[Effect of ferulic acid on cholesterol efflux in macrophage foam cell formation and potential mechanism].

The formation of macrophage-derived foam cells is a typical feature of atherosclerosis (AS). Reverse cholesterol efflux (RCT) is one of important factors for the formation of macrophage foam cells. In this study, macrophage form cells were induced by oxidized low density lipoprotein (ox-LDL) and then treated with different concentrations of ferulic acid, so as to observe the effect of ferulic acid on the intracellular lipid metabolism in the ox-LDL-induced macrophage foam cell formation, the cholesterol efflux and the mRNA expression and protein levels of ATP binding cassette transporter A1 (ABCA1) and ATP binding cassette transporter G1 (ABCG1) that mediate cholesterol efflux, and discuss the potential mechanism of ferulic acid in resisting AS. According to the findings, compared with the control group, the ox-LDL-treated group showed significant increase in intracellular lipid content, especially for the cholesterol content; whereas the intracellular lipid accumulation markedly decreased, after the treatment with ferulic acid. The data also demonstrated that the mRNA and protein expressions of ABCA1 and ABCG1 significantly increased after macrophage foam cells were treated with different concentrations of ferulic acid. In summary, ferulic acid may show the anti-atherosclerosis effect by increasing the surface ABCA1 and ABCG1 expressions of macrophage form cells and promoting cholesterol efflux.

Determination of nine bioactive phenolic components usually found in apple juice by simultaneous UPLC-MS/MS.

The functional food ingredients of apple juice can significantly change during processing, transportation, and storage, thus affecting the quality of the product. A simple and derivation-free analytical method based on ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was developed and optimized for the simultaneous determination of functional food ingredients in apple juice bought in the market. Cleanup steps and chromatographic conditions were optimized to remove interference and decrease the matrix effect. The nine target analytes were separated on an Acquity UPLC system equipped with a BEH C18 column and detected by electrospray ionization source (ESI) operating in positive subsection acquisition mode under multiple reaction monitoring (MRM) conditions. The results showed that p-hydroxybenzoic acid, protocatechuate, caffeic acid, chlorogenic acid, epicatechin, phloridzin, hyperoside, procyanidin B2, and rutin could be sufficiently separated for content determination within 6 min. In the concentration range of 20 µg/L-50 mg/L, nine standard samples exhibited a good linear fit with correlation coefficients above .985.

The oxidation metabolites of endomorphin 1 and its fragments induced by free radicals.

Endomorphin 1 (EM1), an endogenous micro-opioid receptor agonist, acts as a free radical scavenger in vitro and an antioxidant in vivo. The modification of EM1 by ROS and the properties of the OM attracted our attention. In vitro assays were performed via RP-HPLC, spectrophotometric measurements, EPR and amino acid analysis, Schmorl's reaction to define the formation of melanin-like compounds transformed from EM1, collectively named EM1-melanin and by solubility assay, radioligand-binding assay, NADH oxidation, superoxide anion scavenging assay to study some physical and chemical properties of EM1-melanin. Possible pathways of the formation of EM1-melanin were proposed.

Asymmetric Michael addition of trisubstituted carbanion to nitroalkenes catalyzed by sodium demethylquinine salt in water.

A mild method for the asymmetric synthesis of quaternary and tertiary carbon centers has been developed through Michael addition of trisubstituted carbon nucleophile to nitroalkenes catalyzed by low loading sodium demethylquinine salt in water.

Endomorphin 1 effectively protects cadmium chloride-induced hepatic damage in mice.

The antioxidative capacity of endomorphin 1 (EM1), an endogenous mu-opioid receptor agonist, has been demonstrated by in vivo assays. The present study reports the effect of EM1 on hepatic damage induced by cadmium chloride (Cd(II)) in adult male mouse. Mouse were given intraperitoneally (i.p.) a single dose of Cd(II) (1mg/kg body weight per day) and the animals were co-administrated with a dose of EM1 (50 microM/kg body weight per day) for 6 days. Since hepatic damage induced by Cd(II) is related to oxidative stress, lipid peroxidation (LPO), protein carbonyl (PCO), superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) were evaluated. The parameter indicating tissue damage such as liver histopathology was also determined. In addition, the concentrations of Cd and zinc (Zn) in the liver were analyzed. The intoxication of Cd(II) lead to the enhanced production of LPO and PCO, treatment with EM1 can effectively ameliorate the increase of LPO and PCO compared to the Cd(II) group. The increased activities of CAT, SOD and the elevated GSH induced by Cd(II) may relate to an adaptive-response to the oxidative damage, the effect of EM1 can restore the elevated antioxidant defense. Our results suggested that the structure features and the ability of chelating metal of EM1 may play a major role in the antioxidant effect of EM1 in vivo and opioid receptors may be involved in the protection of hepatic damage induced by Cd(II).

Protective effects of blueberries (Vaccinium corymbosum L.) extract against cadmium-induced hepatotoxicity in mice.

The oxidative status and morphological changes of mouse liver exposed to cadmium chloride (Cd(II)) and therapeutic potential of blueberry (Vaccinium corymbosum L.) extract against Cd(II)-induced hepatic injury were investigated. A variety of parameters were evaluated, including lipid peroxidation (LPO), protein carbonyl (PCO) level, DNA fragment, as well as antioxidative defense system (i.e., superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH)). Elemental analysis and evaluation of morphological changes and NO levels were also performed. Exposure to Cd(II) led to increased LPO and PCO as well as DNA fragment and a reduction of SOD and CAT activities, however, the content of GSH elevated probably due to biological adaptive-response. In contrast, co-treatment of anthocyanin (Ay) inhibited the increased oxidative parameters as well as restored the activities of antioxidative defense system in a dose-dependent manner. Ay administration regained these morphological changes caused by intoxication of Cd(II) to nearly normal levels. Moreover, the accumulation of Cd(II) in liver may be one of the reasons for Cd(II) toxicity and Ay can chelate with Cd(II) to reduce Cd(II) burden. The influence of Cd(II) on the Zn and Ca levels can also be adjusted by the co-administration of Ay. Exposure to Cd(II) led to an increase of NO and Ay reduced NO contents probably by directly scavenging. Potential mechanisms for the protective effect of Ay have been proposed, including its anti-oxidative and anti-inflammatory effect along with the metal-chelating capacity. These results suggest that blueberry extract may be valuable as a therapeutic agent in combating Cd(II)-induced tissue injury.