical vein were cultured as monolayers on permeable membrane filters. Endothelial permeability was monitored by measuring transendothelial electrical resistance and movement of low density lipoprotein (LDL) across the endothelial monolayer. Results : Along with increased movement of LDL, $H_2O_2$-induced increase in endothelial permeability was paralleled by a decrease in transendotheliaI electrical resistance. The effect of $H_2O_2$ was mimicked by phorbol 12-myristate 13-acetate (PMA), a potent activator of proteinkinase C. Calphostin-C, a protein kinase C inhibitor, effectively blocked the increase in endothelial permeability induced by $H_2O_2$ or PMA, indicating that activation of protein kinase C is associated with the $H_2O_2-induced$ permeability change. SHCS effectively protected the endothelial monolayer against $H_2O_2-induced$ increase in permeability, whereas, it did not affect PMA-induced change. Forskolin, a potent activator of adenylyl cyclase, antagonized $H_2O_2$ to increase endothelial permeability. In addition, in ${H_2O_2}-treated$ cens, intracenular cAMP concentration was significantly decreased, indicating that impaired cAMP production as well as activation of proteinkinase C is a mechanism underlying ${H_2O_2}>-induced$$H_2O_2$ with regard to its effect on intracellular cAMP content. However, SHCS itself did not affect resting cAMP concentration in endothelial cells. Conclusions : These results suggest that SHCS might operate as an effective protectant against oxidant-induced destruction of endothelial barrier function. The mechanism does not appear to involve direct interaction with protein kinase C- or cAMP-associated signaling mechanism.

• 대한한의학회지
• /
• 제20권3호
• /
• pp.77-86
• /
• 1999

This study was undertaken to evaluate the effect of Sunghyangchungi-san (SHCS) on the oxidant-induced contraction and lipid peroxidation in rabbit carotid artery. Vascular rings isolated from rabbit carotid artery were exposed to t-butyl hydroperoxide (t-BHP), an extrinsic oxidant, and the effect of SHCS on the changes of vascular tension and lipid peroxidation induced by t-BHP was determined. t- BHP induced a slowly developing and sustained contraction of the arterial rings. SHCS effectively relaxed the arterial rings that were pre-contracted by t-BHP. The responses to SHCS were partially dose-dependent at concentrations lower than 0.5 mg/ml. When SHCS was applied prior to the exposure to t-BHP, it inhibited the t-BHP-induced contraction as well. t- BHP increased lipid peroxidation in a dose-dependent manner. SHCS as well as well-known anti-oxidants GSH and DPPD reduced significantly lipid peroxidation induced by t-BHP. SHCS partially blocked the increase in $^{45}Ca$ uptake induced by t-BHP. In contrast to SHCS, anti-oxidants GSH and DPPD failed to inhibit significantly the t- BHP-induced contraction or $^{45}Ca$ uptake. From the above results, it is suggested that SHCS relaxed t-BHP-induced contraction of rabbit carotid artery independently of its anti-oxidant action, and inhibition of $Ca^{2+}$ influx may contribute to the underlying mechanism.

• 대한한의학회지
• /
• 제19권2호
• /
• pp.228-243
• /
• 1998

This study was undertaken to evaluate the effect of Sunghyangchungisan (SHCS) on the regulation of vascular tone. Vascular rings isolated from rabbit carotid artery were myographed isometrically in isolated organ baths and the effect of SHCS on contractile activities were determined. SHCS relaxed the arterial rings which were pre-contracted by phenylephrine(PE). The responses to SHCS were partially dose-dependent at concentrations lower than 0.5 mg/ml. When SHCS was applied prior to the exposure to PE, it inhibited the PE-induced contraction by a similar magnitude which was comparable to the relaxation of pre-contracted arterial rings. Washout of SHCS after observing its relaxant effect resulted in a full recovery of PE-induced contractions, indicating that the action mechanism is reversible. The observation that SHCS did not change the $ED_{50}$ of PE on its dose-response curve ruled out the possible interaction of SHCS and ${\alpha}-receptor$. The relaxant effect of SHCS was not affected by removal of endothelium, and pretreatment of the arterial rings with methylene blue or nitro-L-arginine. This results suggest that the action of SHCS is not mediated by endothelium nor soluble guanylate cyclase. SHCS relaxed high $K^{+}-induced$ contractions as well, whereas it failed to relax phorbol ester-induced contractions. When contraction was induced by additive application of $Ca^{2+}$ in arterial rings which were pre-depolarized by high $K^+$ in a $Ca^{2+}-free$ solution, the relaxant effect of SHCS was attenuated by increasing the $Ca^{2+}$ concentration. SHCS, when applied to the arterial rings pre-contracted by PE and then relaxed by nifedipine, a $Ca^{2+}$ channel blocker, did not show additive relaxation. From above results, it is suggested that SHCS relax PE-induced contraction of rabbit carotid artery in an endothelium-independent manner, and inhibition of $Ca^{2+}$ influx may contribute to the underling mechanism.

• 한방재활의학과학회지
• /
• 제18권2호
• /
• pp.33-43
• /
• 2008

Objectives : Sunghyangjungki-san(Xingxiangzhengqi-san) is a herb decoction prescribed frequently for stroke patients. The present study investigated neuroprotective effects of Sunghyangjungki-san(Xingxiangzhengqi-san) against the ischemic damage of the rat brain. Neuronal cell death under the cerebral ischemia is distinguished with the delayed cell death through apoptosis. Consequently, the effects of Sunghyangjungki-san(Xingxiangzhengqi-san) was evaluated with Bax and Bcl-2 expressions as apoptosis related factors in the brain tissues. Methods : The ischemic damage was induced by the middle cerebral artery occlusion(MCAO) method in Sprague-Dawley rats. Water extract of Sunghyangjungki-san(Xingxiangzhengqi-san) was treated for 5 days after the MCAO. Neurological scores and infarct size with TTC were measured. Bax and Bcl-2 expressions in the brain tissues were observed with immunohistochemistry. Results : Sunghyangjungki-san(Xingxiangzhengqi-san) treatment improved neurological score significantly at 5 days after the MCAO. Sunghyangjungki-san(Xingxiangzhengqi-san) treatment decreased infarct size by the MCAO, but it was not significant statistically. Sunghyangjungki-san(Xingxiangzhengqi-san) treatment attenuated Bax positive neurons significantly in the cerebral penumbra and the caudate putamen. Bcl-2 positive neurons were increased, but not significant. Sunghyangjungki-san(Xingxiangzhengqi-san) treatment increased Bcl-2/Bax expression ratios significantly in the cerebral penumbra and the caudate putamen. Conclusions : These results suggest that Sunghyangjungki-san(Xingxiangzhengqi-san) has a neuroprotective effect on the stroke with modulation of apoptosis related factors.

• 대한본초학회지
• /
• 제32권4호
• /
• pp.61-68
• /
• 2017

Objectives : Jema-sunghyangjungkisan (JSGS, Jima Xingxiang Zhengqi san) and yeoldahanso-tang (YDHST, Reduo hanshao decoction) are traditional herbal formulas which commonly used to prevent and treat stroke in traditional korean medicine. However, JSGS and YDHST extracts have not been previously reported to have anti-inflammatory effects. Therefore, We measured the anti-inflammatory effects of JSGS and YDHST extracts on lipopolysaccharide (LPS)-stimulated murine macrophage cell line, RAW 264.7 cells. Methods : To investigate the anti-inflammatory activities of JSGS and YDHST extracts, tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin (IL)-6, nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) were examined in RAW 264.7 cells with LPS of $1{\mu}g/m{\ell}$. Results : JSGS and YDHST extracts did not have any cytotoxicity in RAW 264.7 cells. $TNF-{\alpha}$ concentration decreased 49.67% at $500{\mu}g/m{\ell}$ by JSGS but, YDHST has no statistically significant effect at all concentration. IL-6 accumulation on JSGS and YDHST extracts in LPS-stimulated RAW 264.7 cells reduced 22.03% and 41.44% at $500{\mu}g/m{\ell}$ respectively. In addition, JSGS has no inhibitory effects on NO accumulation and YDHST reduced 10.08% at $500{\mu}g/m{\ell}$. Moreover, JSGS and YDHST treatment does-dependently reduced the $PGE_2$ production. In particular, YDHST ($500{\mu}g/m{\ell}$) extract was more effective compared with $10ng/m{\ell}$ of indomethacin which is the $PGE_2$ positive control. Conclusions : Our results suggest that treatment of JSGS and YDHST extracts decreased the LPS-stimulated inflammation. Therefore, in the present study, we demonstrated that JSGS and YDHS may be used as a potential anti-inflammatory therapeutic agent.

• 혜화의학회지
• /
• 제9권1호
• /
• pp.387-397
• /
• 2000

연구배경(硏究背景): He-Ne laser 정맥혈관내(靜脈血管內) 조사(照射) (Intravascular Laser Irradiation of Blood : ILIB)가 말초(末梢) 및 뇌혈관순환장애(腦血管循環障碍), 뇌기능장애(腦機能障碍), 동맥경화(動脈硬化) 등의 예방(豫防)과 치료(治療) 목적(目的)으로 사용(使用)되고 있으나 이에 대한 한의학(韓醫學)에서의 연구(硏究)는 찾아보기 힘들다. 이에 저자(著者)는 발병(發病) 48시간(時間) 이내(以內)에 내원(來院)하여 뇌전산화단층촬영(腦電算化斷層撮影)으로 진단(診斷)된 초기(初期) 뇌경색(腦梗塞) 환자(患者)에서 ILIB의 효과(效果)를 평가(評價)하고자 본(本) 연구(硏究)를 시행(施行)하였다. 아울러 흰쥐의 국소(局所) 뇌허혈(腦虛血)에 미치는 영향(影響)을 측정(測定)하였다. 방법(方法) : 대상(對象) 환자(患者) 40명(名)을 UC-SHJGS(우황청심환(牛黃淸心丸)-성향정기산(星香正氣散))만을 투여(投與)한 대조군(對照群)과 UC-SHJGS 투여(投與)와 ILIB를 병용(倂用)한 치료군(治療群)으로 나누어 시행(施行)하였다. 대상환자(對象患者)는 모두 변증(辨證)과 무관(無關)하게 UC, SHJGS만을 투여(投與)하고 침치료(鍼治療)는 중풍칠처혈(中風七處穴)로 한정(限定)하였으며 5일간(日間)의 치료기간(治療期間) 동안 치료군(治療群)에서는 출력(出力) 1.8-2.5mW의 He-Ne laser를 1일(日) 1회(回) 50분(分) 동안 조사(照射)하였다. 동물실험(動物實驗)은 흰쥐를 대상(對象)으로 중대뇌동맥(中大腦動脈)을 결찰(結紮)하여 국소(局所) 뇌허혈(腦虛血)을 유발(誘發)하고 대조군(對照群)과 ILIB를 실시(實施)한 실험군(實驗群)으로 나누어 그 허혈면적(虛血面積)과 부종율(浮腫率)을 측정(測定)하였다. 결과(結果) : 1. 증상호전지수(症狀好轉指數)는 대조군(對照群)과 치료군(治療群) 사이에 유의(有意)한 차이(差異)가 없었다. 2. 치료전후(治療前後) 측정(測定)한 내경동맥(內頸動脈) siphon부(部)의 혈관반응성(血管反應性)은 대조군(對照群)과 치료군(治療群)에서 모두 유의성(有意性)있는 변화(變化)가 없었다. 3. 치료전후(治療前後) 측정(測定)한 요골동맥(橈骨動脈)의 혈관반응성(血管反應性)은 대조군(對照群)과 치료군(治療群)에서 모두 유의성(有意性) 있는 변화(變化)가 없었다. 4. 치료전후(治療前後) 측정(測定)한 PT, a-PTT은 대조군(對照群)과 치료군(治療群)에서 모두 유의성(有意性)있는 변화(變化)가 없었고, fibrinogen은 치료군(治療群)에서 치료전(治療前)보다 유의성(有意性) 있게 증가(增加)하였으나 평균값이 정상(正常) 범위(範圍)에서 벗어나지 않았다. 5. 국소(局所) 뇌허혈(腦虛血) 동물(動物) 실험(實驗)에서는 실험군(實驗群)에서 신경학적(神經學的) 결손(缺損), 허혈(虛血) 면적율(面積率), 부종율(浮腫率)이 유의성(有意性)있게 감소(減少)하였다 결론(結論) : 이상(以上)의 연구(硏究) 결과(結果) 뇌경한(腦硬寒)의 초기(初期) 치료(治療)에서 기존(旣存)의 한의학(韓醫學) 치료(治療)에 ILIB를 추가(追加)하는 것이 치료(治療) 효과(效果)를 증가(增加)시킨다는 증거(證據)는 없었으며 동물(動物) 실험(實驗)에서는 뇌경색(腦梗塞)의 치료(治療)에 응용(應用)할 수 있는 가능성(可能性)을 보여주고 있으나 그 효과(效果)와 적응증(適應症)을 구체적(具體的)으로 증명(證明)하기 위한 체계적(體系的)이고 다양(多樣)한 임상실험(臨床實驗)이 지적(持績)되어야할 것으로 생각된다.