vitamin d 
We Have Found 644 Papers
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Born (osteoporosis)
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Bioactive Compound
Type of Study
Mechanism Keyword
  • Decrease Of Hfs-induced Inflammation In Inguinal Adipose Tissue, Characterized By A Decreased Expression Of Chemokine Mrna Levels

  • Via The Suppression Of Mtor Signaling Pathway

  • By Regulation Of The Cell Cycle, Apoptosis, And Inflammation

  • Modulate Il-33 Signaling

  • Through Vdr And Mutp53 Interaction Followed By The Modulation Of P21/cdk2

  • Regulating The Expression Of Nlrp6

  • Increasing The Vdr/p-rhoa/p-ezrin Pathway

  • By Inhibiting The Perk-atf4-chop Pathway

  • Did Not Affect Gingival Il-1b And Il-10, Serum B-alp And Trap-5b Levels, Or Alveolar Bone

  • Mediated Through The Sirt3–sod2–mtros Signaling Pathway

  • Inhibits Il-12 Production

  • Restoring The Lpmc Macrophage Subtype Balance

  • Calcitriol-enhanced Autophagy

  • Inhibit The Activation Of Th1 And Th17 Cells

  • Via The Paraventricular Nuclei And Energy Homeostasis Via The Arcuate Nuclei

  • Anti-infammatory Efect

  • Interaction Between Vitamin D3 And Muscarinic M3 Receptors In Regulating Insulin Secretion From Pancreas

  • Induction Of Fatty Acid Oxidation

  • Ampk/nf-b Signaling

  • Nf-κb- Dmt1 Signaling.

  • Promotion Of Fa Oxidation

  • Inhibiting Nf-b And Mapk Signaling Pathways In Svcs But Not By The Inhibition Of Macrophage Infiltration

  • Transcript Levels Of The Gastrointestinal Glutathione Peroxidase 2, Which Acts As A Radical Scavenger, Were Significantly Down-regulated

  • Downregulates Catg Expression And Inhibits Cd4 þ T Cell Activation

  • Increased Colonic Cyp27b1 Levels, Leading To Upregulation Of Local 1,25-dihydroxy Vitamin D Production

  • Abrogating Mlck-dependent Tight Junction Dysregulation During Colonic Inflammation

  • Inhibiting Akt/mtor Signaling And Inducing Apoptosis

  • Anti-inflammatory Effects

  • Through Downregulation Of Tlr4 And Jak1/stat3 Signaling In The Gingival Epithelium

  • Unfavorable Effect On Central Obesity And Body Composition

  • Inactivating Nf-κb Pro-inflammatory Signaling

  • Regulation Of Ahr/nf-κb/nlrp3 Inflammasome Pathway By Vd3

  • Decreasing Tlr9 Expression

  • Promote Cathelicidin And Ameliorate The Severity Of Diabetic Periodontitis

  • Through Downregulating Cd44

  • Blocked Tgf-β Signaling, Nf-κb Signaling, Stat3 Signaling, And Activated Nrf2 Singling

  • Inhibitory Effect On The Pro-inflammatory Cytokines

  • Through A Vdr-dependent C-raf/mek/erk Pathway

  • Decreasing Hba1c And Increasing Sirt1 And Irisin

  • Mediated By P-stat-6 And Smad-7 Signal

  • By Partially Inhibiting Chemokine Production

  • Inhibiting The Progression Of Apoptosis

  • By Suppressing Vegfr2 And Erk1/2 Activation And Downregulating Adam33

  • Through The Hmgb1/tlr4/nf-κb Signaling Pathway

  • Promote Apoptosis

  • Interleukin (il)-4, Il-12, Il-13, Interferon-γ, And Ovalbumin-specific Immunoglobulin E Secretion And The Expression Of P-jak1/p-stat6/socs5

  • Through Modulating Cholinergic Transmission In The Prefrontal Cortex

  • Via The Suppression Of Tgf-β/smad Signaling And Activation Of The Nrf2/ho-1 Pathway

  • Alleviated Tau Accumulation And Rescued Methylated Pp2a By Increasing The Expression Of Lcmt-1 And Mthfr

  • Inhibited The Increase Of Bone Turnover And Prevented The Reduction Of Cancellous Bone Mass After A Long Time Postovariectomy. Key Words: 24r,25(oh)2d3—bone Turnover—bone Mineral Content—ovariectomized Dogs—histomorphometry.

  • Inhibiting The Erk1/2 Pathway

  • Maintaining Bp By Regulating Expression Of Genes Involved In Hypertension Pathways But Did Not Induce Dna Damage Or Changes In The Tbars And Gsh Levels

  • By Elevating The Th1 Subtype And The Proportion Of Cd4+cd25+foxp3+tregs In Offspring

  • Significantly Abrogate Damage Related To Oxidative Stress Mediated Neuroinflammation

  • Blocking The P53-p21 Signaling Pathway

  • Vdr-dependent Mechanisms

  • Inhibition Of Oxidative Stress Via Activation The Pi3k/akt/nrf2 Pathway

  • Modulation Of The Intersection Between Insulin/akt/ Gsk-3β And Canonical/non-canonical Wnt/β-catenin Trajectories

  • Vitamin D3 Supplementation Appears To Play A Role In Maintaining Bp By Regulating Expression Of Genes Involved In Hypertension Pathways But Did Not Induce Dna Damage Or Changes In The Tbars And Gsh Levels.

  • Regulating Snail/e-cad/emt Pathway

  • Aβ42 Plays A Crucial Role

  • Inhibited Inflammatory Cytokines And Decreased Bbb Disruption In Tbi Rats

  • Improving Bdnf Levels And Attenuating No And Brain Tissue Oxidative Damage

  • Through Increasing The Immune Level Of Mice.

  • Moreover, The Osteoporosis-associated M-csfr And Rankl Factors Were Both Significantly Downregulated By The Ca/ Vitd-m/zn-m Treatment In Bone Tissues Of Ovx Rats.

  • Decreased Neuro-inflammation And Amyloid β Load As Well As Hyperphosphorylation Of Mapk-38, Erk1/2

  • Pi3k/akt/foxo1 Signaling Pathway Is Involved In The Osteoprotective Effect Of 1,25d By Attenuating Autophagy

  • Hdac2 Activator

  • There Are Further Effects On Increasing Transcription Factor Osterix Expression And Preosteoblast Proliferation When These Were Combined With Vitamin D3.

  • The Proliferation Rate Of Splenic Lymphocytes Was Higher In The Ifn-α + Vd Group Compared With The Ifn-α Group. Ifn-α + Vd Was Found To Achieve Higher Efficacy Than Ifn-α Alone For The Treatment Of Hepatitis B In Mice, Possibly Through Increasing The Immune Level Of Mice.

  • It Is Concluded That, Besides Sharing The Hypotensive Effect Of Calcium, Vitamin D Treatment Of Shr Has An Effect On The Duodenum Smooth Muscle Which Might Be Due To Calmodulin-dependent Activation Of Calcium-dependent Potassium Channels

  • Might Potentially Accelerate Rv Dysfunction

  • Modulation Of Renineangiotensin System, Inflammation And Pth

  • Increases Lpa Receptor-1 (lpa R1) Expression And Production Of Lysophosphatidic Acid (lpa), And Subsequent Lpa R1/3-dependent Signaling

  • Inhibiting Rb And Chk1 Phosphorylation

  • Suggest That Ed-71 May Exert Its Effect As A Unique Vdr Ligand With Stronger Effect On Bone Compared To The Natural Ligand, 1,25(oh)2d3.

  • Reducing The Ip-10 Production From Pbmcs And Isgs Expression In The Liver.

  • Through Reducing Oxidative Stress

  • This Would Be Useful In Understanding Whether The Effects Of Vitamin D On The Brain Are Independent Of The Homeostatic Pathways That Regulate Serum Calcium And Phosphorus.

  • By Acting As A Negative Regulator Of Renin

  • Oral 1,25(oh)2d Administration Decreased 1-84pth Levels, Probably Due To A Suppression Of Parathyroid Production, And Did Not Stimulate Bone Resorption. Since Only Bone Gla Protein Increased, It Is Unclear Whether Or Not Bone Formation Was Actually Stimulated.

  • 1,25(oh)2d3 Promotes The Production Of Igf-i And B2 Microglobulin In Osteoporotic Patients In Parallel To The Marker Of Osteoblastic Function

  • Cbd103 Expression

  • Suggest That Vitamin D Supplementation May Ameliorate Symptoms Of Mdd, Particularly In Females, Via A Serotonin-dependent Mechanism

  • Serotonin-dependent Mechanism

  • Vitamin D And Calcium Supplementation Is Associated With Altered Mineral And Organic Matrix Properties.

  • The Effect Of Topical Clat And Hu Was Dependent On Serum 25hd Levels

  • Vitamin D Supplementation Was Effective In Ameliorating The Severity Of Gad Symptoms By Increasing Serotonin Concentrations And Decreasing The Levels Of The Inflammatory Biomarker Neopterin In Gad Patients.

  • Vitamin D3 Therapy In Obese Hypertensives Modified Rpf, Map, And Tissue Sensitivity To Angii Similar To Converting Enzyme Inhibition.

  • Vitamin D Supplementation In Obese Hypertensive Patients With Low 25-hydroxyvitamin D Reduces Hba1c.

  • Abrogates The Development Of Diseases Associated With Excess Ras Activity

  • A Theoretical Disadvantage Of Calcium Supplements Is That They Depress Bone Turnover By Suppressing Serum Levels Of Parathyroid Hormone And 1,25-dihydroxyvitamin D.

  • Increasing Foxp3 Expressing Cd4+cd25+ Treg Cell Frequency

  • In Both Instances, The Vitamin D Metabolites Exert Their Effects On Pkc Through Changes In Arachidonic Acid Via The Action Of Pla2. In Addition, Pkc By Itself May Mediate The Production Of Pge2.

  • Decreasing Brain Oxidative Stress And Inhibiting Neuroinflammation

  • Erk1/2 Pathway

  • These Changes Were Reflected In A Significant Improvement In Visual Function, Revealing That Vitamin D3 Is A Route To Avoiding The Pace Of Age-related Visual Decline.

  • By Inhibiting The Nf-κb Pathway In Asthmatic Mice

  • Results Suggest That The Pi3k/akt/foxo1 Signaling Pathway Is Involved In The Osteoprotective Effect Of 1,25d By Attenuating Autophagy In Diabetes

  • By Lowering The Expression Of Cyp27a1 And Regulating The Levels Of 27-ohc And Sam

  • By Down-regulating The Activity Of Wnt/β-catenin Signaling Pathway

  • Reducing Nitric Oxide Formation In Serum And The Expression Of Nuclear Factor Kappa B P65 In The Lung

  • Decrease Aβ-related Biomarkers

  • Findings Outlined In The Current Study Demonstrated That 1,25(oh)2d3 Was A Promising Therapeutic Modality For Treatment Of Pah, Function Of Which Was Exerted Through Mir-204 Mediated Tgfbr2 Signaling.

  • Regular Vitamin-d Treatment Can Improve ‘anhedonia-like Symptoms’ In Rats Subjected To Cms, Probably By Regulating The Effect Of Dopamine-related Actions In The Nac.

  • 1,25(oh)2d Deficiency Accelerated Age-related Bone Loss By Activating The P16/p19 Senescence Signaling Pathway, Inhibiting Osteoblastic Bone Formation, And Stimulating Osteoclastic Bone Resorption, Osteocyte Senescence, And Senescence-associated Secretory Phenotype (sasp).

  • Rc Cells To 1α,25-(oh)2d3 But It Blocked The Effect Of Rhtgf-β1, Indicating That Decreases In Stathmin By Vitamin D3 Metabolites May Not Be Modulated By Pkc, Whereas Increases In Stathmin Via Rhtgf-β1 May Be Regulated Via A Pkc-dependent Mechanism

  • Inhibiting The P16/p19 Pathway

  • Via The Combination Of Vitamin D3 And Ifn

  • Reduced Numbers Of Lung Th2/th17 Cells

  • Regulation Of Bdnf And The Nt-3/nt-4 Signaling Pathways

  • High Dose Of Vitamin D3 (5.0 Mg/kg Sc) Could Improve The Depression-like Profile In Long-term Ovx Adult Female Rats Subjected To The Cums Procedure, Which Might Be Mediated By The Regulation Of Bdnf And The Nt-3/nt-4 Signaling Pathways In The Hippocampus, As Well As The Corticosterone/acth Levels Of The Blood Serum

  • By Downregulating Hrc

  • Calmodulin-dependent Activation Of Calcium-dependent Potassium Channels

  • Vitd Regulates Infection Through Cbd103 Expression

  • 24r,25(oh)2d3 Increases Lpa Receptor-1 (lpa R1) Expression And Production Of Lysophosphatidic Acid (lpa), And Subsequent Lpa R1/3-dependent Signaling, Thereby Decreasing P53 Abundance. Lpa Also Increases The Bcl-2/bax Ratio. In Addition, 24r,25(oh)2d3 Acts By Increasing Pkc Activity. 24r,25(oh)2d3 Stimulates 1-hydroxylase Activity, Resulting In Increased Levels Of 1,25(oh)2d3, And It Increases Levels Of Phospholipase A2 Activating Protein, Which Is Required For Rapid 1,25(oh)2d3dependent Activation Of Pkc In Gc Cells. These Results Suggest That 24r,25(oh)2d3 Modulates Growth Plate Development By Controlling The Rate And Extent Of Rc Chondrocyte Transition To A Gc Chondrocyte Phenotype.

  • Reduce Inflammation

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