1,3,5-Trimethylbenzene (1,3,5-TMB) was used as the pore-enlarging modifier to expand the pore size of MCM-41 (mobil company of matter) mesoporous silica nanoparticles. The solvent impregnation method was adopted to assemble non-water-soluble β-carotene into the pore channel of MCM-41. The MCM-41 and drug assemblies were characterized by TEM, FT-IR, elemental analysis and N2 adsorption-desorption. The results showed that MCM-41 has good sphericity and regular pore structure. The research also investigated the optimal loading time, the drug loading and the vitro stability of the β-carotene. As a drug carrier, the modified MCM-41 showing a shorter drug loading time, the drug loading as high as 85.58% and the stability of β-carotene in drug assemblies has improved. The study of this new formulation provides a new way for β-carotene application.
Drug Carriers ; chemistry ; Drug Delivery Systems ; Drug Stability ; Nanoparticles ; chemistry ; Silicon Dioxide ; chemistry ; beta Carotene ; chemistry ; pharmacology

Blakeslea trispora is a natural source of carotenoids, including β-carotene and lycopene, which have industrial applications. Therefore, classical selective breeding techniques have been applied to generate strains with increased productivity, and microencapsulated β-carotene preparation has been used in food industry (Li et al., 2019). In B. trispora, lycopene is synthesized via the mevalonate pathway (Venkateshwaran et al., 2015). Lycopene cyclase, which is one of the key enzymes in this pathway, is a bifunctional enzyme that can catalyze the cyclization of lycopene to produce β-carotene and exhibit phytoene synthase activity (He et al., 2017).
Citric Acid Cycle ; Fermentation ; Gas Chromatography-Mass Spectrometry/methods* ; Lycopene/metabolism* ; Mucorales/metabolism* ; Nicotine/pharmacology* ; beta Carotene/biosynthesis*

OBJECTIVES: Primary tumor treatment through surgical resection and adjuvant therapy has been extensively studied, but there is a lack of effective strategies and drugs for the treatment of tumor metastases. Here, we describe a functional product based on a combination of compounds, which can be used as an adjuvant therapy and has well-known mechanisms for inhibiting cancer metastases, improving anti-cancer treatment, and enhancing immunity and antioxidant capacity. Our designed combination, named MVBL, consists of four inexpensive compounds: L-selenium-methylselenocysteine (MSC), D-‍α‍-tocopheryl succinic acid (VES), β‍-carotene (β‍-Ca), and L-lysine (Lys). METHODS: The effects of MVBL on cell viability, cell cycle, cell apoptosis, cell migration, cell invasion, reactive oxygen species (ROS), and paclitaxel (PTX)-combined treatment were studied in vitro. The inhibition of tumor metastasis, antioxidation, and immune enhancement capacity of MVBL were determined in vivo. RESULTS: MVBL exhibited higher toxicity to tumor cells than to normal cells. It did not significantly affect the cell cycle of cancer cells, but increased their apoptosis. Wound healing, adhesion, and transwell assays showed that MVBL significantly inhibited tumor cell migration, adhesion, and invasion. MVBL sensitized MDA-MB-231 breast cancer cells to PTX, indicating that it can be used as an adjuvant to enhance the therapeutic effect of chemotherapy drugs. In mice, experimental data showed that MVBL inhibited tumor metastasis, prolonged their survival time, and enhanced their antioxidant capacity and immune function. CONCLUSIONS This study revealed the roles of MVBL in improving immunity and antioxidation, preventing tumor growth, and inhibiting metastasis in vitro and in vivo. MVBL may be used as an adjuvant drug in cancer therapy for improving the survival and quality of life of cancer patients.
Mice ; Animals ; beta Carotene ; Lysine/pharmacology* ; Antioxidants/pharmacology* ; Quality of Life ; Paclitaxel/pharmacology* ; Apoptosis ; alpha-Tocopherol ; Succinates/pharmacology* ; Cell Line, Tumor ; Cell Proliferation ; Neoplasms

OBJECTIVEThe aim of this investigation was to study the effects of fat-soluble extracts from vegetable powder (FEFVP) and beta-carotene on the proliferation and apoptosis of cultured YTMLC-90 lung cancer cells.

METHODSThe lung cancer cells were continuously exposed to a broad range of concentration of FEFVP and beta-carotene. The proliferation was evaluated in MTT test. The induction of apoptosis was evaluated by morphological change, DNA fragmentation analysis, and DNA content analysis combined with flow cytometric analysis.

RESULTSBoth FEFVP and beta-carotene were found to inhibit cell proliferation and to induce morphologic changes consistent with apoptosis in YTMLC-90 cancer cells, including cellular shrinkage, chromatin condensation and nuclear fragmentation. DNA agarose gel electrophoresis showed DNA fragmentation 'ladder'. Flow cytometric analysis revealed decreased DNA content and the presence of a sub-G1 apoptotic peak.

CONCLUSIONThese findings are consistent with the induction of apoptosis. Moreover, the effects of FEFVP are stronger than those of beta-carotene. FEFVP inhibits the growth of YTMLC-90 probably via the induction of apoptosis cancer cells.

Antioxidants ; pharmacology ; Apoptosis ; Cell Division ; DNA Damage ; Flow Cytometry ; Humans ; Lung Neoplasms ; pathology ; Plant Extracts ; pharmacology ; Powders ; Tumor Cells, Cultured ; Vegetables ; chemistry ; beta Carotene ; pharmacology

OBJECTIVETo investigate the protective effects of beta-carotene in rats against the development of chronic bronchitis induced by cigarette smoking.

METHODSForty-two Male Wistar rats were randomly divided into three study groups: (1) control (n = 15), animals underwent no treatment; (2) cigarette smoking (n = 15), animals developed chronic bronchitis through long-term cigarette smoking twice a day for 75 d; (3) beta-carotene plus cigarette smoking animals (n = 12) were given 1 ml or 15 mg/kg beta-carotene orally every day just before cigarette smoking. The levels of IL-6, IL-8, NO, superoxide dismutase (SOD) and lipoperoxide (LPO) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue were measured and the pathological changes to lung tissue were analyzed using light microscopy.

RESULTSLong-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. beta-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis.

CONCLUSIONSQuantitative oral intake of beta-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.

Animals ; Bronchitis ; blood ; etiology ; prevention & control ; Interleukin-6 ; blood ; Interleukin-8 ; blood ; Male ; Nitric Oxide ; blood ; Rats ; Rats, Wistar ; Smoking ; adverse effects ; Superoxide Dismutase ; blood ; beta Carotene ; pharmacology

To investigate association between breast cancer risk and nutrients intake in Korean women, a case-control study was carried out, at Seoul, Korea. Incident cases (n=224) were identified through the cancer biopsy between February 1999 and December 2000 at two University hospitals in Seoul. Hospital-based controls (n=250) were selected from patients in the same hospitals, during the same periods. Food intake was investigated semiquantitative frequency questionnaire (98 items) by trained dietitian. Subjects were asked to indicate the average food intake and vitamin supplement for a 12 months period of 3-yr prior to the base-line phase. In investigation of vitamin supplement use, subjects were asked the average frequency of use, duration, dose and the brand name of vitamin supplement (multivitamins, vitamin A, vitamin C and vitamin E). And nutrients were calorie adjusted by the residuals method. In this study, higher breast cancer risk incidence was not observed with higher intake of total fat and saturated fatty acids, however statistically significant trends with breast cancer incidence for total saturated fatty acids were found (p trend =0.0458). In analyses of vitamins, beta-carotene and vitamin C were significantly associated with decreasing risk of breast cancer. In analyses, results from dietary plus supplement of vitamin was not associated with breast cancer risk in this study. In conclusion, our findings suggest that antioxidant vitamins such as beta-carotene and vitamin C intake could lower the breast cancer risk in Korean women.
Adult ; Aged ; Antioxidants/pharmacology ; Ascorbic Acid/metabolism ; Breast Neoplasms/diagnosis/*epidemiology ; Case-Control Studies ; Dietary Fats/*metabolism ; *Dietary Supplements ; Female ; Human ; Incidence ; Korea ; Middle Aged ; Odds Ratio ; Questionnaires ; Time Factors ; Vitamin E/metabolism ; Vitamins/*metabolism ; beta Carotene/metabolism

beta-Carotene has shown antioxidant and antiinflammatory activities; however, its molecular mechanism has not been clearly defined. We examined in vitro and in vivo regulatory function of beta-carotene on the production of nitric oxide (NO) and PGE2 as well as expression of inducible NO synthase (iNOS), cyclooxygenase-2, TNF-alpha, and IL-1beta. beta-Carotene inhibited the expression and production of these inflammatory mediators in both LPSstimulated RAW264.7 cells and primary macrophages in a dose-dependent fashion as well as in LPS-administrated mice. Furthermore, this compound suppressed NF-kappaB activation and iNOS promoter activity in RAW264.7 cells stimulated with LPS. beta-Carotene blocked nuclear translocation of NF-kappaB p65 subunit, which correlated with its inhibitory effect on IkappaBalpha phosphorylation and degradation. This compound directly blocked the intracellular accumulation of reactive oxygen species in RAW264.7 cells stimulated with LPS as both the NADPH oxidase inhibitor diphenylene iodonium and antioxidant pyrrolidine dithiocarbamate did. The inhibition of NADPH oxidase also inhibited NO production, iNOS expression, and iNOS promoter activity. These results suggest that beta-carotene possesses anti-inflammatory activity by functioning as a potential inhibitor for redox-based NF-kappaB activation, probably due to its antioxidant activity.
Animals ; Anti-Inflammatory Agents/*pharmacology ; Antioxidants/*pharmacology ; Dinoprostone/metabolism ; Female ; Gene Expression/drug effects ; Inflammation Mediators/*metabolism ; Lipopolysaccharides/pharmacology ; Macrophages/*drug effects ; Mice ; Mice, Inbred BALB C ; NF-kappa B/*antagonists & inhibitors/genetics/metabolism ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Research Support, Non-U.S. Gov't ; beta Carotene/*pharmacology

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