Antioxidative effects of berberine pre-treatment on hydrogen peroxide-induced PC12 cell toxicity

Oxidative stress has been implicated in the pathogenesis of Alzheimer＇s disease. Oxidative damage could be prevented by augmenting the endogenous defense capacity against oxidative stress by antioxidant intake. As an effective alkaloid component of Chinese herbal medicine Rhizoma coptidis extract, berberine exhibits antioxidative properties and ameliorates memory impairment in a rat model of Alzheimer＇s disease. The present study investigated the protective effects of berberine on H2O2-induced PC12 cell toxicity. Results demonstrated that berberine protects PC12 cells from H2O2-induced apoptosis and increases PC12 cell viability. Lactate dehydrogenase release, reactive oxygen content, and malonyl dialdehyde levels were significantly decreased （P 〈 0.01）. The protective effects of berberine on H2O2-induced PC12 cell toxicity were achieved via the antioxidative effects of berberine.

Protective effect of paeonol on beta-amyloid 25-35- induced toxicity in PC12 cells

BACKGROUND：Paeonol is a primary phenolic component of the Chinese medicinal herb Cortex moutan. Recent studies have shown that paeonol has anti-inflammatory, analgesic, and antioxidative effects as well as a significant cardioprotective effect against myocardial ischemia. OBJECTIVE： To investigate the protective effect of paeonol on β-amyloid 25-35-induced toxicity in PC12 cells and analyze its mechanism of action. DESIGN, TIME AND SETTING： A controlled repeated-measures cell-based study was performed in the Department of Pharmacology of Guangdong Medical College between September 2006 and December 2007. MATERIALS： Paeonol was supplied by Xuancheng Baicao Plant Industry and Trade Company, China. PC12 cells were a kind gift from Dr. Haitao Zhang at Guangdong Medical College. β-amyloid 25-35 was purchased from Sigma Company, USA. Lactate dehydrogenase （LDH） and malondialdehyde （MDA） kits were purchased from Nanjing Jiancheng Bioengineering Research Institute, China. METHODS： PC12 cells were maintained in Dulbecco＇s modified eagle＇s medium （DMEM） supplemented with 100 mL/L heat-inactivated horse serum and 50 mL/L fetal bovine serum at 37 ℃ and cultured in an incubator with 5% CO2. The medium was renewed every other day. Batches of cells were assigned into three groups. （1） Paeonol group： cells were preincubated with different concentrations of paeonol （12, 25 or 50 μmol/L） for one hour and β-amyloid 25-35 was added to the medium; （2） control group： cells were cultured in DMEM supplemented with 100 mL/L heat-inactivated horse serum and 50 mL/L fetal bovine serum; and （3） β-amyloid 25-35 group： β-amyloid 25-35 was added to the medium. MAIN OUTCOME MEASURES： When PC12 cells in each group were cultured for 24 hours, the cell viability was determined using the MTT reduction assay, LDH release into the culture media was measured by 2,4-dinitrophenylhydrazine chromatometry and MDA content was measured using a thiobarbituric acid assay. RESULTS： When PC12 cells were treated withβ-amyloid 25-35 （50 μmol/L） for 24 hours, their viability was significantly lower compared with the control group （P 〈 0.01）. When the cells were treated with paeonol for one hour prior to incubation withβ-amyloid 25-35, their viability was significantly increased compared with theβ-amyloid 25-35 group （P 〈 0.05–0.01）. LDH activity and MDA level in the β-amyloid 25-35 group were significantly increased compared with the control group （P 〈 0.01）. When the cells were treated with different concentrations of paeonol, LDH activity and MDA level in PC12 cells were significantly decreased compared with theβ-amyloid 25-35 group （P 〈 0.01）. CONCLUSION： Paeonol protects PC12 cells againstβ-amyloid 25-35-induced toxicity and the protective effect of paeonol is probably achieved through its antioxidative effects.