ubiquinone and Autoimmune-Diseases

In this review, the author shows that simultaneous multiple disorders caused by reactivation of Epstein-Barr virus can lead to salivary gland disorders as part of Sjogren's syndrome (SS). Therefore, clinicians must differentiate SS from other diseases when diagnosing and treating salivary gland disorders. In particular, the author explains how microbial infection in SS overcomes immunological tolerance, leading to pathological changes, and how cytokine overexpression and endocrine disrupters contribute to glandular tissue injury. Also, the author suggests that involvement of reactive oxygen species is a common pathogenesis of salivary gland disorders and SS, so regulation of oxidative stress is an effective treatment for both. The results of clinical studies on restoring salivary gland function and regenerating salivary glands with tissue stem cells may provide clues on elucidating the cause of SS.

Topics: Antioxidants; Arthritis, Rheumatoid; Autoantigens; Autoimmune Diseases; Cytokines; Diagnosis, Differential; Dioxins; Epstein-Barr Virus Infections; Estrogens; Female; Genetic Predisposition to Disease; Herpesvirus 4, Human; Humans; Interleukin-10; Lymphocytes; Male; Mikulicz' Disease; Oxidative Stress; Reactive Oxygen Species; Salivary Glands; Sjogren's Syndrome; Stem Cell Transplantation; Ubiquinone; Virus Activation; Virus Diseases

Though affecting many thousands of patients, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) should be considered an orphan disease, since the cause remains elusive and no treatment is available that can provide complete cure. There is reasonable insight into the pathogenesis of signs and symptoms, and treatments specifically directed to immunological, inflammatory and metabolic processes offer relief to an increasing number of patients. Particular attention is given to the importance of co-morbidity requiring appropriate therapy. Promising results are obtained by treatment with Metformin, or possibly Momordica charantia extract, which will correct insulin resistance, with Meldonium improving the transportation of glucose into the mitochondria, with sodium dichloroacetate activating pyruvate dehydrogenase, and with nutraceutical support reducing oxidative and inflammatory impairment.

Topics: Adult; Animals; Antiviral Agents; Autoimmune Diseases; Comorbidity; Dichloroacetic Acid; Dietary Supplements; Drug Evaluation, Preclinical; Drug Therapy, Combination; Endocrine System Diseases; Fatigue Syndrome, Chronic; Female; Humans; Infections; Insulin Resistance; Male; Mental Disorders; Methylhydrazines; Middle Aged; Mitochondria; Neuroimaging; Pyruvate Dehydrogenase Complex; Severity of Illness Index; Thiamine; Thioctic Acid; Tomography, Emission-Computed, Single-Photon; Ubiquinone

Coenzyme Q10 (CoQ10), also known as ubiquinone, is a fat-soluble antioxidant. Although CoQ10 has not been approved as medication by the Food and Drug Administration, it is widely used in dietary supplements. Some studies have shown that CoQ10 has anti-inflammatory effects on various autoimmune disorders. In this study, we investigated the anti-inflammatory effects of liposome/gold hybrid nanoparticles encoded with CoQ10 (LGNP-CoQ10). Both CoQ10 and LGNP-CoQ10 were administered orally to mice with collagen-induced arthritis (CIA) for 10 weeks. The inflammation pathology of joint tissues of CIA mice was then analyzed using hematoxylin and eosin and Safranin O staining, as well as immunohistochemistry analysis. We obtained immunofluorescence staining images of spleen tissues using confocal microscopy. We found that pro-inflammatory cytokines were significantly decreased in LGNP-CoQ10 injected mice. Th17 cell and phosphorylated STAT3-expressed cell populations were also decreased in LGNP-CoQ10 injected mice. When human peripheral blood mononuclear cells (PBMCs) were treated with CoQ10 and LGNP-CoQ10, the IL-17 expression of PBMCs in the LGNP-CoQ10-treated group was significantly reduced. Together, these results suggest that LGNP-CoQ10 has therapeutic potential for the treatment of rheumatoid arthritis.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Arthritis, Experimental; Arthritis, Rheumatoid; Autoimmune Diseases; Cell Line; Cytokines; Disease Models, Animal; Gold; Humans; Inflammation; Interleukin-17; Leukocytes, Mononuclear; Liposomes; Male; Metal Nanoparticles; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; STAT3 Transcription Factor; T-Lymphocytes, Regulatory; Th17 Cells; Ubiquinone

Coenzyme Q. Our study confirmed the strong anti-inflammatory effects of coenzyme Q. There is significant synergy between coenzyme Q

Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Autoimmune Diseases; Cell Line, Tumor; Cytokines; Disease Models, Animal; Drug Synergism; Female; Glucans; Humans; Mice; Mice, Inbred BALB C; Neoplasms, Experimental; Phagocytosis; RAW 264.7 Cells; Ubiquinone

Coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant synthesized in human body. This enzyme promotes immune system function and can be used as a dietary supplement. Rheumatoid arthritis (RA) is an autoimmune disease leading to chronic joint inflammation. RA results in severe destruction of cartilage and disability. This study aimed to investigate the effect of CoQ10 on inflammation and Th17 cell proliferation on an experimental rheumatoid arthritis (RA) mice model. CoQ10 or cotton seed oil as control was orally administrated once a day for seven weeks to mice with zymosan-induced arthritis (ZIA). Histological analysis of the joints was conducted using immunohistochemistry. Germinal center (GC) B cells, Th17 cells and Treg cells of the spleen tissue were examined by confocal microscopy staining. mRNA expression was measured by real-time PCR and protein levels were estimated by enzyme-linked immunosorbent assay (ELISA). Flow cytometric analysis (FACS) was used to evaluate Th17 cells and Treg cells. CoQ10 mitigated the severity of ZIA and decreased serum immunoglobulin concentrations. CoQ10 also reduced RANKL-induced osteoclastogenesis, inflammatory mediators and oxidant factors. Th17/Treg axis was reciprocally controlled by CoQ10 treatment. Moreover, CoQ10 treatment on normal mouse and human cells cultured in Th17 conditions decreased the number of Th17 cells and enhanced the number of Treg cells. CoQ10 alleviates arthritis in mice with ZIA declining inflammation, Th17 cells and osteoclast differentiation. These findings suggest that CoQ10 can be a potential therapeutic substance for RA.

Topics: Animals; Arthritis, Experimental; Autoantibodies; Autoimmune Diseases; B-Lymphocytes; Bone Resorption; Cell Differentiation; Disease Models, Animal; Germinal Center; Humans; Immunophenotyping; Immunosuppressive Agents; Interleukin-17; Leukocytes, Mononuclear; Mice; Osteoclasts; Spleen; T-Lymphocyte Subsets; Th17 Cells; Ubiquinone; Zymosan