Jae Kuk Yoo

Anticomplementary activity of triterpenoids from the whole plant of Aceriphyllum rossii against the classical pathway.

To provide a better understanding of the anti-complement activity of triterpenoids, seven unusual pentacyclic triterpenoids bearing a carboxyl group at C-27 were evaluated for their anticomplement activities against the classical pathway of the complement system. The triterpenoids were isolated from the whole plant of Aceriphyllum rossii of the family Saxifragaceae and were determined to be 3alpha,23-isopropylidenedioxyolean-12-en-27-oic acid (1), 3-oxoolean-12-en-27-oic acid (2), 3alpha-hydroxyolean-12-en-27-oic acid (3), beta-peltoboykinolic acid (4), 3alpha,23-diacetoxyolean-12-en-27-oic acid (5), 23-hydroxy-3-oxoolean-12-en-27-oic acid (6) and aceriphyllic acid A ( 7). Among them, compounds 2, 3, and 5 showed significant anticomplement activity on the classical pathway with IC (50) values of 71.4, 98.5, and 180.7 microM, respectively, whereas compounds 1, 4, 6, and 7 were inactive. Our findings suggest that both the ketone at C-3 and the methyl at C-23 in the oleanane triterpenoids with a carboxyl group at C-27 are important for the anticomplement activity against the classical pathway.

Neuroprotection of Ilex latifolia and caffeoylquinic acid derivatives against excitotoxic and hypoxic damage of cultured rat cortical neurons.

Ilex latifolia (Aquifoliaceae), one of the primary components of “Ku-ding-cha”, has been used in Chinese folk medicine to treat headaches and various inflammatory diseases. A previous study demonstrated that the ethanol extract of I. latifolia could protect against ischemic apoptotic brain damage in rats. The present study investigated the protective activity of I. latifolia against glutamate-induced neurotoxicity using cultured rat cortical neurons in order to explain a possible mechanism related to its inhibitory effect on ischemic brain damage and identified potentially active compounds from it. Exposure of cultured cortical neurons to 500 μM glutamate for 12 h triggered neuronal cell death. I. latifolia (10–100 μg/mL) inhibited glutamate-induced neuronal death, elevation of intracellular calcium ([Ca2+]i), generation of reactive oxygen species (ROS), the increase of a pro-apoptotic protein, BAX, and the decrease of an anti-apoptotic protein, BcL-2. Hypoxia-induced neuronal cell death was also inhibited by I. latifolia. 3,4-Dicaffeoylquinic acid (diCQA), 3,5-diCQA, and 3,5-diCQA methyl ester isolated from I. latifolia also inhibited the glutamate-induced increase in [Ca2+]i, generation of ROS, the change of apoptosis-related proteins, and neuronal cell death; and hypoxia-induced neuronal cell death. These results suggest that I. latifolia and its active compounds prevented glutamate-induced neuronal cell damage by inhibiting increase of [Ca2+]i, generation of ROS, and resultantly apoptotic pathway. In addition, the neuroprotective effects of I. latifolia on ischemia-induced brain damage might be associated with the anti-excitatory and anti-oxidative actions and could be attributable to these active compounds, CQAs.

Protective Effect of an Ethanol Extract Mixture of Curcuma longae Radix, Phellinus linteus, and Scutellariae Radix on Oxidative Neuronal Damage

Previous work demonstrated that an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix markedly inhibits (25-35)-induced neurotoxicity. The present study was performed to further verify the neuroprotective effect of HS0608 on oxidative and ischemic cerebral injury using cultured rat cortical neurons and rats. Exposure of cultured cortical neurons to hydrogen peroxide () induced neuronal apoptotic death. At , HS0608 inhibited neuronal death, elevation of intracellular calcium concentration (), and generation of reactive oxygen species (ROS) induced by in primary cultures of rat cortical neurons. In vivo, HS0608 prevented cerebral ischemic injury induced by 2-h middle cerebral artery occlusion (MCAO) and 24-h reperfusion. The ischemic infarct and edema were significantly reduced in rats that received HS0608 (200 mg/kg). These results suggest that the anti-oxidative properties of HS0608 may be responsible for its neuroprotective effect against focal cerebral ischemic injury and that HS0608 may have a therapeutic role in neurodegenerative diseases such as stroke.

Inhibition of human neutrophil elastase by ergosterol derivatives from the mycelium of Phellinus linteus.

Inhibition of human neutrophil elastase by ergosterol derivatives from the mycelium of Phellinus linteus