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The present study investigated the neuroprotective effects of aucubin on hydrogen peroxide (H2O2)-induced apoptosis in PC12 cells. Exposure of PC12 cells to 0.25 mm H2O2 induced a leakage of lactate dehydrogenase and decreased cell viability, as shown by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. In a dose over 0.1 mm, aucubin increased PC12 cellular viability and markedly attenuated H2O2-induced apoptotic cell death. Quantitation of apoptosis by flow cytometry indicated that aucubin inhibited H2O2-induced apoptosis in PC12 cells. Nuclear damage was alleviated by aucubin, as shown by Hoechst staining. In addition, the levels of malondialdehyde were reduced and the activity of superoxide dismutase, catalase and glutathione peroxidase was augmented in these cells. These results indicated that aucubin inhibited H2O2-induced apoptosis in PC12 cells through regulation of the endogenous oxidant–antioxidant balance. Our results suggest that aucubin is a potential protective agent for the treatment of oxidative-stress-induced neurodegenerative disease. Copyright © 2011 John Wiley & Sons, Ltd.

Excess production of reactive oxygen species by macrophages has been implicated in many inflammatory diseases. The present study investigated the inhibitory effect of the stem bark extract of Acanthopanax senticosus on the production of superoxide anion and hydrogen peroxide in mouse peritoneal macrophages in vitro and in vivo. Exposure of mouse peritoneal macrophages to A. senticosus extract significantly suppressed superoxide anion production induced by zymosan in a dose-dependent manner. Similarly, exposure of mouse peritoneal macrophages to A. senticosus extract significantly inhibited hydrogen peroxide production induced by phorbol 12-myristate 13-acetate (PMA) in a dose-dependent manner. Intraperitoneal administration of A. senticosus extract to KM mice reduced the ex vivo production of zymosan induced-superoxide anion and PMA-induced hydrogen peroxide by their peritoneal macrophages. Exposure to A. senticosus extract did not affect the cell viability or systemic toxicity. A. senticosus inhibited reactive oxygen species production by mouse peritoneal macrophages in vitro and in vivo and may be partly responsible for the antiinflammatory function.

Excess nitric oxide (NO) production has been implicated in inflammatory diseases. The present study investigated the inhibitory effect of the stem bark extract of Acanthopanax senticosus (A. senticosus) on NO production in murine macrophages in vitro and in vivo. In vitro exposure of RAW264.7 cells to 1, 10, 50, 100, 250, 500 and 1000 µg/mL of A. senticosus extract significantly suppressed NO production induced by lipopolysaccharide (LPS) and interferon gamma (IFN-γ) in a dose-dependent manner. In vitro exposure of mouse resident peritoneal macrophages to 1, 10, 100 and 1000 µg/mL of A. senticosus extract significantly suppressed NO production induced by LPS and IFN-γ in a dose-dependent manner. In vivo administration of A. senticosus extract (50, 100 and 200 mg/kg) to KM mice dose-dependently inhibited LPS and IFN-γ induced production of NO in isolated mouse peritoneal macrophages ex vivo. Exposure to A. senticosus extract had no effect on cell viability and systemic toxicity. The results demonstrated that the stem bark extract of A. senticosus extract inhibits NO production in murine macrophages in vitro and in vivo. Copyright © 2007 John Wiley & Sons, Ltd.