• 대한한방내과학회지
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• 제34권4호
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• pp.447-455
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• 2013

This clinical case reports the effect of Chilgi-tang, a kind of traditional Korean herbal medicine, on $3^{rd}$ degree AV block patients also known as complete heart block. Complete heart block caused by degeneration of electrical conduction system of heart may result in weakness, dizziness, syncope, etc. Two clinical cases reported herein are diagnosed as $3^{rd}$ degree AV block caused by psychological stress with chief complaints of syncope and dyspnea respectively. The chief complains of cases cured remarkably after Chilgi-tang medication. In one case, $3^{rd}$ degree AV block was disappeared. In conclusion, we suggest that Chilgi-tang can be a potential treatment for complete heart block due to psychological stress.

• 대한한의학회지
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• 제31권2호
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• pp.1-18
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• 2010

Objective: The water extract of Chilgi-tang (CGT) has been traditionally used in treatment of heart diseases caused by stress in Oriental Medicine. However, little is known about the mechanism by which CGT rescues neuronal cells from injury damage. Therefore, this study was designed to evaluate the protective effects of CGT on Neuro-2A cells by glucose deprivation-induced cell death. Methods: We investigated how cell death induced by glucose deprivation was associated with increased reactive oxygen species (ROS) generation. Result: The CGT treatment prior to glucose deprivation insult significantly reduced the number of cell deaths and the glucose deprivation-induced increase in ROS. Nitric oxide (NO) was also attenuated by CGT treatment. In addition, we demonstrated that the anti-cell death effect of CGT was blocked by heme oxygenase-1 (HO-1) activation. Finally, pretreatment of cells with a hemin, HO-1 inducer, reduced glucose deprivation-induced cell death. In contrast, pretreatment of cells with a ZnPP, HO-1 activity inhibitor, attenuated CGT-induced inhibition of cell death. Conclusions: These findings indicate that ROS plays an important role in glucose deprivation-induced cell death and that CGT may prevent glucose deprivation-induced cell death by inhibiting the ROS generation through HO-1 activation in Neuro-2A cells.