Oral administration of microencapsulated B. Longum BAA-999 and lycopene modulates IGF-1/IGF-1R/IGFBP3 protein expressions in a colorectal murine model.

PMID: 

Int J Mol Sci. 2019 Aug 31 ;20(17). Epub 2019 Aug 31. PMID: 31480481

Abstract Title: 

Oral Administration of MicroencapsulatedBAA-999 and Lycopene Modulates IGF-1/IGF-1R/IGFBP3 Protein Expressions in a Colorectal Murine Model.

Abstract: 

The Insulin-like growth factor-I/Insulin-like growth factor-I receptor (IGF-1/IGF-1R) system is a major determinant in colorectal cancer (CRC) pathogenesis. Probiotics (, BF) and lycopene (LYC) have been individually researched for their beneficial effects in the prevention of CRC. However, the effect of a combined treatment of microencapsulated BF and LYC on IGF-1/IGF-1R/IGFBPs (Insulin-like growth factor-binding proteins) expression in an azoxymethane (AOM)-dextran sulfate sodium (DSS)-induced CRC model have not been demonstrated. BF was microencapsulated by the spray drying technique, with high viability, and daily gavaged with LYC for 16 weeks to CD-1 mice in an AOM-DSS model. The results indicated that BF- and BF + LYC-treated groups had significantly lower inflammation grade, tumor incidence (13-38%) and adenocarcinoma (13-14%) incidence compared to the AOM + DSS group (80%), whereas LYC treatment only protected against inflammation grade and incidence. Caecal, colonic and fecal pH andβ-glucuronidase (β-GA) values were significantly normalized by BF and LYC. Similarly, BF and BF + LYC treatments significantly reduced both the positive rate and expression grade of IGF-1 and IGF-1R proteins and normalized Insulin-like growth factor-binding protein-3 (IGFBP3) expression. Based onintestinal parameters related to the specific colon carcinogenesis in an AOM-DSS-induced model, LYC and microencapsulated BF supplementation resulted in a significant chemopreventive potential through the modulation of IGF-1/IGF-1R system.

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zingerone modulates hyperglycaemia, hyperlipidaemia, oxidative biochemical markers and degenerative changes in β-cells of treated diabetic groups.

PMID: 

Arch Physiol Biochem. 2019 Aug 7:1-7. Epub 2019 Aug 7. PMID: 31389247

Abstract Title: 

Modulatory effect of zingerone against STZ-nicotinamide induced type-2 diabetes mellitus in rats.

Abstract: 

The objective of this research was to explore the role of zingerone on hyperglycemia, hyperlipidemia, insulin level, oxidative biochemical markers and histological alterations inβ-cells of type-2 diabetic rats. The outcome of this study illustrates reduction in glucose and insulin levels significantly in zingerone-treated diabetic groups. Lipid parameters were resumed to normal in zingerone-treated diabetic group as demonstrated by significant reduction in triglycerides, cholesterols (total, low-density and very low-density) levels along with significant increase high-density cholesterols levels. Zingerone-treated diabetic groups exhibited significant reduction in LPO levels and restoration of GSH contents. Administration of zingerone to treated diabetic groups indicated improvement in antioxidant enzymes (GPx, GR, GST, SOD and CAT). Administration of zingerone to treated diabetic groups minimized degeneration of pancreatic β-cells as witnessed from histopathological studies. Our results demonstrate that zingerone modulates hyperglycaemia, hyperlipidaemia, oxidative biochemical markers and degenerative changes in β-cells of treated diabetic groups.

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Zingerone induced caspase-dependent apoptosis in MCF-7 cells and prevents 7,12-dimethylbenz(a)anthracene-induced mammary carcinogenesis.

PMID: 

J Biochem Mol Toxicol. 2019 Sep 2:e22387. Epub 2019 Sep 2. PMID: 31476248

Abstract Title: 

Zingerone induced caspase-dependent apoptosis in MCF-7 cells and prevents 7,12-dimethylbenz(a)anthracene-induced mammary carcinogenesis in experimental rats.

Abstract: 

Breast cancer is a prevalent of tumoregenesis in women and reports for the maximum mortality and morbidity in the global. Ginger (Zingiber officinale) is the mainly widespread spice and herbal remedies used in the world. Since antique periods, ginger has been used in Greece, India and China for the curing of upset stomach, nausea, diarrhea, colds, and headaches. The current work was planned to explore the anticancer properties of zingerone (ZO) toward 7,12-dimethylbenz(a)anthracene (DMBA)-treated mammary carcinogenesis in Sprague-Dawley (SD) rats and MCF-7 mammary cancer cells. The mammary carcinogenesis was produced through a single dosage of DMBA (20 mg/kg bwt) mixed in soya oil (1 mL) administrated intragastrically with a gavage. We found improved concentrations of lipid peroxidation (LOOH and TBARS), carcinoembryonic antigen, lowered levels of enzymatic (CAT, GPx, and SOD), and nonenzymatic (vitamin E, GSH, and vitamin C) antioxidant in mammary tissues and plasma of DMBA-induced cancer bearing animals. Moreover, augmented concentrations of phase I (Cyt-band CYP) and reduced levels of phase II (GR and GST) detoxification microsomal proteins in mammary tissues were noticed. ZO administrations significantly reverted back to all these parameters in this way, showing efficient of anticancer effect. Furthermore, our in vitro study also supported the anticancer effect of the treatment of ZO were noticed loss of cell viability, improved reactive oxygen species formation, and reduced MMP. Furthermore, the status of apoptosis proteins such as Bcl-2, Bax, and Bid expressions was determined by using Western blot analysis techniques. Overall, these results proposed the anticancer effect of ZO toward DMBA-induced mammary cancer in SD animals and Michigan cancer foundation-7 mammary cancer cells.

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In vitro antioxidant and in vivo lipid-lowering properties of Zingiber officinale crude aqueous extract.

PMID: 

Evid Based Complement Alternat Med. 2019 ;2019:9734390. Epub 2019 Jul 9. PMID: 31360211

Abstract Title: 

Antioxidant andLipid-Lowering Properties ofCrude Aqueous Extract and Methanolic Fraction: A Follow-Up Study.

Abstract: 

Over the past decades, cardiovascular diseases have become the leading cause of death all over the world, and among these diseases there is atherosclerosis caused mainly by an increase in plasmatic cholesterol levels and by strong oxidation caused by free radicals. For these reasons and others, we explored in this report the hypolipidemic and the antioxidant effects ofcrude aqueous and methanolic extract. The hypolipidemic study was carried out in high-fat-fed mice model. Animals were subdivided into four groups and were orally treated with the aqueous extract once daily for twelve weeks at two doses: 250 and 500 mg/Kg. During the treatment, the body weight, total cholesterol, triglycerides, and high-density lipoproteins have been defined every four weeks. The antioxidant activity has been studied using radical scavenging activity,-carotene bleaching, reducing power assay, and the TBARs tests. The daily oral administration of the extracts for twelve weeks significantly improved the lipid profile in a dose-dependent manner, from the first until the twelfth week, and also showed a significant antioxidant effect. These findings may be potentially contributive to the validation of the medicinal use ofto treat hyperlipidemia and cardiovascular complications.

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Pre-treatment with beta carotene gives protection against nephrotoxicity induced by bromobenzene.

PMID: 

Appl Biochem Biotechnol. 2019 Aug 13. Epub 2019 Aug 13. PMID: 31407161

Abstract Title: 

Pre-treatment with Beta Carotene Gives Protection Against Nephrotoxicity Induced by Bromobenzene via Modulation of Antioxidant System, Pro-inflammatory Cytokines and Pro-apoptotic Factors.

Abstract: 

Bromobenzene is an environmental toxin which causes hepatotoxicity, and the secondary metabolites on biotransformation cause nephrotoxicity. The objective of this study was to assess the alleviation of the nephrotoxic effect of bromobenzene by beta carotene in female Wistar albino rats. Beta carotene (10 mg/kg b.w.p.o.) was delivered orally to the rats for 9 days before bromobenzene (10 mM/kg b.w.p.o.) was intragastrically intubated. Kidney markers, antioxidant status and lipid peroxidation were evaluated. In addition, the levels of TNF-α, IL-6 and IL-1β were measured in serum and in kidney tissue homogenate using ELISA. Caspase, COX-2 and NF-κB were measured with the help of Western blotting. Histopathological analysis of the kidney was done for the control and experimental rats. Bromobenzene induction caused elevation in levels of creatinine, urea, uric acid, cytokines and lipid per oxidation along with deterioration in histological observations and antioxidant status. Pre-treatment with beta carotene significantly (*p 

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The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects.

PMID: 

Biomolecules. 2019 Sep 2 ;9(9). Epub 2019 Sep 2. PMID: 31480727

Abstract Title: 

β-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer's Disease.

Abstract: 

Alzheimer's disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson's, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular,β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in theprotocol, and they were classified into five groups (Group I-control, Group II-disease, Group III-standard, Group IV-V-β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by themolecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could beuseful for the treatment of neurodegenerative diseases such as Alzheimer's disease.

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WARNING: A form of planetary climate change no one is talking about

I need to be perfectly candid with you. Our planet is facing a health crisis scenario so extreme that one might easily mistake it for a badly written science fiction film.

But the facts speak for themselves, and the growing concern around the world is entirely valid…

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β-Carotene is a potent anti-inflammatory agent that improves the barrier functions of atopic dermatitis skin.

PMID: 

Exp Dermatol. 2019 Sep ;28(9):1044-1050. Epub 2019 Aug 8. PMID: 31287602

Abstract Title: 

Effects ofβ-carotene on oxazolone-induced atopic dermatitis in hairless mice.

Abstract: 

Skin acts as a barrier, which protects internal tissues and promotes moisture retention. Atopic dermatitis (AD) is an inflammatory skin disease associated with a variety of genetic and environmental factors that involve helper T cells.β-Carotene (provitamin A) exhibits antioxidant activity and activates the immune system. However, it is not clear whether inflammation in AD skin is improved by posttreatment with β-carotene. In the current study, we investigated the effects of β-carotene on the skin of hairless mice with oxazolone-induced inflammation/oedema (Ox-AD mice). We found that skin inflammation was significantly reduced by oral administration of β-carotene. In addition, treatment with β-carotene suppressed protein levels of TNF-α, IL-1β and MCP-1, as well as mRNA expression associated with IL-1β, IL-6, IL-4 and Par-2 in skin tissues. Furthermore, the mRNA and protein levels of filaggrin, a structural protein in the epidermal stratum corneum, were elevated by β-carotene administration as compared with Ox-AD mice. β-Carotene significantly reduced the activity of proMMP-9, but not proMMP-2. These resultssuggest that in Ox-AD mice, β-carotene improves skin inflammation by suppressing the expression of inflammatory factors, promoting filaggrin expression and reducing MMP-9 activity. β-Carotene is a potent anti-inflammatory agent that improves the barrier functions of AD skin.

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