Protective effect of a phenolic-rich fraction from Schisandra chinensis against H2O2-induced apoptosis in SH-SY5Y cells.

We have investigated the neuroprotective effects of a phenolic-rich fraction (PRF) on the hydrogen peroxide (H(2)O(2))-induced apoptosis of cultured SH-SY5Y cells. The PRF was obtained from the 80% ethanol extract of the fruits of Schisandra chinensis by Sepabeads SP-850 column chromatography. Cell viability assays revealed that pretreating SH-SY5Y cells with PRF (10-200 mugmL(-1)) resulted in significant dose-dependent protection against H(2)O(2)-induced cell death. The protective effect of PRF against H(2)O(2)-induced apoptosis was assessed by flow cytometric analysis of DNA contents using propidium iodide (PI) staining. Pre-incubation of cells with PRF at different concentrations for 24 h partially protected apoptosis by H(2)O(2) (150 muM). Moreover, cells treated with PRF reduced H(2)O(2)-induced caspase-3 activation and poly (ADP-ribose) polymerase cleavage and exerted an apparent suppressive effect on oxidative stress induced by reactive oxygen species (ROS). We concluded that PRF may be useful in the treatment and prevention of neurodegenerative diseases associated with elevated ROS levels.

Phenolic-rich fraction from Rhus verniciflua Stokes (RVS) suppress inflammatory response via NF-kappaB and JNK pathway in lipopolysaccharide-induced RAW 264.7 macrophages.

The effects of phenolic-rich fraction (PRF) from Rhus verniciflua Stokes (Anacardiaceae) on the activities of cellular signaling molecules that mediate inflammatory responses in LPS-induced RAW 264.7 macrophages were investigated. At various concentrations of PRF significantly inhibited NO, PGE(2) and TNF-alpha production in LPS-induced RAW 264.7 macrophage cells. The PRF also significantly inhibited iNOS and COX-2 protein expression in LPS-induced RAW 264.7 macrophage in a concentration-dependent manner. Transcription factor NF-kappaB plays a key role for the inducible expression of genes mediating proinflammatory effects and here, we show that PRF can inhibit the induction of NF-kappaB activity. The PRF effectively inhibited the iNOS and COX-2 protein expression through suppression of phospho-JNK1/2 activation. Study using PDA HPLC has found that the PRF contains several low molecular compounds (i.e. p-coumaric acid, fustin, kaempferol-3-O-glucoside, sulfuretin, butein, kaempferol). Our results indicate that the anti-inflammatory properties of PRF might result from the inhibition of pro-inflammatory mediators (e.g., NO, PGE(2) and TNF-alpha) by suppression of such signaling pathways as NF-kappaB and JNK1/2.

Effects of wild ginseng (Panax ginseng C.A. Meyer) leaves on lipid peroxidation levels and antioxidant enzyme activities in streptozotocin diabetic rats.

The aim of this study was to examine the possible antioxidant activities of wild Panax ginseng leaf extract intake in streptozotocin (STZ)-induced diabetic rats (WGLE). Initial blood glucose levels increased abruptly after streptozotocin injection. After 4 weeks of WGLE supplementation, blood glucose levels were lower in animals fed 40 mg/kg (266 mg/dL) and 200 mg/kg (239 mg/dL) than those in no-WGLE fed diabetic rats (464 mg/dL). The concentration of blood TBARS, which are considered the main products of glucose oxidation in blood, was also lowered by WGLE supplementation. These results indicate that WGLE supplementation is involved in suppressing a sudden increase in blood glucose levels and a consequent decrease in TBARS levels in diabetic rats. TBARS levels in the liver, kidney and spleen of WGLE-fed diabetic groups were also significantly lower than in the control diabetic group indicating that oral administration of WGLE effectively suppresses lipid peroxidation that occurs in the organs of diabetic rats. Antioxidant activities of WGLE supplementation further extend in suppressing activities of antioxidant related enzymes, such as glutathione peroxidase (GSH-Px), catalase (CAT) and superoxide dismutase (SOD), in organs of diabetic rats. These results confirm the effectiveness of WGLE supplementation in detoxifying free radicals that are produced excessively in diabetic-induced complications.