Ik‐Hyun Cho
경희대학교 화학과 · 생화학·유전·분자생물학
이 교수의 연구실은 주로 한방약재 및 천연물 유래 성분의 생리적·약리적 기능을 규명하고, 특히 다낭성 난소증후군(PCOS), 우울증, 헌팅턴병, 파킨슨병 등 신경질환 및 내분비계 질환에 대한 신약 개발을 목표로 하고 있습니다. 주로 한국인삼(Panax ginseng)과 그 유래 성분인 지노티닌, 그리고 전통 한약처방(Kyung-Ok-Ko)의 신경보호 및 항염증 작용을 중심으로 기전 연구를 수행하고 있으며, 특히 산화 스트레스와 신경염증을 조절하는 분자 기전에 초점을 맞추고 있습니다. 또한, 동물 모델 기반의 약리적 효과 평가와 함께 임상 연계 가능성을 고려한 후속 연구를 지속적으로 진행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Complete animal models investigating the pathogenesis and treatment of polycystic ovarian syndrome (PCOS) are not completely established. Although dehydroepiandrosterone (DHEA)-induced pre-pubertal rat model for PCOS has been widely used, the model exhibits weaknesses such as decreased ovary weight. Here, we report an innovative DHEA-induced PCOS model that addresses limitations of the pre-pubertal model. The 21-day-old (pre-pubertal) and 42-day-old (post-pubertal) female rats were subcutaneousl
Kyung-Ok-Ko (KOK), a traditional herbal prescription composed of Rehmannia glutinosa Liboschitz var. purpurae, Lycium chinense, Aquillaria agallocha, Poria cocos, Panax ginseng, and honey, has been widely used in traditional Oriental medicine as a vitalizing medicine or as the prescription for patients with age-associated disorders such as amnesia and stroke. However, the potential protective value of KOK for the treatment of polycystic ovarian syndrome (PCOS) is largely unknown. We investigated
Panax ginseng Meyer (P. ginseng; Korean ginseng) is well known for its medicinal properties. It can alleviate pathological symptoms, promote health, and prevent potential diseases via its anti-inflammatory, antioxidant, homeostatic, and other positive effects on biological metabolism. Although many studies have determined effects of P. ginseng on various diseases, such as cardiovascular, neurological, and immunological diseases, little is known about the effect of P. ginseng on autoimmune diseas
Taken together, our findings suggest that PGE exerts antidepressant-like effect of CRS-induced depression by antineuroinflammatory and antioxidant (nuclear factor erythroid 2 related factor 2/heme oxygenase-1 activation) activities by inhibiting the hypothalamo-pituitary-adrenal axis mechanism. Further studies are needed to evaluate the potential of components of <i>P. ginseng</i> as an alternative treatment of depression, including clinical trial evaluation.
Korean red ginseng (KRG) possesses neuroprotective activity. However, the potential neuroprotective value of KRG for the striatal toxicity is largely unknown. We investigated whether KRG extract (KRGE) could have a neuroprotective effect in a 3-nitropropionic acid- (3-NP) induced (i.p.) Huntington's disease (HD) model. KRGE (50, 100, and 250 mg/kg/day, p.o.) was administrated 10 days before 3-NP injection (pre-administration), from the same time with 3-NP injection (co-administration), or from t
Gintonin is a ginseng-derived lysophosphatidic acid receptor (LPAR) ligand. Although previous <i>in vitro</i> and <i>in vivo</i> studies demonstrated the therapeutic role of gintonin against Alzheimer's disease, the neuroprotective effects of gintonin in Parkinson's disease (PD) are still unknown. We investigated whether gintonin (50 and 100 mg/kg/day, p.o., daily for 12 days) had neuroprotective activities against neurotoxicity in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mo
Herbal medicines are thought to be promising resources in the development of effective therapeutic agents for PCOS. Further studies that include methodological quality assessment and quantitative synthesis of outcomes are recommended.
These results provide that KRGE could prevent DHEA-induced PCOS via antiinflammatory and antioxidant activities. Thus, KRGE may be used in preventive and therapeutic strategies for PCOS-like symptoms.
Toll-like receptor 2 (TLR2) was recently shown to contribute to secondary brain damage after intracerebral hemorrhage (ICH), although the molecular mechanisms of this contribution are elusive. In this study, we tested the hypothesis that hemin functions as a TLR2 endogenous agonist, causing proinflammatory astrocyte activation and secondary brain damage after ICH. Hemin administration to the mouse brain striatum induced ICH injury and neurological deficits, however, the brain injury volume and n