• 대한한의학회지
• /
• 제18권1호
• /
• pp.480-498
• /
• 1997

간경변(肝硬變)은 간장손상(肝腸損傷)을 주로 나타내는 만성(慢性) 전신성(全身性) 질환(疾患)이다. 이것은 각종 병인(病因)이 지속적(持續的) 또는 반복적(反復的)으로 간조직(肝組織)에 작용하여 간세포(肝細胞)의 변성(變成) 괴사(壞死) 섬유성(纖維性) 조직(組織) 증식(增殖) 등의 병리변화(病理變化)를 일으켜 결국 간조직(肝組織)의 정상구조(正常構造)가 변하여 간(肝)의 형태이상(形態異常)과 경화(硬化)를 유발하는 것이다. 한의학(韓醫學)에서는 간경변(肝硬變)의 단계에 따라 표현이 다른데 협통(脇痛), 복창(腹脹), 황달(黃疸), 적취(積聚), 창(脹), 단복창(單腹脹), 수(水), 석수(石水), 간수(肝水)의 범주(範疇)에 해당된다. 울증(鬱症)은 정지부서(情志不舒), 기기울결(氣機鬱結)로 울체(鬱滯)하고 발월(發越)하지 못하여 발생하는 병증(病症)으로, 기울(氣鬱)은 기체혈어성(氣滯血瘀性) 병변(病變)인 적취(積聚)의 전단계(前段階)로 설명되고, 간경변(肝硬變)의 초기상태(初期狀態)에서 나타나는 증상(症狀)들과 유사하다고 볼 수 있으므로, 본(本) 연구(硏究)에 사용된 목향조기산(木香調氣散)과 해울조위탕(解鬱調胃湯)은 기울(氣鬱)에 적용되는 처방(處方)으로서 초기(初期) 간경변(肝硬變)의 섬유화(纖維化) 진행억제(進行抑制)에도 유효할 것으로 사료(思料)된다. 이에 본 연구에서는 담도결찰술(膽道結紮術) 및 Dimethylnitrosamine으로 만성간염(慢性肝炎) 및 간경변증(肝硬變症)을 유발한 후 목향조기산(木香調氣散)과 해울조위탕(解鬱調胃湯)을 투여한 결과 다음과 같은 결론을 얻었다. 1. 담도결찰(膽道結紮)로 인한 혈청(血淸) total bilirubin과 direct bilirubin의 상승은 목향조기산(木香調氣散)과 해울조위탕(解鬱調胃湯)의 투여로 모두 억제되는 효과를 보였으며 두 처방(處方)간의 차이는 보이지 않았다. 2. 담도결찰(膽道結紮)로 인한 혈청(血淸) AST의 상승은 목향조기산(木香調氣散)과 해울조위탕(解鬱調胃湯)을 투여한 두 실험군(實驗群) 모두에서 억제되는 양상을 보였으며, 목향조기산(木香調氣散)을 투여한 실험군(實驗群)에서 억제되는 보다 나았으나 그 차이는 크지 않았다. 3. 담도결찰(膽道結紮)로 인한 血淸 ALT의 상승은 목향조기산(木香調氣散)과 해울조위탕(解鬱調胃湯)을 투여한 두 실험군(實驗群) 모두에서 억제되는 양상을 보였으며, 목향조기산(木香調氣散)의 억제효과가 해울조위탕(解鬱調胃湯)보다는 유의성이 인정되었다.

• 대한한의학방제학회지
• /
• 제4권1호
• /
• pp.99-112
• /
• 1996

• 대한한방내과학회지
• /
• 제17권1호
• /
• pp.290-299
• /
• 1996

The purpose of this research was to investigate the effects of water extract of Mockhyangjokisan on the blood pressure in rabbits The following results have been obtained : 1. The drug significantly increased arteral blood pressure in rabbits. 2. The drug did'nt effect the increase of arteral blood pressure by pretreated atropine and propranolol in rabbits. 3. The drug inhibited the increase of arteral blood pressure by pretreated regitine in rabbits.

• 동의생리병리학회지
• /
• 제20권6호
• /
• pp.1538-1542
• /
• 2006

The study was designed to investigate the effects of MokhwyangJoki-san Extract (MJSE) on the change of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats, and further to determine the mechanism of MJSE. The results in normal rats were as follows ; MJSE significantly increased rCBF in a dose-dependent manner, and MABP did not change in a dose-dependent manner. This results were suggested that MJSE significantly increased rCBF by dilating pial arterial diameter. The MJSE-induced increase in rCBF was significantly inhibited by pretreatment with methylene blue (10 ${\mu}g/kg$, i.p.), an inhibitor of guanylate cyclase, and was not changed by indomethacin (1 ${\mu}g/kg$, i.p.), an inhibitro of cyclooxygenase. The MJSE-was not changed MABP was decreased by pretreatment with indomethacin but was not changed by methylene blue. This results were suggested that the mechanism of MJSE was mediated by guanylate cyclase.

• 동의생리병리학회지
• /
• 제25권5호
• /
• pp.807-815
• /
• 2011

This study was designed to investigate the effects of Mokhyangjoki-san extract (MJS) on the improvement in cerebral blood flow (rCBF) in cerebral ischemic rats, and further to determine cytokines production (IL-1${\beta}$, TNF-${\alpha}$, IL-10, TGF-${\beta}$) of MJS. The results in cerebral ischemic rats were as follows ; The rCBF was significantly and stably increased by MJS (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. In cytokine production in serum from femoral arterial blood 1 hr after middle cerebral arterial occlusion, MJS significantly decreased IL-1${\beta}$ and TNF-${\alpha}$ production, and increased IL-10 production compared with control group. In cytokine production in serum from femoral arterial blood 1 hr after reperfusion, MJS significantly decreased IL-1${\beta}$ and TNF-${\alpha}$ production compared with control group. IL-10 and TGF-${\beta}$1 production in MJS group were significantly increased compared with control group. These results suggested that MJS significantly and stably increased rCBF by inhibiting the production IL-1${\beta}$ and TNF-${\alpha}$, and accelerating that of IL-10 and TGF-${\beta}$. The result in nerve cells was as follows ; MJS significantly inhibited lactate dehydrogenase activity in vitro in a dose-dependent manner. This result suggested that MJS prevented the neuronal death.