vitamin d 
We Have Found 644 Papers
Bird Score
Ingredients
Main Function
Skin
Born (osteoporosis)
Asthma
Intestine
Blood Glucose
Diabetes
Obesity
Hypertension
Women's Monopause
Hepatitis
Osteoporosis
Fatty Liver
Periodontitis
Muscle
Urination
Growth Plate
Memory
Stress
Gastric Cancer
Eye Disease
Helicobacter Pylori
Immune
Sleeping Disturbance
Breast Cancer
Alzheimer's Disease (ad)
Fatigue
Bone Loss
Osteoporotic
Allergic Rhinitis
Major Depressive Disorder
Born (osteoarthritis)
Cognitive Impairment
Lung Cancer
Bone
Osteoarthritis
Periodontiti
Thyroid Cancer
Lung Carcinoma
Alopecia
Depressive Symptoms
Cognitive Function
Essential Hypertension
Bronchial Asthma
Bacterial Vaginosis (bv)
Dry Eye Syndrome
Hepatic Steatosis
Cognitive
Lung Tumor
Age-related Macular Degeneration
Bone Health
Vulvovaginal Candidiasis (vvc)
Liver Injury
Arterial Hypertension
Cognitive Dysfunction
Anxiety And Depression
Pulmonary Hypertension
Tuberculosis (tb)
Nonatopic Asthma
Dry Eye Symptoms
Breast-cancer
Growth Cartilage
Psychological Distress
Primary Sjögren’s Syndrome
Mild Cognitive Impairment (mci)
Generalized Anxiety Disorder
Ocular Surface
Diabetic Retinopathy
Hair Loss
Dry Eye Disease
Pulmonary Metastasis
Bioactive Compound
Type of Study
Mechanism Keyword
  • Inhibiting Nf-b And Mapk Signaling Pathways In Svcs But Not By The Inhibition Of Macrophage Infiltration

  • Via The Suppression Of Mtor Signaling Pathway

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

  • Through Downregulating Cd44

  • Regulating The Expression Of Nlrp6

  • By Inhibiting The Perk-atf4-chop Pathway

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

  • Mediated Through The Sirt3–sod2–mtros Signaling Pathway

  • Calcitriol-enhanced Autophagy

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

  • Inhibits Il-12 Production

  • Restoring The Lpmc Macrophage Subtype Balance

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

  • Anti-inflammatory Effects

  • Downregulates Catg Expression And Inhibits Cd4 þ T Cell Activation

  • Nf-κb- Dmt1 Signaling.

  • Promotion Of Fa Oxidation

  • Anti-infammatory Efect

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

  • Decrease Of Hfs-induced Inflammation In Inguinal Adipose Tissue, Characterized By A Decreased Expression Of Chemokine Mrna Levels

  • Induction Of Fatty Acid Oxidation

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

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

  • Ampk/nf-b Signaling

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

  • Modulate Il-33 Signaling

  • Inhibiting Akt/mtor Signaling And Inducing Apoptosis

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

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

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

  • Promote Cathelicidin And Ameliorate The Severity Of Diabetic Periodontitis

  • Decreasing Tlr9 Expression

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

  • Inactivating Nf-κb Pro-inflammatory Signaling

  • Decreasing Hba1c And Increasing Sirt1 And Irisin

  • Unfavorable Effect On Central Obesity And Body Composition

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

  • Inhibitory Effect On The Pro-inflammatory Cytokines

  • Abrogating Mlck-dependent Tight Junction Dysregulation During Colonic Inflammation

  • Inhibit The Activation Of Th1 And Th17 Cells

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

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

  • Promote Apoptosis

  • 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.

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

  • Inhibiting The Progression Of Apoptosis

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

  • Inhibiting The Erk1/2 Pathway

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

  • Through Increasing The Immune Level Of Mice.

  • Blocking The P53-p21 Signaling Pathway

  • 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.

  • Hdac2 Activator

  • Aβ42 Plays A Crucial Role

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

  • Regulating Snail/e-cad/emt Pathway

  • Through Modulating Cholinergic Transmission In The Prefrontal Cortex

  • By Inhibiting The Nf-κb Pathway In Asthmatic Mice

  • 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

  • Vdr-dependent Mechanisms

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

  • Significantly Abrogate Damage Related To Oxidative Stress Mediated Neuroinflammation

  • 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.

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

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

  • 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.

  • By Partially Inhibiting Chemokine Production

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

  • Inhibited Inflammatory Cytokines And Decreased Bbb Disruption In Tbi Rats

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

  • 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

  • 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.

  • Modulation Of Renineangiotensin System, Inflammation And Pth

  • Cbd103 Expression

  • 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.

  • Through Reducing Oxidative Stress

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

  • By Acting As A Negative Regulator Of Renin

  • 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.

  • 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.

  • Serotonin-dependent Mechanism

  • 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.

  • 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.

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

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

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

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

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

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

  • 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.

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

  • Increasing Foxp3 Expressing Cd4+cd25+ Treg Cell Frequency

  • Decreasing Brain Oxidative Stress And Inhibiting Neuroinflammation

  • Erk1/2 Pathway

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

  • Might Potentially Accelerate Rv Dysfunction

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

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

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

  • Decrease Aβ-related Biomarkers

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

  • 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.

  • 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.

  • 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

  • Via The Combination Of Vitamin D3 And Ifn

  • Reduced Numbers Of Lung Th2/th17 Cells

  • Inhibiting The P16/p19 Pathway

  • 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

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

  • By Downregulating Hrc

  • Calmodulin-dependent Activation Of Calcium-dependent Potassium Channels

  • 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.

  • Vitd Regulates Infection Through Cbd103 Expression

  • Reduce Inflammation

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