Effect of Chungpaesagan-tang on ischemic damage induced by MCAO inspontaneously hypertensive rats > Volume 08 - 2008

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Oriental Pharmacy and Experimental Medicine
Volume 08 - 2008
Date: April 01, 2008

Journal: Pages 430-439

December 2008 | Effect of Chungpaesagan-tang on ischemic damage induced by MCAO inspontaneously hypertensive rats…

Ko-Eun Kim2, Soo-Yong Kim1, Eun-Young Kim1, Bum-Hoi Kim5, Jung-Won Shin4, Hyun-Sam Lee1,Young-joo Sohn3,*, Hyuk-Sang Jung1 and Nak-Won Sohn2



​Chungpaesagan-tang (CPSGT) is most frequently used to treat ischemic brain injury in tradition Koreanmedicine. Clinically, cerebral ischemia is likely to be accompanied by preexisting or complicatingdisease. However, animal models used to examine the effects of herbal medicines on cerebral ischemiahave not given this issue sufficient consideration. The present study was undertaken to determine theeffects of CPSGT on focal cerebral ischemia in normal and SHR rats subjected to transient middlecerebral artery occlusion (MCAO). Animals were divided into four groups: Normal (Sprague-Dawley)rats subjected to MACO (the NC+MCAO group), normal rats subjected to MCAO and thenadministered CPSGT (NC + MCAO + CP), SHR rats subjected to MCAO (SHR + MCAO), and SHR ratssubjected to MCAO and then administered CPSGT (SHR + MCAO + CP). MCAO was performed usingthe intraluminal method. CPSGT was administrated orally twice (1 and 4 h) after MCAO. All animalswere sacrificed at 24 h postoperatively. Brain tissues were stained with hematoxylin & eosin, to examinethe effect of CPSGT on ischemic brain tissues. In addition, changes in TNF-α expression in ischemic areaswere examined by immunostaining. CPSGT was found to significantly reduce infarction areas in normaland SHR rats and infarction volumes in SHR rats. Similarly, CPGST markedly increased neuronnumbers and sizes in all treated groups, except cell sizes in SHRs. Furthermore, CPSGT reduced TNF-αexpression in MCAO administered SHR rats. The findings of the present study suggest that CPSGTeffectively ameliorates neuron damage caused by MACO-induced cerebral ischemia, and that it has asignificant neuroprotective effect after cerebral ischemia in SHR.

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