Antioxidant and antibacterial activities of extracts from Conyza bonariensis growing in Yemen.

This study aims to examine the antioxidant and antibacterial activities and phenolic contents of Conyza bonariensis growing in Yemen. The whole plants of C. bonariensis were ultrasonically extracted by ethanol. The antioxidant activity of the extract was determined by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and ß-carotene bleaching (BCB). The effectiveness of the extract on the growth inhibition of some indicators of foodborne illness bacteria were investigated by agar well diffusion assay. The total phenols (TP), total flavonoids (TF), total tannins (TT), and total anthocyanins (TA) were determined by Folin-Ciocalteu method, aluminium chloride method, Folin and Ciocalteu method, and pH-differential method, respectively. The extract of C. bonariensis possessed TP 144.1 mg/g, TF 143 mg/g, TT 0.99mg/g, and TA 0.97mg 100g, with 94.57% inhibition of DPPH and 92.47% inhibition of BCB, and strong inhibitory effects against tested bacteria, which was approximate to those of peel extract of Punica granatum.

Lipoic acid attenuates high-fat-diet-induced oxidative stress and B-cell-related immune depression.

OBJECTIVE: This study investigated whether spleen oxidative stress induced by a high-fat diet (HFD) influences the expression of genes involved in B-cell activation, thus leading to B-cell-related immunosuppression. METHODS: Male C57BL/6 mice were randomly assigned to one of three groups with eight mice in each group. The control group consumed an ordinary diet (4.9% fat, w/w). The other two groups were fed an HFD (21.2% fat) and an HFD plus 0.1% lipoic acid (LA). After 10 wk, plasma and spleen oxidative stress biomarkers including superoxide dismutase, catalase, glutathione peroxidase, total antioxidant capacity, reduced glutathione/oxidized glutathione ratio, and malondialdehyde were examined. The B-cell-related immune function was evaluated by examining the number of B cells, and the apoptotic percentages of splenic lymphocytes were determined by flow cytometry. Furthermore, the B-cell activation and reactive oxygen species scavenger-related genes differentially expressed between mice fed an HFD and those fed an HFD supplemented with LA were identified through complementary DNA microarray. RESULTS: The HFD induced marked decreases in the number of B cells and significantly increased the apoptotic percentages of splenic lymphocytes, accompanied by oxidative stress and increased oxidative damage, in the plasma and spleen. In addition, complementary DNA array analysis results showed that the HFD induced the decreased expression of genes associated with antioxidant defense, such as superoxide dismutase-3 (1.5-fold), metallothionein-1 (3.03-fold), glutathione peroxidase-5 (17.15-fold), and peroxiredoxin-4 (1.5), and B-cell activation, such as immunoglobulin heavy chain 6 (2.46-fold), immunoglobulin κ-chain (1.74-fold), Fc receptor (1.41-fold), and RAS-related C3 botulinum substrate-1 (7.46). The LA supplement prevented the buildup of oxidative stress and upregulated related gene expressions. CONCLUSION: These results indicate a role for LA as a possible effective supplement with an HFD to prevent the development of oxidative stress and to attenuate B-cell damnification by increasing the gene expression of the B-cell receptor signaling pathway.

Effects of duodenal redox status on calcium absorption and related genes expression in high-fat diet-fed mice.

OBJECTIVE: This study investigated whether duodenal redox imbalance induced by high-fat diet (HFD) influenced expression of genes involved in transcellular calcium absorption, thus leading to reduced intestinal calcium absorption. METHODS: Male C57BL/6 mice were randomly assigned to one of four groups with eight mice in each group. The control group consumed an ordinary diet (4.9% fat, w/w). The other three groups were fed a HFD (21.2% fat), the HFD plus 0.1% lipoic acid, or the HFD plus an additional 0.9% calcium supplement. After 9 wk, plasma and duodenal oxidative stress biomarkers including malondialdehyde, superoxide dismutase, catalase, total antioxidant capacity, reduced glutathione/oxidized glutathione ratio, and reactive oxygen species were examined. The intestinal calcium absorption state was evaluated through examining the calcium balance, bone mineral density, and calcium metabolism biomarkers. Furthermore, quantitative reverse transcription-polymerase chain reaction was carried out to analyze the changes in expression of transcellular calcium absorption-related genes. RESULTS: The HFD induced marked decreases in intestinal calcium absorption and bone mineral density of the whole body, accompanied by redox imbalance and increased oxidative damage in duodenum; duodenal expression of calbindin-D(9K), plasma membrane calcium ATPase (PMCA(1b)), and sodium-calcium exchanger was significantly down-regulated by 1.9-, 2.7-, and 1.5-fold, respectively. Furthermore, duodenal glutathione and oxidized glutathione (GSH/GSSG) ratios were strongly positively correlated with the apparent calcium absorption rate and the expression of PMCA(1b) and Calbindin-D(9K), whereas reactive oxygen species levels were negatively correlated with them. CONCLUSION: Our results demonstrated that a HFD-induced duodenal oxidation state could significantly down-regulate expression of calbindin-D(9K), PMCA(1b), and sodium-calcium exchanger, thus causing an inhibitory effect on intestinal calcium absorption.

Lipoic acid prevents high-fat diet-induced dyslipidemia and oxidative stress: a microarray analysis.

OBJECTIVE: We previously found that lipoic acid (LA) improved high-fat diet (HFD)-induced dyslipidemia in rats. To elucidate the molecular mechanisms of that effect, we carried out experiments aimed at analyzing biochemical parameters and gene expression profiles. METHODS: C57BL/6 mice were randomly assigned to one of three groups (n = 8). The control group consumed an ordinary diet (4.89% fat, w/w). The other two experimental groups were fed with an HFD (21.45% fat, w/w) or an HFD plus 0.1% LA. After 6 wk, plasma lipid level and antioxidant status were examined. To investigate the molecular mechanisms underlying the effects of LA on lipid metabolism and oxidative stress, we examined gene expression profiles in liver using the GeneChip microarray system. The differential expression of genes of interest identified by microarray technique was validated by real-time reverse transcription-polymerase chain reaction. RESULTS: HFD resulted in significant alterations in lipid profiles and a depressed antioxidant defense system. LA supplementation induced decreases in lipid peroxidation, plasma cholesterol, triacylglycerols, and low-density lipoprotein cholesterol and an increase in high-density lipoprotein in HFD-fed mice. DNA microarray analysis of the liver showed that LA ingestion upregulated the expression of genes related to beta-oxidation and free radical scavenger enzymes, whereas those involved in cholesterol synthesis were downregulated. CONCLUSION: LA can prevent HFD-induced dyslipidemia by modulating lipid metabolism, especially by increasing beta-oxidation and decreasing cholesterol synthesis, and oxidative stress by increasing those of free radical scavenger enzyme gene expression.

Effect of zinc sulphate and zinc methionine on growth, plasma growth hormone concentration, growth hormone receptor and insulin-like growth factor-I gene expression in mice.

1. The current experiment was conducted to investigate the effect of zinc sulphate (ZnSO4) and zinc methionine (Zn-Met) on growth and their effect on plasma growth hormone (GH) concentration, growth hormone receptor (GHR) and insulin-like growth factor I (IGF-I) mRNA expression in mice. 2. Ninety male KunMing (KM) mice were randomly divided into three treatments. The control group was fed on a basal diet containing 11.67 mg/kg of zinc. The ZnSO4 group and Zn-Met group were fed on the diets supplemented with ZnSO4 or Zn-Met at 30 mg/kg (containing zinc of 40.05 and 40.75 mg/kg, respectively). The mice were offered the test diets for 10 days. Weight gains and food intake were measured at the end of the experiment, zinc contents in liver and serum were determined using atomic absorption spectrophotometry; GH was determined by radioimmunoassay, the levels of GHR and IGF-I mRNA were determined with reverse transcript polymerase chain reaction. 3. Both ZnSO4 and Zn-Met enhanced weight gain and food intake in the mice, Zn-Met improved the growth and food intake more effectively than ZnSO4 did (P < 0.05). The both forms of zinc had no effect on GH and the level of GHR mRNA expression (P > 0.05) and they up-regulated the expression of IGF-I mRNA (P < 0.05). As compared to ZnSO4, Zn-Met enhanced the level of IGF-I mRNA significantly (P < 0.05). 4. Both ZnSO4 and Zn-Met had no effect on plasma GH and the expression of GHR mRNA, but they enhanced the expression of IGF-I mRNA. Zinc methionine enhanced the weight gain and up-regulated IGF-I mRNA expression more effectively than ZnSO4.