Hydroxyethylpuerarin attenuates focal cerebral ischemia-reperfusion injury in rats by decreasing TNF-alpha expression and NF-kappaB activity.

This study is to investigate the effect of hydroxyethylpuerarin on the expression of tumor necrosis factor-alpha (TNF-alpha) and activity of nuclear factor kappa B (NF-kappaB) after middle cerebral artery occlusion (MCAO) in rats. Rats were subjected to cerebral ischemia-reperfusion injury induced by MCAO. Hydroxyethylpuerarin (10, 20, 40 mg x kg(-1), iv) was administered just 30 min before occlusion and immediately after reperfusion. After a 24 h reperfusion following 2 h of MCAO, the number of viable neurons in hippocampal CA1 region was counted by hematoxylin and eosin (HE) staining. TNF-alpha protein and its mRNA expression were examined with radioimmunoassay (RIA) and reverse transcriptasepolymerase chain reaction (RT-PCR) respectively. NF-KB activity was observed by electrophoretic mobility shift assay (EMSA), and inhibition of NF-kappaB alpha (IkappaBalpha) protein expression was evaluated by Western blotting analysis. Animals treated with hydroxyethylpuerarin had a significant increase in neuronal survival in comparison with vehicle-treated group. Hydroxyethylpuerarin significantly reduced the protein and mRNA expression of TNF-alpha following 2 h of ischemia with 24 h of reperfusion. NF-kappaB DNA binding activity and the degradation of IkappaBalpha in the cytoplasm also decreased by hydroxyethylpuerarin treatment. The protective effects of hydroxyethylpuerarin against ischemia-reperfusion injury may be mediated by decreasing the expression of TNF-alpha and the activity of NF-kappaB in rats.

Effects of scutellarin on apoptosis induced by cobalt chloride in PC12 cells.

The present study investigated the protective effects of scutellarin on cobalt chloride (CoCl2)-induced apoptosis in PC12 cells. Incubation of PC12 cells with 500 microM CoCl2 for 24 h resulted in significant apoptosis as evaluated by the crystal violet, electron microscopy and flow cytometry assays. The increase of caspase-3 activity, decrease of Bcl-XL expression, phosphorylation of p38 mitogen-activated protein kinase (MAPK) and accumulation of intracellular reactive oxygen species (ROS) were also seen in CoCl2-treated PC12 cells. Scutellarin at 0.1, 1 and 10 microM significantly protected against the apoptotic cell death induced by CoCl2. Scutellarin decreased caspase-3 activity, increased Bcl-XL expression, inhibited p38 phosphorylation and attenuated ROS production. These results demonstrate that scutellarin can protect PC12 cells from cobalt chloride induced apoptosis by scavenging ROS, inhibiting p38 phosphorylation, up-regulating Bcl-XL expression and decreasing caspase-3 activity, and may reduce the cellular damage in pathological conditions associated with hypoxia-mediated neuronal injury.

[Protective effect of effective parts of Zingiber Offecinal on vascular endothelium of the experimental hyperlipidemic rats].

OBJECTIVE: To observe the influence of effective parts of Zingiber Officinale on serum IL-6, TNF-alpha in oroler to investigate the protective effects of the effective parts of Zingiber Officinal (EPZ) on endothelium of the experimental hyperlipidemic rats and the mechanism of its effects. METHODS: The hyperlipidemia model of rats was constructed by feeding high-fat forage and filled with the effective parts of Zingiber Officinale 200 mg/kg, 400 mg/kg, 800 mg/kg every day for 13 weeks. Blood was drawn to determine both the level of serum IL-6 and TNF-alpha. All the aortaes were taken to oberserve morphologic change and the intima-media thickness were detected. RESULTS: The effective parts of Zingiber Officinale could markedly decrease intima-media thickness, but had no marked influence in the level of serum IL-6 and TNF-alpha. CONCLUSION: The Effect Parts of Zingiber Officinale has the effect of protection of the endothelia of hyperlipidemia rats, which has nothing with the level of serum IL-6 and TNF-alpha.

Anti-inflammatory effect of hydroxyethylpuerarin on focal brain ischemia/reperfusion injury in rats.

The objective of this study is to investigate the anti-inflammatory effect of hydroxyethylpuerarin on focal brain ischemia injury in rats and to explore its mechanisms of action. After 24 h of reperfusion following 2 h of cerebral ischemia, the infiltration of neutrophils was observed by myeloperoxidase (MPO) activity determination, the expression of intercellular adhesion molecule-1 (ICAM-1) was observed by western blot and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, and the nuclear translocation and DNA binding activity of nuclear factor-kappaB (NF-kappaB) were observed by western blot and electrophoretic mobility shift assay (EMSA). The results showed that hydroxyethylpuerarin could obviously inhibit the MPO activity and ICAM-1 expression following 2 hours of ischemia with 24 hours of reperfusion. The nuclear translocation and DNA binding activity were also decreased by hydroxyethylpuerarin treatment. These results suggested that hydroxyethylpuerarin could inhibit neutrophil-mediated inflammatory response after brain ischemia reperfusion in rats. This effect may be mediated by down-regulation of ICAM-1 and NF-kappaB activity.