Neuroprotective effects of constituents of the root bark of Dictamnus dasycarpus in mouse hippocampal cells.

Glutamate-induced oxidative injury causes neuronal degeneration related to many central nervous system diseases, such as Parkinson's disease, Alzheimer's disease, epilepsy and ischemia. The bioassay-guided fractionation of the EtOH extract of the root bark of Dictamnus dasycarpus Trucz. provided one neuroprotective limonoid, obacunone, together with a degraded limonoid, fraxinellone and two alkaloids, dictamine and haplopine. At concentrations of 100-150 microM, obacunone showed the potent neuroprotective effects on glutamateinduced neurotoxicity and induced the expression of heme oxygenase (HO)-1 in the mouse hippocampal HT22 cells. In addition, we found that obacunone increased p38 MAPK phosphorylation and induced HO-1 expression via p38 MAPK pathway. These results suggest that obacunone isolated from the root bark of D. dasycarpus increases cellular resistance to glutamate-induced oxidative injury in mouse hippocampal HT22 cells, presumably through the p38 MAPK pathway-dependent HO-1 expression. These results suggest that obacunone could be the effective candidates for the treatment of ROS-related neurological diseases.

Tribuli fructus constituents protect against tacrine-induced cytotoxicity in HepG2 cells.

A new phenolic amide, tribulusimide D (4-hydroxy-N-[3-(4-hydroxy-3-methoxyphenyl)-1-oxo-2-propen-1-yl]-3-methoxybenzamide) (1), together with a known phenolic amide, terrestriamide ((E)-3-(4-hydroxy-3-methoxyphenyl)-N-[2-(4-hydroxyphenyl)-2-oxoethyl]-prop-2-enamide) (2) and a flavonol glycoside, quercetin-3-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranoside (3) were isolated from the H2O extract of Tribuli Fructus. Compounds 1 and 3 showed significant hepatoprotective activities, with EC50 values of 13.46 +/- 0.2 and 7.06 +/- 0.7 microM, respectively, against tacrine-induced cytotoxicity in HepG2 cells.

Protective effect of sauchinone by upregulating heme oxygenase-1 via the P38 MAPK and Nrf2/ARE pathways in HepG2 cells.

Sauchinone, a unique lignan isolated from the roots of Saururus chinensis (Lour.) Baill. (Saururaceae), is reported to exert potent hepatoprotective, anti-inflammatory actions and inhibitory effects on bone resorption. This study investigated the potency of sauchinone as a hepatic heme oxygenase (HO)-1 inducer and its protective effects in HepG2 cells. Treatment of the cells with sauchinone induced HO-1 expression and increased HO activity in a concentration- and time-dependent manner. This expression conferred cytoprotection against oxidative injury induced by T-butyl hydroperoxide. HO-1 expression by sauchinone also suppressed T-butyl hydroperoxide-induced reactive oxygen species generation in HepG2 cells. Moreover, sauchinone promoted the nuclear accumulation of the nuclear factor, E2-related factor 2 (Nrf2), and increased the promoter property of the antioxidant response element (ARE). Furthermore, treatment of the cells with a p38 MAPK inhibitor (SB203580) reduced sauchine-induced HO-1 expression and its protective effects. These results suggest that sauchinone increases the cellular resistance of HepG2 cells to T-butyl hydroperoxide-induced oxidative injury, presumably through the p38 MAPK pathway-Nrf2/ARE-dependent HO-1 expression.