Neuroprotective effects of butterbur and rough aster against kainic Acid-induced oxidative stress in mice.

The separate and combined neuroprotective effects of rough aster (Aster scaber) and butterbur (Petasite japonicus) extracts against oxidative damage in the brain of mice challenged with kainic acid were examined by comparing behavioral changes and biochemical parameters of oxidative stress. Rough aster butanol extract (400 mg/kg) and/or butterbur butanol extract (150 or 400 mg/kg) were administered to male ICR mice, 6-8 weeks old, through a gavage for 4 days consecutively, and on day 4, kainic acid (50 mg/kg) was administered intraperitoneally. Compared with the vehicle-treated control, no significant changes in body and brain weight were observed in mice administered rough aster or butterbur butanol extract. Administration of kainic acid only, causing a lethality of approximately 54%, resulted in a significant decrease of total glutathione level and increase of thiobarbituric acid-reactive substances (TBARS) value in brain tissue. The administration of butterbur or rough aster extract (400 mg/kg) decreased the lethality (50%) of kainic acid to 25%, alleviated the behavioral signs of neurotoxicity, restored the cytosolic glutathione level of brain homogenate to approximately 80% (P < .05), and reduced kainic acid-induced increases in TBARS values. In contrast to no significant neuroprotection by butterbur extract at a low dose (150 mg/kg), the combination of rough aster extract and butterbur extract reduced the lethality to 12.5%. Moreover, the combination delayed the onset time of behavioral signs by twofold, and significantly preserved the level of cytosolic glutathione peroxidase and glutathione reductase activities. However, the other biochemical parameters were not altered significantly by the combination. Thus, the combination of two vegetable extracts significantly increased the neuroprotective action against kainic acid-induced neurotoxicity. Based on these findings, the combination of butterbur extract and rough aster extract contains a functional agent or agents that protect against oxidative stress in the brain of mice.

Neuroprotective effect of rough aster butanol fraction against oxidative stress in the brain of mice challenged with kainic acid.

The neuroprotective effect of the butanol fraction from the methanol extract of Aster scaber Thunb. (rough aster butanol fraction) on oxidative damage in the brain of mice challenged with kainic acid was examined using behavioral signs and biochemical parameters of oxidative stress. The rough aster butanol fraction (0.4-1.0 g/kg) was administered to ICR male mice, 6-8 weeks, through a gavage for 4 days consecutively, and on the third day, kainic acid (50 mg/kg) was ip administered. When compared to the vehicle-treated control, no significant changes in body and brain weight were observed in mice administered the rough aster butanol fraction. Administration of kainic acid only, causing a lethality of approximately 54%, resulted in a significant decrease of total glutathione level and an increase of the thiobarbituric acid-reactive substances (TBARS) value in brain tissue. When the rough aster butanol fraction was examined for neuroprotective action, the rough aster butanol fraction (0.4 g/kg) alleviated the lethality (25%) of kainic acid and the behavioral sign of its neurotoxicity. Moreover, administration of the rough aster butanol fraction at a dose of 0.4 g/kg restored the glutathione level in the cytosolic portion of brain homogenate to approximately 80% (p < 0.05). Also, the rough aster butanol fraction (0.4 g/kg) led to a significant reduction of kainic acid-induced increase of TBARS value. In addition, the glutathione peroxidase activity was restored significantly (p < 0.05) in the cytosolic portion of brain homogenate, whereas glutathione reductase activity was not. On the basis of these results, the rough aster butanol fraction is suggested to contain a functional agent to prevent oxidative stress in the brain of mice.

Ixeris dentata extract maintains glutathione concentrations in mouse brain tissue under oxidative stress induced by kainic acid.

The neuroprotective effects of a water fraction from the methanol extract of Ixeris dentata (WFID) against oxidative stress in the brain of mice challenged with kainic acid were examined by evaluating behavioral characteristics and biochemical parameters of oxidative stress. Male ICR mice were divided into three groups: a control group that received no treatment and two groups challenged with kainic acid either with or without WFID (1.0 g/kg) for 4 consecutive days. On day 3 kainic acid (50 mg/kg) was intraperitoneally administered in the two challenged groups. When compared with the vehicle-treated control, no significant changes in body and brain weights were observed in mice administered WFID. Administration of kainic acid only caused a lethality of approximately 62.5%, and resulted in a significant decrease of total glutathione concentrations in the brain tissue. When WFID was investigated for neuroprotective action, WFID reduced the lethality (37.5%) of kainic acid, and the behavioral signs of its neurotoxicity. Moreover, the administration of WFID restored the glutathione concentrations in the cytosolic fraction of brain homogenate to control levels (P <.05). Furthermore, glutathione peroxidase activity was restored significantly (Plt;.05) in the cytosolic portion of brain homogenate, whereas glutathione reductase activity was not. These results suggest that I. dentata contains a functional agent that protects against oxidative stress in the brains of mice.