Objective: To investigate the improving effect of astaxanthin (AST) on the sperm quality of rats with ornidazole (ORN)-induced oligoasthenozoospermiaand its action mechanism. METHODS: Forty adult male SD rats were equally randomized into groups A (solvent control), B (low-dose ORN ［400 mg/（kg·d）］), C (high-dose ORN ［800 mg/（kg·d）］), D (low-dose ORN ［400 mg/（kg·d）］ + AST ［20 mg/（kg·d）］), and E (high-dose ORN ［800 mg/（kg·d）］ + AST ［20 mg/（kg·d）］), all treated intragastrically for3 weeks.After treatment, the epididymal tails ononeside was taken for determination of sperm concentration and activity, and the epididymideson the other side harvested for measurement of the activities of GSH-Px, GR, CAT and SOD and the MDA contentin the homogenate. RESULTS: Compared with group A, sperm motilityin the epididymal tail andGSH-Px and SOD activities in theepididymiswere markedly decreased while the MDAcontent significantlyincreased in group B (P<0.05), spermmotility and concentrationin the epididymal tail, testisindex, and the activities of GSH-Px, GR, CAT and SOD in the epididymis were remarkably reduced while theMDA contentsignificantly increased in group C(P<0.05). In comparison with group B, group D showed markedly increased sperm motility (［45.3±8.7］% vs ［66.3±8.9］%, P<0.05) in the epididymal tail and SOD activity in the epididymis (［116.7±25.3］ U/mg prot vs ［146.1±23.8］ U/mg prot, P<0.05), decreased MDA content(［1.68±0.45］ nmol/mg prot vs ［1.19±0.42］ nmol/mg prot, P<0.05).Compared with group C, group Eexhibited significant increases in the weight gained (［89.0±9.5］ vs ［99.9±4.1］ %, P<0.05) and sperm motility (［17.9±3.5］% vs ［27.3±5.3］ %, P<0.05) but a decrease in the content of MDA (［2.03±0.30］ nmol/mg prot vs ［1.52±0.41］ nmol/mg prot, P<0.05). CONCLUSIONS AST can improve spermquality in rats with ORN-inducedoligoasthenozoospermia, which may be associated with its enhancing effect on the antioxidant capacity of the epididymis.
Animals ; Antioxidants ; pharmacology ; Asthenozoospermia ; prevention & control ; Epididymis ; drug effects ; metabolism ; Male ; Oligospermia ; prevention & control ; Ornidazole ; Oxidative Stress ; Protective Agents ; pharmacology ; Radiation-Sensitizing Agents ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sperm Count ; Sperm Motility ; Spermatozoa ; drug effects ; metabolism ; Xanthophylls ; pharmacology

We examined the effect of a combination of astaxanthin (AX) supplementation, repeated heat stress, and intermittent reloading (IR) on satellite cells in unloaded rat soleus muscles. Forty-nine male Wistar rats (8-week-old) were divided into control, hind-limb unweighting (HU), IR during HU, IR with AX supplementation, IR with repeated heat stress (41.0-41.5 °C for 30 min), and IR with AX supplementation and repeated heat stress groups. After the experimental period, the antigravitational soleus muscle was analyzed using an immunohistochemical technique. Our results revealed that the combination of dietary AX supplementation and heat stress resulted in protection against disuse muscle atrophy in the soleus muscle. This protective effect may be partially due to a higher satellite cell number in the atrophied soleus muscle in the IR/AX/heat stress group compared with the numbers found in the other groups. We concluded that the combination treatment with dietary AX supplementation and repeated heat stress attenuates soleus muscle atrophy, in part by increasing the number of satellite cells.
Animals ; Body Weight ; Dietary Supplements ; Fibrinolytic Agents/pharmacology* ; Heat-Shock Response ; Hindlimb ; Hot Temperature ; Immunohistochemistry ; Male ; Muscle, Skeletal ; Muscular Atrophy/drug therapy* ; Oxidative Stress ; Rats ; Rats, Wistar ; Satellite Cells, Skeletal Muscle/cytology* ; Xanthophylls/pharmacology*

This study is to investigate the protective effect of astaxanthin against injured hepatocyte L-02 cells induced by sodium azide (NaN3) and reveal the possible mechanisms. Hepatocyte L-02 cells were exposed to 100 mmol.L-1 NaN3 with various concentrations of astaxanthin pre-incubated, then the cell viability was measured by MTT method; The level of reactive oxygen species (ROS) was determined by DCFH-DA method; The changes of mitochondrial membrane potential (MMP) and apoptosis ratio were detected by JC-1 method and Annexin V-FITC/PI double stain method, respectively. Results showed that after cells were exposed to 100 mmol.L-1 NaN3 for 3 hours, the cell viability significantly decreased; ROS level and the percentage of late phase apoptosis increased obviously; MMP was also declined. When cells were pretreated with astaxanthin, the cell damage and late phase apoptosis ratio reduced and MMP was maintained. However, the level of ROS showed insignificant decrease (P>0.05). The beneficial concentration of astaxanthin in improving cell viability and MMP was not in a dose dependent manner and the most effective of which was 0.10 nmol.L-1 (P<0.01). In order to reveal its possible non-antioxidant mechanism, mitochondrial membrane was imitated and H+ transferring function of astaxanthin was also detected by bilayer lipid membrane (BLM) method. Results showed that 2.0% astaxanthin could transfer H+ efficiently. These suggested the mechanisms of astaxanthin in protection of hepatocyte L-02 cells not via its ROS quenching capability but via its H+ transferring function, which improved the mitochondrial function and had the sequence biology effects.
Antioxidants ; pharmacology ; Apoptosis ; drug effects ; Cell Line ; Cell Survival ; drug effects ; Hepatocytes ; cytology ; drug effects ; Humans ; Hydrogen-Ion Concentration ; Membrane Potential, Mitochondrial ; drug effects ; Protons ; Reactive Oxygen Species ; metabolism ; Sodium Azide ; toxicity ; Xanthophylls ; pharmacology

OBJECTIVETo investigate the effect of Astaxanthin on enhancing the function of anti-oxidative damage in osteoblast.

METHODSMC3T3-E1 osteoblasts were randomly divided into five groups, including control group, model group, Astaxanthin group [low-dose (1 x 10(-7) mol/L), middle-dose (1 x 10(-6) mol/L), high-dose (1 x 10(-5) mol/L)], in which the activity of cells, activity of superoxide dismutase (SOD), the content of reactive oxygen species (ROS), lipid oxygen (LPO) and membrane fluidity were tested and compared.

RESULTSCompared with Astaxanthin groups, the activity of cells, SOD activity and membrane fluidity in the model group were significantly decreased (P < 0.01). However, the contents of ROS and LPO were significantly raised (P < 0.01).

CONCLUSIONH2O2 can cause oxidative damage of MC3T3-E1 osteoblasts, but Astaxanthin can prevent or decrease its influence.

Animals ; Antioxidants ; chemistry ; pharmacology ; Cell Line ; Hydrogen Peroxide ; metabolism ; Lipid Peroxidation ; drug effects ; Membrane Fluidity ; drug effects ; Mice ; Osteoblasts ; drug effects ; metabolism ; Oxidative Stress ; drug effects ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism ; Xanthophylls ; chemistry ; pharmacology

OBJECTIVETo study the chemical constituents of Chaetomorpha basiretorsa and screen for bioactive leading compounds.

METHODCompounds were isolated by normal phase silica gel and Sephadex LH-20 gel column chromatography, reverse phase MPLC and reverse phase HPLC. Their structures were elucidated by spectroscopic methods including MS, IR and 1D, 2D NMR. Cytotoxicity of the compounds was screened by using standard MTT method. The purified compounds' inhibition against proliferation of dog vascular smooth muscle cells was also screened by MTT assay.

RESULTFive compounds were isolated from C. basiretorsa and their structures were identified as euphol (I), loloilide (II), 4-cumylphenol (III), zeaxanthin (IV) and lactucaxanthin (V).

CONCLUSIONAll these compounds were obtained from this genus for the first time. Compound (III), 4-cumylphenol, was a new nature product. All compounds were inactive (IC50 > 10 microg x mL(-1)) in cytotoxicity screening. In inhibition against proliferation of dog vascular smooth muscle cells test, the cell survival ratio to compound I was (0.32 +/- 0.056)% which indicate its potential anti-atherosclerotic bioactivity.

Animals ; Cell Line, Tumor ; drug effects ; Cell Survival ; drug effects ; Chlorophyta ; chemistry ; Dogs ; Humans ; Lanosterol ; analogs & derivatives ; chemistry ; isolation & purification ; pharmacology ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Phenols ; chemistry ; isolation & purification ; pharmacology ; Triterpenes ; chemistry ; isolation & purification ; pharmacology ; Xanthophylls ; chemistry ; isolation & purification ; pharmacology ; Zeaxanthins

OBJECTIVETo investigate the in vivo inhibition of extract of Fructus lycii (FL) on the expressions of cathepsin B (Cat B) and cystatin C (Cys C) in high-fat diet and hydroquinone (HQ) induced model mice with age-related macular degeneration (AMD), and to explore the in vitro effects of lutein and zeaxanthin on hydrogen peroxide (H2O2,) induced expressions of matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of metalloproteinase 2 (TIMP-2) on ARPE-19 cells.

METHODSFifty female 8-month-old C57BL/6 mice were recruited in this research. Ten mice fed with regular diet was taken as the age control group. The rest 40 mice were fed with high fat diet for 6 months, followed by adding HQ (0. 8%) in the drinking water for 3 consecutive months. Then the modeled mice were randomly divided into the model control group (n =10), the high (at the daily dose of 3.75 g/kg), middle (at the daily dose of 2.50 g/kg), and low dose (at the daily dose of 1.25 g/kg) FL groups, 10 in each group. The extract of FL at each dose was respectively administered to mice by gastrogavage for 3 successive months. By the end of the experiment, the mice were killed and their eyeballs were removed. The protein expressions of Cat B and Cys C were observed by immunohistochemical assay. The mRNA and protein expressions of Cat B and Cys C were detected by real-time PCR and Western blot respectively. The drug concentrations of H2O2, lutein, and zeaxanthin were screened and detected using the activity of cell proliferation. The protein expressions of MMP-2 and TIMP-2 were detected using Western blot.

RESULTSCompared with the age control group, the mRNA and protein expressions of Cat B and Cys C were significantly higher in the in vivo model control group (P <0.05, P <0.01). The mRNA expressions of Cat B and Cys C were weaker in the middle and high dose FL groups than in the model control group (P <0. 05, P <0. 01). In in vitro cells, lutein and zeaxanthin could down-regulate the protein expressions of MMP-2 and TIMP-2 in H202 induced ARPE-19 cells (P <0. 05, P <0. 01).

CONCLUSIONSExtract of FL could down-regulate the high protein expressions of Cat B and Cys C in high-fat diet and HQ induced model mice. Lutein and zeaxanthin could down-regulate the protein expressions of MMP-2 and TIMP-2 in H202 induced ARPE-19 cells.

Animals ; Cathepsin B ; metabolism ; Cystatin C ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Female ; Hydrogen Peroxide ; Lutein ; pharmacology ; Macular Degeneration ; prevention & control ; Matrix Metalloproteinase 2 ; metabolism ; Mice ; Mice, Inbred C57BL ; Pigment Epithelium of Eye ; drug effects ; metabolism ; Tissue Inhibitor of Metalloproteinase-2 ; metabolism ; Xanthophylls ; pharmacology ; Zeaxanthins

OBJECTIVETo investigate the effects of various carotenoids on the proliferation, cell cycle, apoptosis and expression of bcl-2 gene in breast cancer cell MCF-7.

METHODSTime and dose effects of individual carotenoids were detected using the MTT assay. The effects of individual carotenoids on cell cycle and the apoptosis were observed by flow cytometry. The expression of bcl-2 mRNA gene was detected using the RT-PCR method.

RESULTSAll 4 carotenoids tested inhibited the proliferation of MCF-7 cell line, but with different potencies. beta-carotene and lycopene were the most active inhibitors (inhibition rate 88.2% and 87.8%, respectively) followed by zeaxanthin and astaxanthin. All 4 carotenoids did not induce cell apoptosis. Cell cycle progression was blocked at G(2)/M phase with 60 micromol/L lycopene and at G(0)/G(1) phase with 60 micromol/L zeaxanthin dipalmitate. Carotenoids down regulated bcl-2 gene expression.

CONCLUSIONCarotenoids could inhibit the proliferation of human beast cancer MCF-7 cell line in vitro and the action of carotenoids may be worked through different pathways.

Breast Neoplasms ; drug therapy ; genetics ; pathology ; Canthaxanthin ; pharmacology ; Carotenoids ; pharmacology ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured ; Xanthophylls ; Zeaxanthins ; beta Carotene ; analogs & derivatives ; pharmacology

OBJECTIVE: To investigate the protective effect of fucoxanthin (FX) against diabetic cardiomyopathy and explore the underlying mechanism. METHODS: Rat models of diabetes mellitus (DM) induced by intraperitoneal injection of streptozotocin (60 mg/kg) were randomized into DM model group, fucoxanthin treatment (DM+FX) group and metformin treatment (DM+ Met) group, and normal rats with normal feeding served as the control group. In the two treatment groups, fucoxanthin and metformin were administered after modeling by gavage at the daily dose of 200 mg/kg and 230 mg/kg, respectively for 12 weeks, and the rats in the DM model group were given saline only. HE staining was used to examine the area of cardiac myocyte hypertrophy in each group. The expression levels of fibrotic proteins TGF-β1 and FN proteins in rat hearts were detected with Western blotting. In the cell experiment, the effect of 1 μmol/L FX on H9C2 cell hypertrophy induced by exposure to high glucose (HG, 45 mmol/L) was evaluated using FITC-labeled phalloidin. The mRNA expression levels of the hypertrophic factors ANP, BNP and β-MHC in H9C2 cells were detected using qRT-PCR. The protein expressions of Nrf2, Keap1, HO-1 and SOD1 proteins in rat heart tissues and H9C2 cells were determined using Western blotting. The DCFH-DA probe was used to detect the intracellular production of reactive oxygen species (ROS). RESULTS: In the diabetic rats, fucoxanthin treatment obviously alleviated cardiomyocyte hypertrophy and myocardial fibrosis, increased the protein expressions of Nrf2 and HO-1, and decreased the protein expressions of Keap1 in the heart tissue (P < 0.05). In H9C2 cells with HG exposure, fucoxanthin significantly inhibited the enlargement of cell surface area, lowered the mRNA expression levels of ANP, BNP and β-MHC (P < 0.05), promoted Nrf2 translocation from the cytoplasm to the nucleus, and up-regulated the protein expressions its downstream targets SOD1 and HO-1 (P < 0.05) to enhance cellular antioxidant capacity and reduce intracellular ROS production. CONCLUSION Fucoxanthin possesses strong inhibitory activities against diabetic cardiomyocyte hypertrophy and myocardial fibrosis and is capable of up-regulating Nrf2 signaling to promote the expression of its downstream antioxidant proteins SOD1 and HO-1 to reduce the level of ROS.
Animals ; Antioxidants/metabolism* ; Atrial Natriuretic Factor/pharmacology* ; Cardiomegaly ; Diabetes Mellitus, Experimental/metabolism* ; Fibrosis ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Metformin ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; RNA, Messenger/metabolism* ; Rats ; Reactive Oxygen Species/metabolism* ; Superoxide Dismutase-1/pharmacology* ; Xanthophylls

OBJECTIVETo study the effects of astaxanthin on renal fibrosis and apoptosis induced by partial unilateral ureteral obstruction (UUO) in rats.

METHODSNinety-six male adult SD rats were randomized into 6 equal groups, namely the blank control group, sham-operated group, UUO group, and astaxanthin group at high, medium, and low doses. Left ureteral ligation was performed in UUO and astaxanthin groups, and two days before the operation, the rats in astaxanthin groups were lavaged with 25, 50, or 100 mg/kg astaxanthin daily for 14 days, while the same volume of saline was given to rats in UUO group and sham-operated group. Renal pathological in the rats was observed with HE staining, and the expression levels of TGF-β1, SGK1, and CTGF in the left kidney were detected immunohistochemically; the expression level of Bcl-2 and Bax were detected using Bcl-2 and Bax detection kits.

RESULTSCompared to UUO group, high- and medium-dose astaxanthin groups showed obviously ameliorated renal pathologies and reduced expressions of TGF-β1, SGK1, and CTGF in the left kidney with lessened renal cell apoptosis.

CONCLUSIONAstaxanthin can reduce UUO-induced renal fibrosis and renal cell apoptosis, demonstrating the renoprotective effect of astaxanthin against renal fibrosis.

Animals ; Apoptosis ; drug effects ; Connective Tissue Growth Factor ; metabolism ; Fibrosis ; Immediate-Early Proteins ; metabolism ; Kidney ; drug effects ; metabolism ; pathology ; Kidney Diseases ; metabolism ; pathology ; Male ; Protein-Serine-Threonine Kinases ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; metabolism ; Ureteral Obstruction ; metabolism ; pathology ; Xanthophylls ; pharmacology ; bcl-2-Associated X Protein ; metabolism