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Arachis hypogaea L. stems and leaves (AHSL) were used as raw materials, to extract phenolic acids through 60Co γ irradiation and solvent synergistic method. The extraction conditions were optimized by the response surface methodology of Box-Behnken, following a separation; thereafter, the antioxidant activity of the phenolic acid AHSL was studied. The results showed that the optimal extraction process could be achieved at an absorbed dose of 6.70 kGy and 70% ethanol concentration with 27∶1 liquid-solid ratio (mL∶g). The highest AHSL phenolic acid yield was (2.25±0.11)%. Among the process parameters, the absorbed dose showed the most significant effect on the AHSL phenolic acid yield (p=0.000 1).The phenolic acid content increased to 1.80 fold after extraction and purification with chloroform and ethyl acetate. Concerning the antioxidant activity, AHSL phenolic acid showed better free radical scavenging ability and ferric-reducing power than the ethanol extracts. Moreover, no significant difference could be observed in the hydroxyl radical scavenging effect between AHSL phenolic acid and tea polyphenols under the same concentration (p˃0.05). More than 50% of DPPH free radicals and hydroxyl free radicals could be removed at the AHSL phenolic acid concentration of 100 μg/mL. The results revealed that 60Co γ ray irradiation combined with ethanol extraction is feasible, and the phenolic acid from AHSL has strong antioxidant activity in vitro.

Chlorogenic acid (CGA) is a naturally occurring phenolic acid in human diet. Data obtained from in vivo and in vitro experiments demonstrate that CGA mostly presents anti-oxidant and anti-carcinogenic activities. Here we show that CGA also inhibits lipopolysaccharide (LPS)-induced inflammatory response[AU1] in RAW 264.7 cells. Our results indicated that CGA significantly decreased LPS-induced up-regulation of cyclooxygenase (COX-2) at protein and mRNA levels in RAW 264.7 cells and as a result it inhibited prostaglandin E(2) (PGE(2)) release from LPS-treated RAW 264.7 cells. In the further experiments, LPS-induced activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK)-c-Jun-activator protein (AP-1) pathway were suppressed significantly by CGA. In addition, CGA did not affect phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38. In conclusion, CGA suppresses LPS-induced COX-2 expression via attenuating the activation of NF-kappaB and JNK/AP-1 signaling pathways suggesting that CGA, the polyphenol compound in our food, could exert anti-inflammatory effects through inhibiting PGE(2) production.

The effect of different concentrations of eicosapentaenoic acid (EPA), on rat pheochromocytoma PC12 cells were evaluated using cell viability, lactate dehydrogenase (LDH) activity, flow cytometric DNA analysis and electronic microscopy. A time- and dose-dependent decrease in the cell viability was observed in the cultures of PC12 cells, supplemented with EPA. The incubation with 200 microM EPA for 48 and 72 hr induced a decrease in the cell viability by 53.40 and 53.43%, respectively. Treatment of PC12 cells with EPA induced apoptosis in a concentration-dependent manner, as evidenced by flow cytometry analysis. The highest percentage of apoptotic cells accumulated to 30.32%, following treatment with 200 microM EPA. The LDH levels increased significantly on treatment with 100 and 200 microM EPA, by 144.4 and 197.3%, respectively, compared with the untreated control. In addition, the cell morphology change was also observed by electron microscopy. The results suggest that EPA mediates its effect on the PC12 cells, at least in part, via the induction by apoptosis.