Effect of pulsed electric fields (PEF) on physico-chemical properties, ß-carotene and antioxidant activity of air-dried apricots.

Fresh apricots pre-treated by pulsed electric fields at different intensities [LPEF, 0.65 kV/cm, 100 Hz, 20 µs and total treatment time 30 s; HPEF1, 1.25 kV/cm, 100 Hz, 20 µs and total treatment time 30 s; HPEF2, 1.25 kV/cm, 100 Hz, 20 µs and total treatment time 60 s], along with controls [non-treated, non-treated and sulphite treated, and heat pre-treatment at 80 °C, for 10 min (HC)] and soaked in 0.2% sodium sulphite solution for 1 h and then were subject to hot air drying. The changes in drying rate, polyphenol oxidase, peroxidase, and ß-carotene contents as well as antioxidant activity and colour in pre-treatment and hot air-dried apricot samples were investigated. PEF and heat treatments increased the drying rate of apricots. PEF treatments had no effect on the PPO activity and decreased the POD activity (p < 0.05). HPEF2 treatment retained more ß-carotene, higher antioxidant activity and suffered less browning during processing. Overall, the results indicate that combining sulphite treatment with PEF produces dried apricots with more ß-carotene and antioxidant activity, and better colour.

Xinjiang herbal tea exerts immunomodulatory activity via TLR2/4-mediated MAPK signaling pathways in RAW264.7 cells and prevents cyclophosphamide-induced immunosuppression in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: A multi-herb Chinese medicinal formula consisting of a variety of medicinal and edible materials has long been consumed as a hot drink and immune enhancer for its efficiency to increase disease resistance in Xinjiang, China. However, no fundamental data has been collected associated with traditional consumption. The present work was designed to evaluate the immunostimulatory role of Xinjiang herbal tea (XMT-WE) in RAW 264.7 macrophages and cyclophosphamide (CTX)-induced immunosuppression mice model. MATERIALS AND METHODS: RAW 264.7 cells were treated with various concentrations of XMT-WE. Nitric oxide (NO) levels were determined using Griess reagents, and pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α were investigated with a cytometric bead array kit. The effects on mRNA expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and TNF-α were investigated. Furthermore, activation of nuclear factor (NF)-κB and AP-1 mitogen-activated protein kinase (MAPK) signaling pathways was investigated. RESULTS: Pre-treatment with XMT-WE significantly increased secretion of NO, IL-6, and TNF-α. In addition, XMT-WE markedly increased expression of iNOS, COX-2, and TNF-α as well as AP-1 and NF-κB translocation from the cytoplasm into the nucleus, which was associated with an increase of phosphorylated ERK, JNK, and p38 as well as membrane receptors such as toll-like receptor (TLR) 2 and TLR4. Moreover, XMT-WE promoted the secretion of interleukin-2 (IL-2) and interferon-γ (IFN-γ) in cyclophosphamide (CTX)-induced immunosuppressive mice. CONCLUSION: These results indicated that XMT-WE at 50 µg/ml exerts immunomodulatory activity via TLR2/4-mediated MAPK signaling pathways in RAW 264.7 cells. Furthermore, in vivo experiments revealed that XMT-WE at the dose of 50 and 100 mg/kg strongly stimulated inflammatory cytokines.

Neuroprotective effects of macranthoin G from Eucommia ulmoides against hydrogen peroxide-induced apoptosis in PC12 cells via inhibiting NF-κB activation.

Oxidative stress-mediated cellular injury has been considered as a major cause of neurodegenerative diseases including Alzheimer and Parkinson diseases. The scavenging of reactive oxygen species (ROS) mediated by antioxidants may be a potential strategy for retarding the disease's progression. Macranthoin G (MCG), isolated from Eucommia ulmoides, is a derivative from chlorogenic acid methyl ester and caffeic acid. This study is aimed to investigate the protective role of MCG against the cytotoxicity induced by hydrogen peroxide (H2O2) and to elucidate potential protective mechanisms in rat pheochromocytoma (PC12) cells. The results showed that the treatment of PC12 cells with MCG prior to H2O2 exposure effectively increased the cell viability, and stabilized the mitochondria membrane potential (MMP); furthermore, it enhanced the antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) and the levels of intracellular glutathione (GSH); it also decreased the malondialdehyde (MDA) content, intracellular ROS, caspase-3 activation, as well as cell apoptosis. In addition, the MCG treatment minimized the cell injury by H2O2 via down-regulation of the NF-κB pathway as well as activation of phosphorylation of IκBα, p38, and the extracellular signal-regulated kinase (ERK). These results showed that that MCG is promising as a potential therapeutic agent for neurodegenerative diseases induced by oxidative damage and should be encouraged for further research.