[Antifatigue effects of the composition of Moringa oleifera leaves and Polygonatum polysaccharide and its mechanisms].

Objective: To investigate the anti-fatigue effects of composition of Moringa oleifera leaves and Polygonatum polysaccharide, and to explore the mechanisms. Methods: Thirty male Kunming mice were randomly divided into control (C) and composition of Moringa oleifera leaves and Polygonatum polysaccharide group (MP). There were 15 mice in each group. Group C was given distilled water and the group MP was given composition intragastriclly every day. The volume was 0.5 ml. After 14 days of treatment, weight-bearing swimming experiment was conducted, and exhaustive swimming time was recorded. The bearing weight was 3% of the body weight. In another experiment, 48 male Kunming mice were randomly divided into quiet control group (QC), swimming control group (SC) and composition group (MP). There were 16 mice in each group. The QC and SC groups were given distilled water intragastrically, and the group MP was treated with composition every day for 14 days. The volume was 0.5 ml. On the day 15, 30 minutes after intragastriclly administration of distilled water, blood, liver and hind leg muscle of the QC group were collected immediately. The SC and MP groups were subjected non-weight-bearing swimming experiment, and blood, liver and hind leg muscle were collected after swimming. The fatigue related indexes, oxidant/antioxidant parameters and energy metabolism indicators in serum and tissues were determined by commercial kits. Results: The exhaustive swimming time of mice in MP group was significantly longer than that in the C group (P<0.05). Compared with the control group, non-weight-bearing swimming decreased the contents of serum glucose and GSH, the contents of hepatic glycogen and ATP, the hepatic activities of SOD, LDH and ATPase, and muscle activity of GSH-Px (P< 0.05). However, serum levels of BUN and MDA were increased (P<0.05). Compared with the SC group, the composition remarkably increased the contents of serum glucose and hepatic glycogen, increased serum content of GSH, enhanced hepatic activities of SOD, LDH and ATPase and muscle activity of GSH-Px, and increased the hepatic content of ATP (P<0.05). However, the serum level of BUN was decreased (P<0.05). Conclusion: The Moringa oleifera leaves and Polygonatum polysaccharide composition possesses anti-fatigue effects. Anti-oxidant and improving energy metabolism could be the important mechanisms.

Riboflavin deficiency affects lipid metabolism partly by reducing apolipoprotein B100 synthesis in rats.

Lipid metabolism is dependent on riboflavin status. Apolipoprotein B100 plays an important role in lipids transportation. This study was aimed to investigate the effect of riboflavin status on lipid metabolism and explore its association with apolipoprotein B100 synthesis in vivo. Riboflavin deficiency was developed in rats by feeding riboflavin-deficient diets. Compared to the control rats, the mRNA and protein expressions of apolipoprotein B100 were significantly reduced in riboflavin-deficient rats. Endoplasmic reticulum oxidoreductin 1 (ERO1) and protein disulfide isomerase (PDI), two enzymes involved in the oxidative folding of apolipoprotein B100, were also lowered remarkably in expression at protein level. Meanwhile, total cholesterol and triglyceride levels were decreased in the plasma and increased in the liver of riboflavin-deficient rats. The plasma very low-density lipoprotein cholesterol (VLDL-c) and low-density lipoprotein cholesterol (LDL-c) were also reduced in riboflavin-deficient rats. Our findings demonstrate that riboflavin deficiency affects lipid metabolism partly by reducing apolipoprotein B100 synthesis.

Cytoprotective effects of diosmetin against hydrogen peroxide-induced L02 cell oxidative damage via activation of the Nrf2-ARE signaling pathway.

Oxidative stress is considered a crucial mediator in the pathogenesis of various liver diseases. The flavone diosmetin has been reported to exhibit antioxidant activities; however, the hepatoprotective effects of diosmetin against oxidative stress, and the underlying molecular mechanisms, remain unknown. The present study aimed to investigate the potential hepatoprotective effects of diosmetin on hydrogen peroxide (H2O2)­induced oxidative damage in L02 cells and attempted to evaluate the role of the nuclear factor erythroid 2­related factor 2 (Nrf2)/antioxidant response element pathway in this process. L02 cells were divided into groups: Control (DMSO, diosmetin), H2O2, Trolox or tertiary butylhydroquinone and diosmetin (different doses). Protective effects in L02 cells were determined by CCK­8, cell apoptosis and lactate dehydrogenase leakage assays. Flow cytometry and inverted fluorescence microscope were used to measure the intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP). Protein expression levels were of Nrf2, heme oxygenase­1 (HO­1) and NAD(P)H quinone oxidoreductase­1 (NQO1) were determined by western blotting and mRNA levels were determined by reverse transcription­quantitative polymerase chain reaction. The results revealed that H2O2 induced notable injury to L02 cells, as demonstrated by decreased cell viability, increased lactate dehydrogenase release, apoptotic rate and intracellular ROS production, and by the loss of MMP. Conversely, diosmetin (20­40 µM) significantly reversed the damaging effects of H2O2, which indicated that diosmetin may exhibit potent hepatoprotective potential against H2O2­induced oxidative damage. Furthermore, pretreatment with diosmetin elevated mRNA and protein expression levels of Nrf2, HO­1 and NQO1. The present study is the first, to the best of our knowledge, to demonstrate that activation of the Nrf2/NQO1­HO­1 signaling pathway maybe involved in the cytoprotective effects of diosmetin against oxidative stress. Therefore, diosmetin may be considered a promising therapeutic agent for the treatment of various liver diseases associated with oxidative stress.