• The Journal of Korean Medicine
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• v.18 no.1
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• pp.480-498
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• 1997

This study was to investigate the protective and anticirrhotic effects of Mockhyangjokisan and Haewooljoweetang on the liver cirrhosis or fibrosis induced by prolonged bile duct ligation; a new experimental model for cirrhosis and the intraperitoneal injection of dimethylnitrosamine in the rat. The development of fibrosis or cirrhosis and its inhibition by the two prescriptions were examined by the chemical analysis of AST, ALT, and hydroxyproline. The results obtained were as follows. 1. The increase of serum asparate aminotransferase induced by bile duct ligation was inhibited by the administration of Mockhyangjokisan and Haewooljoweetang extract. 2. The increase of serum alanine aminotransferase induced by bile duct ligation was inhibited by the administration of Mockhyangjokisan and Haewooljoweetang extract. 3. The increased level of serum AST and AL T induced by the intraperitoneal injection of dimethylnitrosamine was inhibited by the administration of Mockhyangjokisan and Haewooljoweetang extract. 4. The increasing level of hydroxyproline volume in the damaged liver tissues in the rat was decreased by the oral administration of Mockhyangjokisan and Haewooljoweetang extract. But there were no significant differences in the inhibition rate between the two experimental groups.

• Herbal Formula Science
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• v.4 no.1
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• pp.99-112
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• 1996

• The Journal of Internal Korean Medicine
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• v.17 no.1
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• pp.290-299
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• 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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1538-1542
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• 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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.5
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• pp.807-815
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• 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.