Diabetes and its complications have been linked to increased levels of free radicals and systemic pro-inflammatory cytokines and to an altered lipid profile. Coenzyme Q10 and curcumin are potent antioxidants and anti-inflammatory agents but are underutilized clinically because of their poor bioavailability when administered orally. We have recently developed poly(D,L-lactic-co-glycolic acid)-based nanoparticles in which we have encapsulated coenzyme Q10 and curcumin to increase the oral bioavailability and therapeutic efficacy of the antioxidant molecules. These formulations when tested in streptozotocin-induced diabetic rats demonstrated protective effects on inflammatory markers as well as lipid metabolism. Coenzyme Q10 nanoparticulates reduced only C-reactive protein levels, whereas curcumin nanoparticles reduced levels of C-reactive protein, interleukin-6 and tumor necrosis factor-α. Administration of both nanoparticulates resulted in significant reductions of plasma triglycerides and total cholesterol and an increase in high-density lipoprotein cholesterol. Together, these data indicate the promise of coenzyme Q10 and curcumin in diabetes when delivered through nanoparticulate formulations.
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http://dx.doi.org/10.1007/s13346-011-0041-3 | DOI Listing |
Mater Today Bio
February 2025
Breast Center, Department of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, PR China.
Cell membrane targeting sonodynamic therapy could induce the accumulation of lipid peroxidation (LPO), drive ferroptosis, and further enhances immunogenic cell death (ICD) effects. However, ferroptosis is restrained by the ferroptosis suppressor protein 1 (FSP1) at the plasma membrane, which can catalyze the regeneration of ubiquinone (CoQ10) by using NAD(P)H to suppress the LPO accumulation. This work describes the construction of US-active nanoparticles (TiF NPs), which combinate cell-membrane targeting sonosensitizer TBT-CQi with FSP1 inhibitor (iFSP1), facilitating cell-membrane targeting sonodynamic-triggered ferroptosis.
View Article and Find Full Text PDFBMJ Open
December 2024
Division of Nephrology, Department of Internal Medicine, Showa University Graduate School of Medicine, Shinagawa-ku, Tokyo, Japan.
Introduction: Coenzyme Q10 (CoQ10) is a fat-soluble vitamin-like quinone. The plasma levels of CoQ10 are reduced in patients with chronic kidney disease (CKD). CoQ10 supplementation can improve mitochondrial function and decrease oxidative stress in these patients.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
Department of Translational Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
Background: Coenzyme Q10 (CoQ10) nephropathy is a well-known cause of hereditary steroid-resistant nephrotic syndrome, primarily impacting podocytes. This study aimed to elucidate variations in individual cell-level gene expression in CoQ10 nephropathy using single-cell transcriptomics.
Methods: We conducted single-cell sequencing of a kidney biopsy specimen from a 5-year-old boy diagnosed with a CoQ10 nephropathy caused by a compound heterozygous COQ2 mutation complicated with immune complex-mediated glomerulonephritis.
Neurobiol Dis
January 2025
Department of Neurology, the First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, Nanning, Guangxi, China. Electronic address:
One of the underlying mechanisms of epilepsy (EP), a brain disease characterized by recurrent seizures, is considered to be cell death. Disulfidptosis, a proposed novel cell death mechanism, is thought to play a part in the pathogenesis of epilepsy, but the exact role is unclear. The gene expression omnibus series (GSE) 33,000 and GSE63808 datasets were used to search for differentially expressed disulfidptosis-related molecules (DE-DRMs).
View Article and Find Full Text PDFCureus
December 2024
Pediatrics Department, Dr. Sulaiman Al Habib Hospital, Riyadh, SAU.
Coenzyme Q2 (CoQ2) mutations are a group of autosomal recessive mitochondria-linked diseases that result in coenzyme Q10 (CoQ10) deficiency (CoQ10: a cofactor in mitochondrial energy production). Its deficiency leads to multiple systemic clinical presentations; however, isolated steroid-resistant nephrotic syndrome (SRNS) is considerably rare. Multiple genetic mutations have been reported with different ranges of severity and prognosis, with variable responses to CoQ10 supplementation.
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