Search results for “TNF-α

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7 articles

Evaluation of Vitamin D3 metabolite (25-OH Vit D3), Neurotransmitter (ACh), and the Expression of Proinflammatory Cytokines (IL-6 and TNF-α) in Tissue Homogenate after Administration of Biofield Energy Healing-based Novel Proprietary Test Formulation and Biofield Treatment per se to the Animals in Vitamin D3 Deficiency Diet (VDD)-induced Sprague Dawley Rats

Mar 2021 DOI 10.14302/issn.2470-5020.jnrt-21-3755
Jana SnehasisCorresponding author Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India.

A novel proprietary test formulation was designed which included minerals, vitamins, β-carotene, cannabidiol isolate,and Panax ginseng extract. This present study was evaluated the impact of the Trivedi Effect® on novel proprietary test formulation in male Sprague Dawley rats, fed with vitamin D3 deficiency diet (VDD). The novel test formulation was divided into two parts; one part was defined as untreated test formulation, while the other part was defined as the Biofield Energy Treated sample, which received the Biofield Energy Healing Treatment by renowned Biofield Energy Healer, Mr. Mahendra Kumar Trivedi. The level of 25-OH Vit. D3 was measured in brain homogenate, which was found to be increased by 20.13%, 24.12%, 45.86%, 14.79%, and 29.96% in the G5 group treated with Biofield Treated test formulation, Biofield Energy Treatment per se to the animals (G6), 15 days pre-treatment of Biofield Energy Treated test formulation (G7), Biofield Energy Treatment per se plus Biofield Energy Treated test formulation from day -15 (G8), and untreated test formulation to the Biofield Energy Treated animals (G9) groups respectively, as compared with the disease control (G2) group. Brain acetylcholine (ACh) level was increased by 61.33% in the G7 group as compared with the untreated test formulation (G4) group. The expression of interleukin-6 (IL-6) was significantly reduced by 43.44% (p≤0.01), 30.93%, 21.42%, 45.99% (p≤0.01), and 60.85% (p≤0.01), respectively as compared with the G4. Lung pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) level was significantly reduced in the G5, G6, G7, and G8 by 24.86%, 32.55% (p≤0.01), 30.12% (p≤0.01), and 42.69% (p≤0.01), respectively, as compared with the G4 group. Altogether, the Biofield Treated test formulation and/or per se treatment to the animals significantly improved the levels of active form of vitamin D3 metabolite (25-OH Vit D3) and neurotransmitter (ACh); consequently significantly lowered the expression of proinflammatory cytokines (IL-6 and TNF-α). Therefore, the energized test formulation or per se treatment could be effectively useful against neuronal damage and inflammation for the management of brain disorders such as Alzheimer’s disease, dementias, brain cancer, epilepsy and other seizure disorders, mental disorders, and Parkinson’s. Thus, the results showed a significant slowdown of disease progression and all other disease-related complications/symptoms in the preventive Biofield Energy Treatment group per se and the Biofield Energy Treated Test formulation groups (viz. G6, G7, G8, and G9) as compared to the disease control group.

Embryology Open Access

Association of Gestational Diabetes and Proinflammatory Cytokines (IL-6, TNF-α and IL-1β)

Oct 2017 DOI 10.14302/issn.3070-5657.je-17-1513
GELEN VolkanCorresponding author Kafkas University, Turkey

Changes to proinflammatory cytokines as a result of gestational diabetes mellitus (GDM), and the pregnancy complications that these changes can cause, are of vital importance to the effective prevention and optimal management. Interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) are cytokines that are associated with gestational diabetes. Therefore, the aim of this review is to draw attention to the relationship between gestational diabetes and these diseases

Lineage-Specific Disruption of Hematopoiesis by Oxaliplatin: Mechanisms of Erythropoietin Resistance and Immune Suppression

Feb 2026 DOI 10.14302/issn.2372-6601.jhor-25-5944
Y. Berezin MikhailCorresponding author

Background Oxaliplatin, a widely used chemotherapeutic agent, is associated with hematologic toxicities such as anemia, leukopenia, and thrombocytopenia. Despite their clinical relevance, the molecular mechanisms underlying lineage-specific bone marrow suppression remain poorly understood. Methods We administered oxaliplatin to mice over eight weeks and performed RNA-sequencing (RNA integrity >8) on bone marrow alongside peripheral blood analysis and cytokine profiling. Transcriptomic data were analyzed to identify differentially expressed genes (DEGs) and enriched pathways. For that, we applied a thematic Gene Ontology (thematicGO) enrichment method that groups GO terms into biologically meaningful categories, such as hematopoietic lineage disruption, cell cycle arrest, and cytokine signaling. Results Oxaliplatin induced broad transcriptional suppression of erythropoiesis and lymphopoiesis, with 3,691 DEGs identified (FDR<0.05, |FC|>1.5). Upregulation of Cdkn1a and downregulation of E2f2 suggest G1/S cell cycle arrest, correlating with repression of key erythroid maturation genes (e.g., Spta1, Slc4a1, Alas2) and hemoglobin subunits (Hba-a1/2, Hbb-bs/t). Despite a ~3000-fold increase in renal Epo expression, bone marrow Epor was reduced, indicating erythropoietin resistance. B and T cell markers were also significantly downregulated, signifying a collapse in adaptive immunity. Notably, neutrophil populations were largely spared. Cytokine analysis in plasma revealed a pro-inflammatory shift with elevated TNF-α and reduced TGF-β, potentially exacerbating hematopoietic dysfunction. Conclusions Oxaliplatin induces a lineage-dependent suppression of hematopoiesis, driven by coordinated cell cycle arrest, metabolic stress, and disrupted cytokine signaling. RNA-seq analysis enabled integration of transcriptomic findings into coherent biological themes. These findings provide mechanistic insights into oxaliplatin’s hematologic toxicity linking bone marrow failure (potentially reversible) via interconnected inflammatory and metabolic pathways and may inform therapeutic strategies to minimize or restore myelosuppression in cancer patients.

Activation of Transcription Factor EB Protects Against Proinflammatory Insults Through NF-κB Inhibition in Keratinocytes

Feb 2026
Xing HuiCorresponding author

Keratinocytes are pivotal in mediating cutaneous inflammation. Identifying anti-inflammatory factors within these cells holds promise for developing novel therapeutic strategies to manage skin inflammation. Transcription factor EB (TFEB) has recently emerged as a key regulator linking cellular energy metabolism to inflammatory processes, primarily through its influence on autophagy and NF-κB signaling. However, whether TFEB activation exerts anti-inflammatory effects in keratinocytes remains unclear. In vitro inflammation model was established in HaCat cells by incubation with proinflammatory mediators LPS and IL-1β. Cell viability and TFEB expression and phosphorylation were measured. The effect of TFEB activation by C1 and adenoviral TFEB overexpression on the expression of proinflammatory genes including COX-2, MCP-1 and IL-6 were detected. Also, IκBα protein level were determined. TFEB phosphorylation is increased while TFEB total protein expression is inhibited by treatment with LPS and IL-1β. Pharmacological activation of TFEB by compound C1 and TFEB overexpression suppressed the expression of COX-2, MCP-1 and TNF-α induced by LPS and IL-1β. TFEB overexpression increased basal IκBα expression and restored IκBα level under LPS treatment. TFEB knockdown reduced TFEB expression and lowered basal expression level of COX-2, MCP-1 and TNF-α. Our findings indicate that TFEB activation can mitigate inflammatory gene expression in keratinocytes triggered by LPS and IL-1β. This implicates TFEB as a significant novel modulator of cutaneous inflammation, highlighting its potential as a therapeutic target. Targeting TFEB could thus be a viable strategy for developing new treatments for chronic inflammatory skin conditions.

Auricular Vagus Nerve Stimulation Improves Chronic Pain and Pain-Related Cytokine Levels: A Clinical Study

Aug 2023 DOI 10.14302/issn.2688-5328.ijp-23-4624
James AndersonCorresponding author

Periauricular Vagus Nerve Stimulation (pVNS) has been proven safe and effective in reducing chronic pain and related comorbidities in numerous clinical studies. This multicenter, interventional study used a non-randomized, interrupted time-series analysis to test the efficacy of an 8-week treatment protocol using the Stivax neurostimulator device. Subjects (n=33, 15 F, 18 M, age 40-77) were recruited at 3 clinic sites in California and Colorado. All subjects had long-term chronic pain and had failed other treatments. Subjects were treated with the Stivax device 3 times (2 weeks on, 1 week off). Subjective assessments of pain (Visual Analog Scale), disability (Oswestry Disability Index), depression (PHQ-9), and activity (IPAQ-E) were collected at baseline and weekly. Objective blood levels of pain-related cytokines collected at the end of weeks 2 and 8. Most subjects reported reduced pain, disability, and depression, with increased activity levels. At the end of week 8, subjects reported an average reduction in pain by 38.5% (3 subjects reported no pain), depression by 43.6% (2 subjects reported no depression), disability by 38.6% (2 subjects reported no disability), and an average 26.1% increase in activity level (5 subjects doubled their activity level). Levels of the pain-related cytokines IL-1ꞵ, IL-2, IL-3, IL-7, IL-10, IL-15, IL-17α, IL-21, TNF-α, IFN-γ, and FLT3-ligand showed improvement at week 8. pVNS is believed to “reset” central sensitization underlying chronic pain and other central sensitization syndromes, engaging the body’s pain modulation systems. Our results indicate that pVNS can clinically significantly improve chronic pain and associated morbidities without adverse effects.

Evaluation of Inflammatory Serum Cytokines after Treatment with the Consciousness Energy Healing Based Proprietary Test Formulation on Combination of Cecal Slurry, LPS and E. Coli Induced Systemic Inflammatory Response Syndrome (SIRS) in Sprague Dawley Rats

Jul 2021 DOI 10.14302/issn.2766-8681.jcsr-21-3885
Jana SnehasisCorresponding author Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India.

Sepsis is a systemic inflammatory response to a confirmed or suspected infection. The transition from sepsis to septic shock causes high rate of mortality. The aim of this experiment was to evaluate the anti-inflammatory potential of the Biofield Energy Treated (Blessed) Proprietary Test Formulation and Biofield Energy Healing (Blessing) Treatment per se to Sprague Dawley rats on Cecal Slurry, LPS, and E. coli-induced systemic inflammatory response syndrome (SIRS) model. In this experiment, various proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10, IL-12, 1L-17, and interferon-γ (IFN-γ) were analysed using ELISA. A test formulation was formulated including minerals (magnesium, zinc, calcium, selenium, and iron), vitamins (ascorbic acid, pyridoxine HCl, vitamin E, cyanocobalamin, and cholecalciferol), Panax ginseng extract, β-carotene, and cannabidiol isolate. The constituents of the test formulation were divided into two parts; one section was defined as the untreated test formulation, while the other portion of the test formulation and three group of animals received Biofield Energy Healing Treatment remotely for about 3 minutes by a renowned Biofield Energy Healer Mr. Mahendra Kumar Trivedi. The level of TNF-α was significantly reduced by 40.50%, 85.36% (p≤0.01), 50.66% (p≤0.01), 87.38% (p≤0.01), and 58.63% (p≤0.01) in G5 (Cecal Slurry, LPS, and E. coli + Biofield Energy Treated test formulation), G6 (Cecal Slurry, LPS, and E. coli + Biofield Energy Treatment per se to animals from day -15), G7 (Cecal Slurry, LPS, and E. coli + Biofield Energy Treated test formulation from day -15), G8 (Cecal Slurry, LPS, and E. coli + Biofield Energy Treatment per se + Biofield Energy Treated test formulation from day -15), and G9 (Cecal Slurry, LPS, and E. coli + Biofield Energy Treatment per se animals + untreated test formulation) groups, respectively as compared to the disease control (G2) group. Additionally, the level of IL-1β was decreased by 17.04%, 15.56%, and 12.59% in G6, G8, and G9 groups, respectively as compared to the untreated test formulation (G4) group. The level of IL-6 was significantly (p≤0.001) reduced by 36.18%, 50.24%, 43.25%, 52.69%, and 38.23% in the G5, G6, G7, G8, and G9 groups, respectively as compared to the G2 group. The level of IL-10 was altered by 70.53%, 49.25%, 60.18%, 41.54%, and 58.89% in G5, G6, G7, G8, and G9 groups, respectively as compared to the G2 group. Moreover, the level of IL-12 was decreased by 30.24%, 31.67%, 29.82%, 45.77%, and 50.54% in the G5, G6, G7, G8, and G9 groups, respectively as compared to the G2. The level of IL-17 was reduced by 48.75%, 59.61%, 59.28%, 62.49%, and 58.65% in the G5, G6, G7, G8, and G9 groups, respectively as compared to the G2. IFN-γ expression was reduced by 49.56%, 24.09%, 23.7%, 56.98%, and 44.94% in G5, G6, G7, G8, and G9 groups, respectively than G2. Overall, the data suggested anti-inflammatory potentials of the Biofield Energy Treated test formulation and Biofield Energy Treatment per se along with preventive measure on the animal with respect to various inflammatory conditions that might be beneficial various types of systemic inflammatory disorders specially sepsis, trauma, septic shock or any types of injuries. Therefore, the results showed the significant slowdown the inflammation-related disease progression and its complications in preventive treatment groups viz. G6, G7, G8, and G9.

Organ Transplantation Open Access

Single Nucleotide Polymorphism Profiles of Patients with Acute Renal Rejection to Personalize Immunosuppressive Therapy: Preliminary Results from An On-Going, Italian Study

Jun 2017 DOI 10.14302/issn.2576-9359.jot-17-1603
Caprara CarlottaCorresponding author  Department of Nephrology, Dialysis and Transplantation; International Renal Research Institute Vicenza (IRRIV); San Bortolo Hospital; Vicenza.

Single-nucleotide polymorphisms (SNPs) in genes involved in immune responses and in the pharmacokinetics/pharmacodynamics of immunosuppressive drugs influence transplant outcomes of patients receiving the same immunosuppressive therapy. The aim of our preliminary study was to determine the SNPs profiles of ABCB1/MDR-1, UGT1A9, IMPDH2, IL-10 and TNF-α genes associated with acute rejection (AR) events in renal allograft recipients. DNA was extracted from whole blood samples of 220 individuals in 3 experimental groups; Case: 41 kidney transplant patients with AR event(s), Control I: 109 kidney transplant patients without AR event, Control II: 70 healthy blood donors. Acute rejection defined as rapid, unexplained rise in serum creatinine was biopsy-proven. 19 SNPs were analyzed by Sanger Sequencing. Analysis of allele and genotype frequencies and gene-disease association tests were performed. Allele frequencies of healthy persons are in line with ones reported from Europe indicating that the studied population is representative. Statistically significant differences only by the comparison of kidney transplant patients with AR event(s) and healthy individuals are found for rs2032582 and rs1045642 SNPs of ABCB1/MDR1, the latter is also not in Hardy-Weinberg equilibrium in our population. Patients with specific alleles for these SPNs are more prone to have acute rejection events. Certain allele variants of ABCB1/MDR1 by modifying the effectiveness of the drugs may compromise the success of the immunosuppressive therapy and put patients at higher risk to reject the new organ. Therefore screening for these polymorphisms before transplantation would help clinicians to more accurately personalize medications.

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