Terminalia chebula extract protects OGD-R induced PC12 cell death and inhibits lps induced microglia activation.

Terminalia chebula, native to Southeast Asia, is a popular medicinal plant in Ayurveda. It has been previously reported to have strong antioxidant and anti-inflammatory efficacy. In this study, we aimed to investigate if fruit extract from T. chebula might protect neuronal cells against ischemia and related diseases by reduction of oxidative damage and inflammation in rat pheochromocytoma cells (PC12) using in vitro oxygen-glucose deprivation followed by reoxygenation (OGD-R) ischemia and hydrogen peroxide (H2O2) induced cell death. Cell survival was evaluated by a 2-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Free radical scavenging, lipid peroxidation and nitric oxide inhibition were measured by diphenyl-1-picrylhydrazyl (DPPH), thiobarbituric acid (TBA) and Griess reagent, respectively. We found that T. chebula extract: (1) increases the survival of cells subjected to OGD-R by 68%, and H2O2 by 91.4%; (2) scavenges the DPPH free radical by 96% and decreases malondialdehyde (MDA) levels from 237.0 ± 15.2% to 93.7 ± 2.2%; (3) reduces NO production and death rate of microglia cells stimulated by lipopolysaccharide (LPS). These results suggest that T. chebula extract has the potential as a natural herbal medicine, to protect the cells from ischemic damage and the possible mechanism might be the inhibition of oxidative and inflammatory processes.

Neuroprotective effect of HT008-1, a prescription of traditional Korean medicine, on transient focal cerebral ischemia model in rats.

HT008-1 is one of the prescriptions used in Traditional Korean Medicine for the treatment of mental and physical weakness. It is composed of Panax ginseng, Acanthopanax senticosus, Angelica sinensis and Scutellaria baicalensis, which have been reported to have various pharmacological effects on the central nervous system. The study investigated whether HT008-1 has neuroprotective effects in a focal cerebral ischemia rat model. Stroke was induced in rats by 2 h of middle cerebral artery occlusion (MCAo) followed by 22 h of reperfusion. HT008-1 (30, 100 and 300 mg/kg) and the component herbs (300 mg/kg) were administered orally twice at 0 and 2 h after ischemia. Oral administration of 300 mg/kg HT008-1 reduced brain infarction by 45.7%, prolonged the latency time by 24.8% in the rotarod test, and enhanced the score by 17.0% in the balance beam test. Only P. ginseng and S. baicalensis showed protective effects, and HT008-1 showed a greater effect than its component herbs. HT008-1 down-regulated the COX-2 and OX-42 expression in the penumbra region. In conclusion, the results show that HT008-1 may be effective in a rat stroke model by an antiinflammatory mechanism and may improve sensory-motor function by reducing damage in the cortex and caudoputamen.

Neuroprotective effect of defatted sesame seeds extract against in vitro and in vivo ischemic neuronal damage.

Sesame (Sesamum indicum L.) is an important oilseed crop that possesses a wide spectrum of pharmacological activities. Many studies have been conducted to investigate its health-promoting effects. Compared to other plant oils, sesame seed oil is highly stable to oxidation and has been demonstrated to have protective effects against ischemia-reperfusion injury in the rat brain. However; the effects of defatted sesame seeds extract (DSE) have not been studied yet. The purpose of this study was to evaluate the protective effect of DSE against ischemia models. For in vitro ischemia, oxygen-glucose deprivation followed by reoxygenation (OGD-R, 4 h OGD followed by 24 h reoxygenation) in HT22 cells was used to investigate the protective effects on cell death and the inhibitory effects on lipid peroxidation. For in vivo ischemia, the middle cerebral artery occlusion (MCAo, 2 h of MCAo followed by 22 h of reperfusion) rat model was used. Twenty-two h after occlusion the rats were assessed for neurobehavioral deficit and infarct volume. DSE (0.1-10 microg/mL) significantly reduced the cell death and inhibited lipid peroxidation induced by OGD-R. DSE (30, 100 and 300 mg/kg, p.o.) given twice at 0 h and 2 h after onset of ischemia reduced brain infarct volume dose-dependently and improved sensory-motor function. The therapeutic time window of DSE (300 mg/kg, p.o.) was 2 h after MCAo in rats. In conclusion, our results show that DSE may be effective in ischemia models by an antioxidative mechanism.