Administration Of Coenzyme Q10 Research Articles

Efficacy of Kirin pill plus vitamin CE and coenzyme Q10 in the treatment of ovarian reserve hypofunction

Purpose: To investigate the efficacy of Kirin pill plus vitamin CE and coenzyme Q10 in the treatment of diminished ovarian reserve (DOR). 
 Methods: 145 patients with ovarian reserve hypofunction hospitalized in Xiangyang Central Hospital, Xiangyang City, China from March 2019 to March 2022 were recruited and assigned randomly to receive either vitamin CE and coenzyme Q10 (control group), or vitamin CE and coenzyme Q10 plus Kirin pills (study group). The parameters/indices determined include menstrual recovery, clinical efficacy, sex hormone and serum anti-mullerian hormone (AMH) levels, changes in the number of ovarian sinus follicles, and levels of CD3+, CD4+ and CD8+ T cell. 
 Results: There were no significant differences (p > 0.05) observed among baseline data, pre-treatment sex hormones, serum AMH, ovarian antral follicle count, CD3+, CD4+, and CD8+ T cell levels. After the intervention, administration of the Kirin pill resulted in significantly lower serum follicle stimulating hormone (FSH) and FSH/luteinizing hormone (LH), elevated AMH levels, and better LH and estradiol (E2) levels in patients compared to the administration of vitamin CE and coenzyme Q10 (control group). The study group also showed superior ovarian reserve function and more ovarian basal sinus follicles than the control group (p < 0.05). 
 Conclusion: Kirin pill plus vitamin CE and coenzyme Q10 treatment regimen optimizes the ovarian reserve function of patients with DOR infertility by improving basal sex hormones, menstrual cycle and menstrual volume, AMH and ovarian basal sinus follicle count. Further clinical trials are required prior to application in clinical practice.

Coenzyme Q10 supplementation in burn patients: a double-blind placebo-controlled randomized clinical trial

BackgroundBurn injuries are important medical problems that, aside from skin damage, cause a systemic response including inflammation, oxidative stress, endocrine disorders, immune response, and hypermetabolic and catabolic responses which affect all the organs in the body. The aim of this study was to determine the effect of coenzyme Q10 (CoQ10) supplementation on inflammation, oxidative stress, and clinical outcomes in burn patients.MethodsIn a double-blind placebo-controlled randomized clinical trial, 60 burn patients were randomly assigned to receive 100 mg CoQ10 three times a day (total 300 mg/day) or a placebo for 10 days. Inflammatory markers including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), oxidative stress markers including total antioxidant capacity (TAC), malondialdehyde (MDA) and superoxide dismutase (SOD) activity, fasting blood glucose (FBG), blood urea nitrogen (BUN), creatinine, white blood cells (WBC), and body temperature were assessed as primary outcomes and albumin, prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), other hematological parameters, blood pressure, O2 saturation, ICU duration, and 28-mortality rate were assessed as secondary outcomes.ResultsFifty-two participants completed the trial. CRP and ESR levels were not significantly different between CoQ10 and placebo groups at the end of the study (P = 0.550 and P = 0.306, respectively). No significant differences between groups were observed for TAC (P = 0.865), MDA (P = 0.692), and SOD activity (P = 0.633) as well. Administration of CoQ10 resulted in a significant increase in albumin levels compared to placebo (P = 0.031). There was no statistically significant difference between the two groups in other measured outcomes (P > 0.05).ConclusionResults showed that in patients with burn injury, CoQ10 administration had no effect on inflammatory markers and oxidative stress, although serum albumin levels were improved after supplementation. Further studies with albumin as the primary outcome are needed to confirm this finding.

Evaluate The Effect of Coenzyme Q10 on The Prevention of Doxorubicin-Induced Acute Cardiotoxicity in Rats.

Objective: This study will evaluate the potential protective effects of coenzyme Q10 on DOX-induced cardiotoxicity in female rats, manifested by changes in biochemical parameters in tissue and serum samples histopathological differences, and compare their changes. Methods:24 female rats were divided into three groups based on weight. The first group received saline, the second group received a cumulative dose of 15 mg/kg of DOX via IP injection, and the third group was pre-treated with CoQ10 before receiving DOX. The data were analysed using a one-way ANOVA test with a Bonferroni post hoc test to compare the markers and histopathological changes in different groups. The GraphPad Prism version 8.1 was used to do the statistical analysis. Results: As indicated by a statistically significant increase (P<0.0001) in TNFα and ICAM-1 level, doxorubicin-induced cardiotoxicity. Additionally, the level of GSH, SOD, and caspase-3 did not differ significantly between the DOX+CoQ10 group and the control group. Furthermore, lesions and histological alterations were induced by the substance. Significant reductions in cardiotoxicity were observed with the administration of coenzyme Q10, as indicated by notable increases (P<0.0001) in SOD, GSH, and TNFα and significant decreases (P<0.0001) in caspase 3 when compared to the DOX group. Also, the CMYO score and lesions exhibited a substantial improvement. Conclusion: In this investigation, coenzyme Q10 exhibited cardioprotective effects against DOX-induced damage to the mouse heart. This phenomenon potentially pertains to inhibiting and safeguarding against oxidative stress, the pathway of apoptosis, and the inflammatory response.

COENZYME Q10 EFFECT ON NMDA RECEPTOR EXPRESSION AND RETINAL GANGLION CELL DENSITY (Experimental Study in Traumatic Optic Neuropathy Model of Wistar Rat)

Abstract
 Introduction & Objectives : Traumatic optic neuropathy is a visual disturbance condition after acute injury to optic nerve. This injury results in retinal ganglion cells ischemic leading to excitotoxicity and apoptosis. Coenzyme Q10 (CoQ10) is an antioxidant and cofactor in electron transport within mitochondria that inhibits glutamate excitotoxicity and thereby preventing retinal ganglion cell apoptosis. This research aims to prove the effect of coenzyme Q10 on NMDA receptor expression and retinal ganglion cell density in rat model of traumatic optic neuropathy.
 Methods : This study use post-test only randomized controlled groups design. Traumatic optic neuropathy wistar rats model was made by optic nerve crushed method, then given oral CoQ10 100mg/kgBW after 1 hour for 14 days in treatment group. Retinal histopathological specimen was made with immunohistochemistry and Haematoxyllin-eosin staining and examined under microscope with 400x magnification. Data was verified and statistically analyzed.
 Results : The NMDA receptor expression in the treatment group was significantly lower than control (p=0.009). The retinal ganglion cell density in the treatment group was significantly higher than control (p=0.009). There was a significant correlation between NMDA receptor expression and retinal ganglion cell density in the treatment group (p = 0.012) with a strong negative correlation direction (r = - 0.652).
 Conclusion : Administration of CoQ10 in traumatic optic neuropathy model rats affects NMDA receptor expression and retinal ganglion cell density. NMDA receptor expression was lower with higher retinal ganglion cell density in the treatment group. NMDA receptor expression was inversely proportional to retinal ganglion cell density in the treatment group.

Coenzyme Q10 mitigates macrophage mediated inflammation in heart following myocardial infarction via the NLRP3/IL1β pathway

BackgroundThe protective effect of Coenzyme Q10 (CoQ10) on the cardiovascular system has been reported, however, whether it can promote early recovery of cardiac function and alleviate cardiac remodeling after myocardial infarction (MI) remains to be elucidated. Whether CoQ10 may regulate the macrophage-mediated pro-inflammatory response after MI and its potential mechanism are worth further exploration.MethodsTo determine the baseline plasma levels of CoQ10 by LC-MS/MS, healthy controls and MI patients (n = 11 each) with age- and gender-matched were randomly enrolled. Additional MI patients were consecutively enrolled and randomized into the blank control (n = 59) or CoQ10 group (n = 61). Follow-ups were performed at 1- and 3-month to assess cardiac function after percutaneous coronary intervention (PCI). In the animal study, mice were orally administered CoQ10/vehicle daily and were subjected to left anterior descending coronary artery (LAD) ligation or sham operation. Echocardiography and serum BNP measured by ELISA were analyzed to evaluate cardiac function. Masson staining and WGA staining were performed to analyze the myocardial fibrosis and cardiomyocyte hypertrophy, respectively. Immunofluorescence staining was performed to assess the infiltration of IL1β/ROS-positive macrophages into the ischemic myocardium. Flow cytometry was employed to analyze the recruitment of myeloid immune cells to the ischemic myocardium post-MI. The expression of inflammatory indicators was assessed through RNA-seq, qPCR, and western blotting (WB).ResultsCompared to controls, MI patients showed a plasma deficiency of CoQ10 (0.76 ± 0.31 vs. 0.46 ± 0.10 µg/ml). CoQ10 supplementation significantly promoted the recovery of cardiac function in MI patients at 1 and 3 months after PCI. In mice study, compared to vehicle-treated MI mice, CoQ10-treated MI mice showed a favorable trend in survival rate (42.85% vs. 61.90%), as well as significantly alleviated cardiac dysfunction, myocardial fibrosis, and cardiac hypertrophy. Notably, CoQ10 administration significantly suppressed the recruitment of pro-inflammatory CCR2+ macrophages into infarct myocardium and their mediated inflammatory response, partially by attenuating the activation of the NLR family pyrin domain containing 3 (NLRP3)/Interleukin-1 beta (IL1β) signaling pathway.ConclusionsThese findings suggest that CoQ10 can significantly promote early recovery of cardiac function after MI. CoQ10 may function by inhibiting the recruitment of CCR2+ macrophages and suppressing the activation of the NLRP3/IL1β pathway in macrophages.Trial registrationDate of registration 09/04/2021 (number: ChiCTR2100045256).

Prospects of Intravenous Coenzyme Q10 Administration in Emergency Ischemic Conditions.

Coenzyme CoQ10 (CoQ10) is an endogenous lipid-soluble antioxidant that effectively protects lipids, proteins, and DNA from oxidation due to its ability to undergo redox transitions between oxidized and reduced forms. Various oxidative stress-associated infectious and somatic diseases have been observed to disrupt the balance of CoQ10 concentration in tissues. As a high molecular weight polar lipophilic compound, CoQ10 exhibits very limited oral bioavailability, which restrains its therapeutic potential. Nevertheless, numerous studies have confirmed the clinical efficacy of CoQ10 therapy through oral administration of high doses over extended time periods. Experimental studies have demonstrated that in emergency situations, intravenous administration of both oxidized and reduced-form CoQ10 leads to a rapid increase in its concentration in organ tissues, offering protection for organ tissues in ischemic conditions. This suggests that the cardio- and neuroprotective efficacy of intravenously administered CoQ10 forms could present new opportunities in treating acute ischemic conditions. Based on these findings, the review provides reasoning supporting further research and implementation of CoQ10 dosage forms for intravenous administration in emergency situations into clinical practice.

Coenzyme Q10 attenuates neurodegeneration in the cerebellum induced by chronic exposure to tramadol

BackgroundChronic use of tramadol can cause neurotoxic effects and subsequently cause neurodegeneration in the cerebellum. The main damage mechanisms identified are oxidative stress and inflammation. Currently, we investigated the effects of coenzyme Q10 (CoQ10) in attenuates of neurodegeneration in the cerebellum induced by chronic exposure to tramadol. Material and methodsSeventy-two male mature albino rats were allocated into four equal groups, including; non-treated group, CoQ10 group (which received CoQ10 at 200 mg/kg/day orally for three weeks), tramadol group (which received tramadol hydrochloride at 50 mg/kg/day orally for three weeks), and tramadol+CoQ10 group (which received tramadol and CoQ10 at the same doses as the previous groups). Tissue samples were obtained for stereological, immunohistochemical, biochemical, and molecular evaluations. Also, functional tests were performed to evaluate behavioral properties. ResultsWe found a significant increase in stereological parameters, antioxidant factors (catalase, glutathione, and superoxide dismutase), and behavioral function scores in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). In addition, malondialdehyde levels, the density of apoptotic cells, as well as the expression of pro-inflammatory (tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 6) and autophagy (lysosome-associated membrane protein 2, autophagy-related 5, beclin 1, and autophagy-related 12) genes were considerably reduced in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). ConclusionWe conclude that the administration of CoQ10 has neuroprotective effects in the cerebellum of rats that have chronic exposure to tramadol.

Investigación del efecto de la coenzima Q10 sobre el daño testicular inducido por ciclofosfamida en ratas macho

Cyclophosphamide (CP) is one of the frequently preferred chemotherapeutic agents Worldwide. CP has negative effects on the testes, spermatogenesis, and reproductive hormones. The aim of this study was to determine the protective effect of Coenzyme Q10 (CoQ10) on the damage caused by CP. CoQ10 is use in the treatment of infertility problems and is naturally found in the testes and seminal fluid. Thirty–six Albino Wistar male rats were divided into six groups (Control, Sham, Cyclophosphamide (CP), Coenzyme Q10 (CoQ10), CP + CoQ10 I, CP + CoQ10 II), with six animals in each group. Semen analysis included investigations of sperm DNA damage, motility, abnormal sperm ratio, and density. Histopathological examination and assessment of oxidative stress parameters in the testes were conducted. Additionally, serum levels of FSH, LH, and Testosterone were measured. CoQ10 administration increased the motility rate, density, and Testosterone levels in testicular damage caused by CP (P&lt;0.05). Furthermore, it was observed that the abnormal sperm ratio, sperm DNA damage, and oxidative stress were reduced (P&lt;0.05). Based on the results of this study, the use of CoQ10 in conjunction with CP has the potential to alleviate male infertility problems that may arise from CP administration.

The Effect Of Coenzim Q10 On The Number Of Lymfocite Cells In Male Wistar Rats With Periodontitis

Periodontal disease is a dental and oral health problem in adult society. One of the periodontal diseases is periodontitis which is an inflammation of the periodontal tissue caused by accumulation of dental plaque which can lead to impaired masticatory function, tooth loss, alveolar bone damage, periodontal ligament damage, pocket formation, and gingival recession. Coenzyme Q10 acts as an antioxidant, the reduced form is ready to give electrons to deactivate ROS or block free radicals which can prevent oxidative stress thereby protecting lymphocyte cells and reducing the immune response which can lead to a reduction in inflammation in the periodontal tissues. The purpose of this study was to determine the effect of coenzyme Q10 on the number of lymphocyte cells in the gingiva of male wistar rats with periodontitis. The research method used is true experimental laboratory quantitative research with a research design that is a posttest only control group design with observation or observing the control group and the treatment group. The number of samples used was 24 rats. Observation of lymphocyte cells was carried out using a light microscope with a magnification of 200x and a magnification of 400x and then counted manually by the observer. The results showed that the significance value obtained in the One-Way ANOVA test was 0.000 (&lt;0.05). Then, based on the results of the Post Hoc Least Significant Difference (LSD) test, it was found that the biggest difference in effect was in the K(-)5 group and the P5 group, where the difference was 59.00 with a significance value of 0.000 (&lt;0.05). It can be concluded that there is an effect of coenzyme Q10 administration on the number of lymphocyte cells in the gingiva of male Wistar rats with periodontitis.

Effects of coenzyme Q10 in a propofol infusion syndrome model of rabbits.

Coenzyme Q (CoQ) might be the main site of interaction with propofol on the mitochondrial respiratory chain in the propofol infusion syndrome (PRIS) because of the structural similarity between coenzyme Q10 (CoQ10) and propofol. To investigate the effects of CoQ10 on survival and organ injury in a PRIS model in rabbits. Sixteen male New Zealand white rabbits were divided into 4 groups: (1) propofol infusion group, (2) propofol infusion and CoQ10, 100 mg/kg was administered intravenously, (3) sevoflurane inhalation was administered, and (4) sevoflurane inhalation and CoQ10, 100 mg/kg intravenously, was administered. Arterial blood gas and biochemical analyses were repeated every 2 h and every 12 h, respectively. Animals that were alive on the 24th hour after anesthesia induction were euthanized. The organ damages were investigated under light and transmission electron microscopy (TEM). The propofol infusion group had the highest troponin T levels when compared with the other three groups at the 12th hour. The propofol + CoQ10 group had lower troponin T levels when compared with the propofol and sevoflurane groups (P < 0.05). Administration of CoQ10 decreased total liver injury scores and total organ injury scores both in the propofol and sevoflurane groups. The propofol and sevoflurane organ toxicities were attenuated with CoQ10 in liver, gallbladder, urinary bladder, and spleen. The addition of CoQ10 to propofol and sevoflurane anesthesia prevented the propofol-associated increase in troponin T levels at the 12th hour of infusion and decreased anesthetic-induced total liver and organ injury scores.

Coenzyme Q 10 in Infertile Men with Idiopathic Asthenozoospermia: A Single Blind Placebo-Controlled, Randomized Trial

Background: Many studies have focused on male infertility. There is limited evidence about the influence of nutrition on quality of semen. Accumulating evidence suggests that oxidative stress plays an important role in the development of male infertility and recently antioxidants have been tried to treat men with idiopathic infertility. Objective: To evaluate the effectiveness of coenzyme Q-10 treatment in improving sperm motility in men with idiopathic asthenozoospermia. Methods: This randomized controlled study conducted in the Department of Reproductive Endocrinology and Infertility, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, from January 2021 to December 2021. Total 74 diagnosed cases of idiopathic asthenozoospermia were selected for medication was included in this study. Eligible man who gave their informed consent was allocated into either Group A (Coenzyme Q-10) or Group B (Placebo) on the basis of computer generated table. Group A received coenzyme Q-10 100 mg two times daily and Group B received placebo for same doses for 12 weeks. Then pretreatment and post treatment semen parameters, including sperm concentration, total motility, progressive motility and morphology was assessed. Results: Post treatment motility (37.8±11.1 vs 26.3±8.8%), progressive motility (30.0±7.9 vs 22.4±7.7) and total motile sperm count (33.5±24.4 vs 21.4±14.3 million) were significantly higher in coenzyme Q-10 group than placebo group (p&lt;0.05). In coenzyme Q-10 group, motility (37.8±11.1 vs 25.2±8.1%), progressive motility (30.0±7.9 vs 22.5±7.0) and total motile sperm count (33.5±24.4 vs 20.0±13.6 million) were significantly increased in post treatment than pretreatment patients (p&lt;0.05), but not found in placebo group. Improvement of sperm motility was significantly higher in coenzyme Q-10 group than placebo group (60.0% vs 5.6%). Conclusion: In conclusion, coenzyme Q10 administration, total motility, progressive motility and total motile sperm count were .....

Coenzyme Q10 exhibits anti-inflammatory and immune-modulatory thereby decelerating the occurrence of experimental cerebral malaria

Cerebral Malaria (CM) is associated with the complex neurological syndrome, whose pathology is mediated by severe inflammatory processes following infection with Plasmodium falciparum. Coenzyme-Q10 (Co-Q10) is a potent anti-inflammatory, anti-oxidant, and anti-apoptotic agent with numerous clinical applications. The aim of this study was to elucidate the role of oral administration of Co-Q10 on the initiation or regulation of inflammatory immune response during experimental cerebral malaria (ECM). For this purpose, the pre-clinical effect of Co-Q10 was evaluated in C57BL/6 J mice infected with Plasmodium berghei ANKA (PbA). Treatment with Co-Q10 resulted in the reduction of infiltrating parasite load, greatly improved the survival rate of PbA-infected mice that occurred independent of parasitaemia and prevented PbA-induced disruption of the blood-brain barrier (BBB) integrity. Exposure to Co-Q10 resulted in the reduction of infiltration of effector CD8 + T cells in the brain and secretion of cytolytic Granzyme B molecules. Notably, Co-Q10-treated mice had reduced levels of CD8 +T cell chemokines CXCR3, CCR2, and CCR5 in the brain following PbA-infection. Brain tissue analysis showed a reduction in the levels of inflammatory mediators TNF- α, CCL3, and RANTES in Co-Q10 administered mice. In addition, Co-Q10 modulated the differentiation and maturation of both splenic and brain dendritic cells and cross-presentation (CD8α+DCs) during ECM. Remarkably, Co-Q10 was very effective in decreasing levels of CD86, MHC-II, and CD40 in macrophages associated with ECM pathology. Exposure to Co-Q10 resulted in increased expression levels of Arginase-1 and Ym1/chitinase 3–like 3, which is linked to ECM protection. Furthermore, Co-Q10 supplementation prevented PbA-induced depletion of Arginase and CD206 mannose receptor levels. Co-Q10 abrogated PbA-driven elevation in pro-inflammatory cytokines IL-1β, IL-18, and IL-6 levels. In conclusion, the oral supplementation with Co-Q10 decelerates the occurrence of ECM by preventing lethal inflammatory immune responses and dampening genes associated with inflammation and immune-pathology during ECM, and offers an inimitable opening for developing an anti-inflammatory agent against cerebral malaria.

The Effects of Coenzyme Q10 on Hormonal and Histopathological Changes in Female Wistar Rats with Polycystic Ovary Syndrome

Background: Polycystic ovary syndrome (PCOS) is one the most common diseases in women in the fertility age. PCOS alters ovarian follicles and affects blood lipid profiles, liver enzymes and hormones. In this study, we tried to investigate the effects of coenzyme Q10 (CoQ10) on PCOS pathological conditions. Methods: Twenty-four female rats were randomly divided into the three groups; 1: control group, 2: PCOS group (received 1 mg/ kg letrozole daily for 21 days, PO) and 3: PCOS+CoQ10 group (received 1 mg/kg letrozole with 10 mg/kg of CoQ10 for 21 days orally). Blood lipid profiles, liver enzymes, blood glucose and testosterone levels were measured and ovarian histopathology was evaluated. Results: Histological examination showed reduced number of antral follicles in PCOS+CoQ10 group as compared with PCOS group (P&lt;0.001). PCOS increased the alanine aminotransferase (ALT) enzyme by acting on the liver (P&lt;0.01). Administration of CoQ10 during PCOS induction was able to reduce ALT levels (P&lt;0.01). PCOS increased the cholesterol (P&lt;0.05), fasting blood sugar (FBS) (P&lt;0.05), triglyceride (P&lt;0.001), low-density lipoprotein (LDL) (P&lt;0.05) and testosterone levels (P&lt;0.001) compared to the control group. However, CoQ10 treatment significantly reduced the above-mentioned parameters compared to the PCOS group. Conclusion: The results of the present study confirm that CoQ10 has a therapeutic potential for PCOS-induced lipid and hormonal changes and ovarian tissue damages. CoQ10 supplementation and its concomitant use with letrozole could inhibit the development of PCOS in rats. Testosterone reduction could be an important mechanism for CoQ10 beneficial effects.

Therapeutic Options for Migraines in the Microsurgical Patient: A Scoping Review.

There exists an increasing array of treatments proposed to prevent, alleviate, and abort symptoms of a migraine; however, for patients who undergo reconstructive microsurgery, caution must be taken to preserve vascular integrity. This study is the first-to-date scoping review of vascular and bleeding risk of current migraine therapies, with the purpose of identifying potential therapeutic agents for postoperative migraine management appropriate for microsurgical patients. Currently available migraine therapeutics were compiled from UpToDate and the American Academy of Family Physicians. A PubMed literature review was performed for each therapeutic's effect on bleeding or vascular involvement. Data were compiled into tables of abortive, symptom-controlling and prophylactic, and non-pharmacologic treatments. Expert microsurgeons reviewed the data to provide recommendations for optimized patient care. Triptans and other ergot derivatives demonstrated strong evidence of vasoconstriction and were greatly advised against for immediate post-microsurgical use. Novel pharmaceutical therapies like Lasmiditan and CGRP antagonists have no literature indicating potential for vasoconstriction or hematoma and remain an investigational option for abortive medical treatment. For symptom control, acetaminophen appears the safest option, with clinical judgment and further research needed for use of NSAIDs. Alternative treatment techniques may include migraine prophylaxis with botulinum toxin injection or nutraceutical treatment via magnesium supplementation or Coenzyme Q10 administration, minimizing the need for additional medication in the postoperative setting. Patients undergoing reconstructive microsurgery have a unique medical profile limiting the therapeutic options available to treat migraines. This review provides preliminary evidence to be considered as a guide for prescribing therapeutics for migraine in the postoperative setting.

Comparative analysis of oxidized fish oil and coenzyme Q10 on the intestinal microecology of largemouth bass Micropterus salmoides at different growth stages

Coenzyme Q10 (CoQ10) is a powerful antioxidant that is gradually being used in aquafeeds. Here, we examined the influence of oxidized fish oil and CoQ10 supplementation on intestinal microbiota of Micropterus salmoides at different growth stages. Three isonitrogenous and isoenergetic diets were formulated to contain 100% fresh fish oil (FFO), 100% oxidized fish oil (OFO) and OFO + 0.1% CoQ10 (QFO) and were fed to Micropterus salmoides (95 ± 0.60 g) for 70 days. Furthermore, three different growth stages (28-day, 49-day, 70-day) were selected to observe the dynamic changes of intestinal microbiota. The growth performance of fish fed QFO were significantly higher than that of fish fed OFO after a 70-day’s feeding. Intestinal microbial community of Micropterus salmoides was significantly affected by different growth stages more than diets. The abundance of phylum Proteobacteria showed an increasing trend, while the abundance of Firmicutes decreased with increased feeding time. Compared with OFO, diet supplemented with CoQ10 significantly increased the abundance of Firmicutes, and decreased Proteobacteria on the 28- and 70-day of feeding. When fish fed OFO and QFO, Simpson and Shannon indices significantly increased with increased feeding time from 28 to 70 days. Fish fed QFO significantly decreased the value of Bray-Curtis distance than those fed FFO on the 70-day of feeding. Moreover, Bray-Curtis distance showed an increased trend with increased feeding time. Notably, intestinal microbial functional prediction indicated that OFO suppressed amino acid metabolism, while long-term oral administration of CoQ10 could improve amino acid metabolism and detoxification of Micropterus salmoides. This study demonstrated that prolonged application of CoQ10 is needed to produce some beneficial effects to Micropterus salmoides.

Effects of Coenzyme Q10 on the Biomarkers (Hydrogen, Methane, SCFA and TMA) and Composition of the Gut Microbiome in Rats.

The predominant route of administration of drugs with coenzyme Q10 (CoQ10) is administration per os. The bioavailability of CoQ10 is about 2-3%. Prolonged use of CoQ10 to achieve pharmacological effects contributes to the creation of elevated concentrations of CoQ10 in the intestinal lumen. CoQ10 can have an effect on the gut microbiota and the levels of biomarkers it produces. CoQ10 at a dose of 30 mg/kg/day was administered per os to Wistar rats for 21 days. The levels of gut microbiota biomarkers (hydrogen, methane, short-chain fatty acids (SCFA), and trimethylamine (TMA)) and taxonomic composition were measured twice: before the administration of CoQ10 and at the end of the experiment. Hydrogen and methane levels were measured using the fasting lactulose breath test, fecal and blood SCFA and fecal TMA concentrations were determined by NMR, and 16S sequencing was used to analyze the taxonomic composition. Administration of CoQ10 for 21 days resulted in a 1.83-fold (p = 0.02) increase in hydrogen concentration in the total air sample (exhaled air + flatus), a 63% (p = 0.02) increase in the total concentration of SCFA (acetate, propionate, butyrate) in feces, a 126% increase in butyrate (p = 0.04), a 6.56-fold (p = 0.03) decrease in TMA levels, a 2.4-fold increase in relative abundance of Ruminococcus and Lachnospiraceae AC 2044 group by 7.5 times and a 2.8-fold decrease in relative representation of Helicobacter. The mechanism of antioxidant effect of orally administered CoQ10 can include modification of the taxonomic composition of the gut microbiota and increased generation of molecular hydrogen, which is antioxidant by itself. The evoked increase in the level of butyric acid can be followed by protection of the gut barrier function.

Protective Effects of L-carnitine and Co-enzyme Q10 Against Oxidative Stress Damage in Hypertension

In this study, it was aimed to investigate the effects of L-carnitine and Co-enzyme Q10 administration together with ACE Inhibitor (ACE inh.) on oxidative stress parameters in liver, brain and kidney tissues in L-NAME hypertensive rats. At the study, divided all rats into eight groups, four groups with 14 days of experiment time and four groups with 28 days of experiment time. At the end of the experiment, the rats were euthanized and their liver, brain and kidney tissues were taken. Malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) activities were measured in tissue supernatants. While NO and MDA levels increased in all tissues, a significant decrease was observed in GSH levels (P&amp;lt;0.001). In conclusion, it is suggested that supplementation of L-carnitine and CoQ10 can be considered as a combination therapy strategy for patients prone to higher levels of oxidative stress and inflammation.

Coenzyme Q10 and N-acetyl cysteine modulates the haematological parameters, markers of oxidative stress and membrane bound phosphatase in spleen toxicity induced by aniline hydrochloride

Aniline is widely used chemical for industrial purpose. Exposure to aniline can lead to various health issues in human being. The most common toxic effect of aniline is splenotoxicity which is produced via the generation of oxidative stress. The present study examines the protective effect of coenzyme Q10 and N-acetyl cysteine on spleen weight, body weight, endogenous antioxidants and membrane bound ATPases in aniline hydrochloride (AH) induced spleen toxicity in rats. Adult male albino rats were divided into five groups, each group consists of six rats. Toxicity was induced by administration of AH (100 ppm, p. o) in drinking water for 30 days. Body weight, markers of oxidative stress and haematological parameters were assessed at the end of treatment period. Treatment rats received Coenzyme Q10 (CoQ10, 10 mg/kg/day/p.o) and N- acetyl cysteine (NAC, 300mg/kg/ day p.o) alone and in combination for 30. AH toxic rats showed a significant elevation of spleen weight, WBC count, iron content, LPO level, NO level and Ca ATPase whereas a significant decrease in body weight, haemoglobin, RBCs level, Protein content, GSH and Na/ K and Mg ATPase were observed. Administration of Coenzyme Q10 (CoQ10, 10 mg/kg/day/p.o) and N- acetyl cysteine (NAC, 300mg/kg/ day p.o) together for 30 consecutive days shows a significant decrease in spleen weight, WBC level, iron content, LPO level, NO level whereas significant increase in body weight, hemoglobin level, RBCs level Protein content, GSH level, Na/ K ATPase, Ca and Mg ATPase when compared with aniline treated group and CoQ10 or NAC alone treated groups. These findings indicate the synergistic &amp; protective effect of CoQ10 and NAC in aniline induced spleen toxicity in rats compared to alone antioxidants.

Protective Effects of L-carnitine and Co-enzyme Q10 Against Oxidative Stress Damage in Hypertension

In this study, it was aimed to investigate the effects of L-carnitine and Co-enzyme Q10 administration together with ACE Inhibitor (ACE inh.) on oxidative stress parameters in liver, brain and kidney tissues in L-NAME hypertensive rats. At the study, divided all rats into eight groups, four groups with 14 days of experiment time and four groups with 28 days of experiment time. At the end of the experiment, the rats were euthanized and their liver, brain and kidney tissues were taken. Malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) activities were measured in tissue supernatants. While NO and MDA levels increased in all tissues, a significant decrease was observed in GSH levels (P

CoQ10 alleviates hepatic ischemia reperfusion injury via inhibiting NLRP3 activity and promoting Tregs infiltration.

Hepatic ischemia-reperfusion injury (IRI) has been concerned as a main complication of liver surgery and transplantation. Previous studies show that reactive oxygen species (ROS) associated inflammation response and contribute to the liver damage during IRI. Coenzyme Q10 (CoQ10) has shown many beneficial effects on abrogating ROS production and ameliorating liver injury. This study found lower CoQ10 level in the process of liver IRI in a mouse model of hepatic IRI. Meanwhile, our results showed that CoQ10 administration significantly attenuate hepatic IRI proved by HE staining, serum ALT/AST. The NOD-like receptor protein 3 (NLRP3) inflammasome is activated by ROS which triggers the activation of inflammatory caspases. In this study, NLRP3 was significantly suppressed by CoQ10 while Foxp3 exhibited increased expression in liver. Furthermore, Kupffer cells (KCs) pretreated with CoQ10 under the condition of hypoxia and reoxygenation contributed to improved CD4+CD25+Foxp3+ regulatory T cells (Tregs) ratio in co-culture system. Furthermore, NLRP3 inflammasome activator treatment in vivo resulted in higher expression of caspase-1 and NLRP3 and reduction of Tregs in liver, which reversed the protection of CoQ10 in the liver injury. Taken together, our study discovered that CoQ10 can suppress NLRP3 activity in KCs and improves Foxp3+ Tregs differentiation depending on M2 macrophage polarization of KCs to ameliorate hepatic IRI.