via Health News Spirulina http://www.greenmedinfo.com/article/s-platensis-may-represent-potential-therapeutic-option-protect-testicular
PMID: Oxid Med Cell Longev. 2016 ;2016:7174351. Epub 2016 Jan 13. PMID: 26881036 Abstract Title: Antioxidant Potential of Spirulina platensis Mitigates Oxidative Stress and Reprotoxicity Induced by Sodium Arsenite in Male Rats. Abstract: The present study aimed to examine the protective role of Spirulina platensis (S. platensis) against arsenic-induced testicular oxidative damage in rats. Arsenic (in the form of NaAsO2 at a dose of 6.3 mg/kg body weight for 8 weeks) caused a significant accumulation of arsenic in testicular tissues as well as a decrease in the levels of testicular superoxide dismutase (SOD), catalase (CAT), reduced glutathione, and zinc. Moreover, it significantly decreased plasma testosterone, luteinizing hormone (LH), triiodothyronine (T3), and thyroxine (T4) levels and reduced sperm motility and sperm count. Arsenic (AS) led to a significant increase in testicular malondialdehyde (MDA), tumour necrosis factor alpha (TNF-α), nitric oxide (NO), and sperm abnormalities. S. platensis at a dose of 300 mg/kg was found to attenuate As-induced oxidative stress, testicular damage, and sperm abnormalities by its potent antioxidant activity. S. platensis may represent a potential therapeutic option to protect the testicular tissue from arsenic intoxication.
via Health News Spirulina http://www.greenmedinfo.com/article/s-platensis-may-represent-potential-therapeutic-option-protect-testicular
0 Comments
Spirulina maxima significantly reduced the number of AOM-induced colon aberrant crypts in mice.3/31/2016
PMID: Pharmacogn Mag. 2015 Oct ;11(Suppl 4):S619-24. PMID: 27013804 Abstract Title: Inhibitory Effect of Spirulina maxima on the Azoxymethane-induced Aberrant Colon Crypts and Oxidative Damage in Mice. Abstract: BACKGROUND: Spirulina maxima (Sm) is a cyanobacterium well known because of its high nutritive value, as well as its anti-inflammatory, anti-hyperlipidemic, antioxidant, and anti-genotoxic activities.OBJECTIVE: To determine the capacity of Sm to inhibit the induction of aberrant colon crypts (AC), as well as the level of lipid peroxidation and DNA oxidative damage in mice treated with azoxymethane (AOM).MATERIALS AND METHODS: Sm (100, 400, and 800 mg/kg) was daily administered to animals by the oral route during 4 weeks, while AOM (10 mg/kg) was intraperitoneally injected to mice twice in weeks 2 and 3 of the assay. We also included a control group of mice orally administered with distilled water along the assay, as well as other group orally administered with the high dose of Sm.RESULTS: A significant decrease in the number of AC with the three tested doses of Sm, with a mean protection of 51.6% respect to the damage induced by AOM. Also, with the three doses of the alga, we found a reduction in the level of lipoperoxidation, as well as in regard to the percentage of the DNA adduct 8-hydroxy-2'- deoxyguanosine.CONCLUSION: Sm possesses anti-precarcinogenic potential in vivo, as well as capacity to reduce the oxidative damage induced by AOM.SUMMARY: Azoxymethane (AOM) induced a high number of colon aberrant crypts in mouse. It also increased the level of peroxidation and of DNA oxidation in the same organ.Spirulina maxima significantly reduced the number of AOM-induced colon aberrant crypts in mouse. It also reduced the AOM-induced lipid and DNA oxidation in mouse.The results suggest a chemopreventive potential for the tested algae.
via Health News Spirulina http://www.greenmedinfo.com/article/spirulina-maxima-significantly-reduced-number-aom-induced-colon-aberrant
PMID: Mol Neurobiol. 2016 Mar 28. Epub 2016 Mar 28. PMID: 27021021 Abstract Title: The Protective Role of Selenium on Scopolamine-Induced Memory Impairment, Oxidative Stress, and Apoptosis in Aged Rats: The Involvement of TRPM2 and TRPV1 Channels. Abstract: Inhibition of Ca(2+) entry into the hippocampus and dorsal root ganglion (DRG) through inhibition of N-methyl-D-aspartate (NMDA) receptor antagonist drugs is the current standard of care in neuronal diseases such as Alzheimer's disease, dementia, and peripheral pain. Oxidative stress activates Ca(2+)-permeable TRPM2 and TRPV1, and recent studies indicate that selenium (Se) is a potent TRPM2 and TRPV1 channel antagonist in the hippocampus and DRG. In this study, we investigated the neuroprotective properties of Se in primary hippocampal and DRG neuron cultures of aged rats when given alone or in combination with scopolamine (SCOP). Thirty-two aged (18-24 months old) rats were divided into four groups. The first and second groups received a placebo and SCOP (1 mg/kg/day), respectively. The third and fourth groups received intraperitoneal Se (1.5 mg/kg/ over day) and SCOP + Se, respectively. The hippocampal and DRG neurons also were stimulatedin vitro with a TRPV1 channel agonist (capsaicin) and a TRPM2 channel agonist (cumene hydroperoxide). We found that Se was fully effective in reversing SCOP-induced TRPM2 and TRPV1 current densities as well as errors in working memory and reference memory. In addition, Se completely reduced SCOP-induced oxidative toxicity by modulating lipid peroxidation, reducing glutathione and glutathione peroxidase. The Se and SCOP + Se treatments also decreased poly (ADP-ribose) polymerase activity, intracellular free Ca(2+) concentrations, apoptosis, and caspase 3, caspase 9, and mitochondrial membrane depolarization values in the hippocampus. In conclusion, the current study reports on the cellular level for SCOP and Se on the different endocytotoxic cascades for the first time. Notably, the research indicates that Se can result in remarkable neuroprotective and memory impairment effects in thehippocampal neurons of rats. Graphical abstract Possible molecular pathways of involvement of selenium (Se) in scopolamine (SCOP) induced apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in the hippocampus neurons of aged rats. The TRPM2 channel is activated byADP-ribose and oxidative stress, although it is inhibited by ACA. The TRPV1 channel is activated by oxidative stress and capsaicin, and it is blocked by capsazepine (CPZ). The beta-amyloid plaque induces oxidative stress in hippocampus. SCOP can result in augmented ROS release in hippocampal neurons, leading to Ca(2+) uptake through TRPM2 and TRPV1 channels. Mitochondria were reported to accumulate Ca(2+) provided that intracellular Ca(2+) rises, thereby leading to the depolarization of mitochondrial membranes and release of apoptosis-inducing factors such as caspase 3 and caspase 9. Se reduced TRPM2 and TRPV1 channel activation through the modulation of aging oxidative reactions and Se-dependent glutathione peroxidase (GSH-Px) antioxidant pathways.
via Health News Spirulina http://www.greenmedinfo.com/article/selenium-has-protective-role-against-scopolamine-induced-memory-impairment
PMID: Comp Biochem Physiol A Mol Integr Physiol. 2016 Mar 9 ;197:16-22. Epub 2016 Mar 9. PMID: 26970583 Abstract Title: Melatonin not only restores but also prevents the inhibition of the intestinal Ca(2+) absorption caused by glutathione depleting drugs. Abstract: We have previously demonstrated that melatonin (MEL) blocks the inhibition of the intestinal Ca(2+) absorption caused by menadione (MEN). The purpose of this study were to determine whether MEL not only restores but also prevents the intestinal Ca(2+) absorption inhibited either by MEN or BSO, two drugs that deplete glutathione (GSH) in different ways, and to analyze the mechanisms by which MEN and MEL alter the movement of Ca(2+) across the duodenum. To know this, chicks were divided into four groups: 1) controls, 2) MEN treated, 3) MEL treated, and 4) treated sequentially with MEN and MEL or with MEN and MEL at the same time. In a set of experiments, chicks treated with BSO or sequentially with BSO and MEL or with BSO and MEL at the same time were used. MEL not only restored but also prevented the inhibition of the chick intestinal Ca(2+) absorption produced by either MEN or BSO. MEN altered the protein expression of molecules involved in the transcellular as well as in the paracellular pathway of the intestinal Ca(2+) absorption. MEL restored partially both pathways through normalization of the O2(-) levels. The nitrergic system was not altered by any treatment. In conclusion, MEL prevents or restores the inhibition of the intestinal Ca(2+) absorption caused by different GSH depleting drugs. It might become one drug for the treatment of intestinal Ca(2+) absorption under oxidant conditions having the advantage of low or null side effects.
via Health News Spirulina http://www.greenmedinfo.com/article/melatonin-prevents-or-restores-inhibition-intestinal-ca2-absorption-caused
PMID: Mov Disord. 2016 Mar 12. Epub 2016 Mar 12. PMID: 26971528 Abstract Title: Hypothalamic volume loss is associated with reduced melatonin output in Parkinson's disease. Abstract: BACKGROUND: Recent studies have suggested that melatonin-a hormone produced by the pineal gland under circadian control-contributes to PD-related sleep dysfunction. We hypothesized that degenerative changes to the neural structures controlling pineal function (especially the suprachiasmatic nuclei of the anterior hypothalamus) may be responsible for reduced melatonin output in these patients. We compared hypothalamic volumes in PD patients with matched controls and determined whether volume loss correlated with reduced melatonin output in the PD group.METHODS: A total of 12 PD patients and 12 matched controls underwent magnetic resonance imaging to determine hypothalamic volume. In addition, PD patients underwent 24-hour blood sampling in a controlled environment to determine serum melatonin concentrations using enzyme-linked immunosorbent assays.RESULTS: PD patients had significantly reduced hypothalamic gray matter volume when compared with matched controls. Melatonin levels were significantly associated with hypothalamic gray matter volume and disease severity in PD patients.CONCLUSION: Melatonin levels are associated with hypothalamic gray matter volume loss and disease severity in PD patients. This provides anatomical and physiological support for an intrinsic sleep and circadian phenotype in PD.© 2016 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
via Health News Spirulina http://www.greenmedinfo.com/article/melatonin-levels-are-associated-hypothalamic-gray-matter-volume-loss-and
PMID: Oncotarget. 2016 Mar 9. Epub 2016 Mar 9. PMID: 26980735 Abstract Title: Melatonin inhibits TPA-induced oral cancer cell migration by suppressing matrix metalloproteinase-9 activation through the histone acetylation. Abstract: Melatonin exerts antimetastatic effects on liver and breast cancer and also inhibits matrix metalloproteinase (MMP) activity. However, the detailed impacts and underlying mechanisms of melatonin on oral cancer cell metastasis are still unclear. This study showed that melatonin attenuated the 12-O-tetradecanoylphorbol-13-acetate-induced migration of oral cancer cell lines, HSC-3 and OECM-1. Zymography, quantitative real-time PCR, and Western blotting analyses revealed that melatonin lessened MMP-9 enzyme activity as well as the expression of MMP-9 mRNA and protein. Furthermore, melatonin suppressed the phosphorylation of the ERK1/2 signalling pathway, which dampened MMP-9 gene transcription by affecting the expression of transcriptional coactivators, such as CREB-binding protein (CREBBP) and E1A binding protein p300 (EP300), and decreasing histone acetylation in HSC-3 and OECM-1 cells. Examinations on clinical samples exhibited that MMP-9, CREBBP, and EP300 were significantly increased in oral cancer tissues. Moreover, the relative level of CREBBP was positively correlated with the expression of MMP-9 and EP300. In conclusion, we demonstrated that melatonin inhibits the motility of HSC-3 and OECM-1 cells in vitro through a molecular mechanism that involves attenuation of MMP-9 expression and activity mediated by decreased histone acetylation.
via Health News Spirulina http://www.greenmedinfo.com/article/inhibition-oral-cancer-metastasis-melatonin-can-provide-crucial-preventive-and
PMID: Pain Ther. 2016 Mar 16. Epub 2016 Mar 16. PMID: 26984272 Abstract Title: Melatonin in Chronic Pain Syndromes. Abstract: Melatonin is a neurohormone secreted by epiphysis and extrapineal structures. It performs several functions including chronobiotic, antioxidant, oncostatic, immune modulating, normothermal, and anxiolytic functions. Melatonin affects the cardiovascular system and gastrointestinal tract, participates in reproduction and metabolism, and body mass regulation. Moreover, recent studies have demonstrated melatonin efficacy in relation to pain syndromes. The present paper reviews the studies on melatonin use in fibromyalgia, headaches, irritable bowel syndrome, chronic back pain, and rheumatoid arthritis. The paper discusses the possible mechanisms of melatonin analgesic properties. On one hand, circadian rhythms normalization results in sleep improvement, which is inevitably disordered in chronic pain syndromes, and activation of melatonin adaptive capabilities. On the other hand, there is evidence of melatonin-independent analgesic effect involving melatonin receptors and several neurotransmitter systems.
via Health News Spirulina http://www.greenmedinfo.com/article/paper-discusses-possible-mechanisms-melatonins-analgesic-properties
PMID: Mediators Inflamm. 2016 ;2016:9050828. Epub 2016 Feb 18. PMID: 26989334 Abstract Title: Melatonin Attenuates Contrast-Induced Nephropathy in Diabetic Rats: The Role of Interleukin-33 and Oxidative Stress. Abstract: Background. Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKD and CIN is unknown. Methods. Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrast-induced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), and melatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50 mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5 mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs and MTCIN + DRs were given 20 mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days. Results. Weobserved increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN+ DRs compared with other groups without MT treatment (p
via Health News Spirulina http://www.greenmedinfo.com/article/inhibition-interleukin-33-melatonin-provides-therapeutic-potential-diabetic
PMID: Head Neck. 2016 Feb 5. Epub 2016 Feb 5. PMID: 26849799 Abstract Title: Vitamin E neuroprotection against cisplatin ototoxicity: Preliminary results from a randomized, placebo-controlled trial. Abstract: BACKGROUND: Few studies have investigated the effect of vitamin E in reducing the cisplatin (CDDP)-induced ototoxicity. This study evaluated vitamin E supplementation as a protecting agent against CDDP-induced ototoxicity.METHODS: Patients who started CDDP were randomly assigned to receive vitamin E supplementation at 400 mg per day (group 1) or placebo (group 2). Audiograms and evoked brainstem responses were obtained at baseline, and after 1, 2, and 3 months.RESULTS: Twenty-three patients affected by solid malignancies were enrolled (13 in group 1 and 10 in group 2). At 1 month, a significant hearing loss in group 2 at both 2000 HZ (right ear: p = .05; left ear: p = .04) and 8000 HZ (right ear: p = .04; left ear: p = .03) was detected when compared to baseline values. Audiograms did not show significant changes. At 1 month, evoked brainstem responses remained unchanged in both arms without significant differences between groups.CONCLUSION: These preliminary findings confirm the neuroprotective properties of vitamin E against the CDDP-induced ototoxicity.© 2016 Wiley Periodicals, Inc. Head Neck, 2016.
via Health News Spirulina http://www.greenmedinfo.com/article/these-preliminary-findings-confirm-neuroprotective-properties-vitamin-e
PMID: J Pineal Res. 2016 Mar 18. Epub 2016 Mar 18. PMID: 26993080 Abstract Title: Melatonin pretreatment enhances the therapeutic effects of exogenous mitochondria against hepatic ischemia-reperfusion injury in rats through suppression of mitochondrial permeability transition. Abstract: We tested the hypothesis that melatonin (Mel) enhances exogenous mitochondria (Mito) treatment against rodent hepatic ischemia-reperfusion (IR) injury. In vitro study utilized three groups of hepatocytes (i.e., non-treatment, menadione, and menadione-melatonin treatment, 4.0 x 10(5) each), while in vivo study involved adult male Sprague-Dawley rats (n=40) equally divided into sham-control (SC), IR (60-min left lobe ischemia + 72-hr reperfusion), IR-Mel (melatonin at 30 min/6h/8h after reperfusion), IR-Mito (mitochondria 15000μg/rat 30 min after reperfusion), and IR-Mel-Mito. Following menadione treatment in vitro, oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptotic (cleaved caspase-3/PARP), DNA-damage (γ-H2AX/CD90/XRCC1), mitochondria-damage (cytosolic cytochrome-C) biomarkers and mitochondrial permeability transition were lower, whereas mitochondrial cytochrome-C were higher in hepatocytes with melatonin treatment compared to those without (all p
via Health News Spirulina http://www.greenmedinfo.com/article/melatonin-pre-treatment-enhances-therapeutic-effects-exogenous-mitochondria |
AuthorWrite something about yourself. No need to be fancy, just an overview. Archives
November 2016
Categories |