Coenzyme Q10 protects skeletal muscle from ischemia-reperfusion through the NF-kappa B pathway

Boroujeni, Mandana Beigi; khayat, Zahra Khanipour; Anbari, Khatereh; Niapour, Ali; Gholami, Mohammadreza; Gharravi, Anneh Mohammad

doi:10.1177/0267659116683790

Cited by 12 publications

(6 citation statements)

References 27 publications

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“…Therefore, it is not surprising that its depletion is associated with a greater propensity to develop immune inflammatory responses through the activation of inflammatory processes such as the nuclear factor-kappa-light-chain-enhancer of activated B cell's (NF-κB) gene expression [16]. Worthy to note, CoQ 10 is endowed with potent antioxidant action able to prevent free radical damage by the regulation of transcriptional pathways in addition to deactivation of inflammatory pathways [17].…”

Section: Organmentioning

confidence: 99%

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

et al. 2020

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Coenzyme Q10 (CoQ10) is a ubiquitous factor present in cell membranes and mitochondria, both in its reduced (ubiquinol) and oxidized (ubiquinone) forms. Its levels are high in organs with high metabolism such as the heart, kidneys, and liver because it acts as an energy transfer molecule but could be reduced by aging, genetic factors, drugs (e.g., statins), cardiovascular (CV) diseases, degenerative muscle disorders, and neurodegenerative diseases. As CoQ10 is endowed with significant antioxidant and anti-inflammatory features, useful to prevent free radical-induced damage and inflammatory signaling pathway activation, its depletion results in exacerbation of inflammatory processes. Therefore, exogenous CoQ10 supplementation might be useful as an adjuvant in the treatment of cardiovascular diseases such as heart failure, atrial fibrillation, and myocardial infarction and in associated risk factors such as hypertension, insulin resistance, dyslipidemias, and obesity. This review aims to summarize the current evidences on the use of CoQ10 supplementation as a therapeutic approach in cardiovascular diseases through the analysis of its clinical impact on patients’ health and quality of life. A substantial reduction of inflammatory and oxidative stress markers has been observed in several randomized clinical trials (RCTs) focused on several of the abovementioned diseases, even if more RCTs, involving a larger number of patients, will be necessary to strengthen these interesting findings.

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Section: Organmentioning

confidence: 99%

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

et al. 2020

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“…An anti-nociceptive effect of the CoQ10 has been studied in a rat model of knee OA and the mechanism of pain suppression was suggested to be caused by an anti-inflammation [ 39 ]. Previous in vivo study has also shown that CoQ10 pretreatment significantly inhibited TNF-α and NF-κβ activation during I/R of skeletal muscle [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…CoQ10 is a potent antioxidant frequently used in clinical practice. It potentially prevents the TQ-induced I/R injury because the CoQ, as part of mitochondrial ETC, regulates ATP and ROS synthesis [ 12 , 19 , 32 , 33 , 34 ]. In aging and chronic arthritis patients, endogenous CoQ10 levels have been shown to significantly decrease, thus inducing mitochondrial vulnerability to I/R processes [ 19 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

CoenzymeQ10 and Ischemic Preconditioning Potentially Prevent Tourniquet-Induced Ischemia/Reperfusion in Knee Arthroplasty, but Combined Pretreatment Possibly Neutralizes Their Beneficial Effects

et al. 2022

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Tourniquet (TQ) use during total knee arthroplasty (TKA) induces ischemia/reperfusion (I/R) injury, resulting in mitochondrial dysfunction. This study aims to determine the effects of coenzyme Q10 (CoQ10) and ischemic preconditioning (IPC), either alone or in combination, on I/R-induced mitochondrial respiration alteration in peripheral blood mononuclear cells (PBMCs) and pain following TKA. Forty-four patients were allocated into four groups: control, CoQ10, IPC, and CoQ10 + IPC. CoQ10 dose was 300 mg/day for 28 days. IPC protocol was three cycles of 5/5-min I/R time. Mitochondrial oxygen consumption rates (OCRs) of PBMCs were measured seven times, at baseline and during ischemic/reperfusion phases, with XFe 96 extracellular flux analyzer. Postoperative pain was assessed for 48 h. CoQ10 improved baseline mitochondrial uncoupling state; however, changes in OCRs during the early phase of I/R were not significantly different from the placebo. Compared to ischemic data, IPC transiently increased basal OCR and ATP production at 2 h after reperfusion. Clinically, CoQ10 significantly decreased pain scores and morphine requirements at 24 h. CoQ10 + IPC abolished analgesic effect of CoQ10 and mitochondrial protection of IPC. In TKA with TQ, IPC enhanced mitochondrial function by a transient increase in basal and ATP-linked respiration, and CoQ10 provides postoperative analgesic effect. Surprisingly, CoQ10 + IPC interferes with beneficial effects of each intervention.

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“…CoQ10 deficiency leads to mitochondrial disorders and cellular dysfunction especially in tissues with high energy requirements like skeletal muscles ( Romero-Moya et al, 2017 , Woodman et al, 2016 ). Boroujeni et al demonstrated the protective effect of CoQ10 in a model of HLI/R through suppression of NFκB and TNF-α ( Boroujeni et al, 2017 ). While the action of CoQ10 as an inhibitor of calcium influx and its favorable aspect on cellular damage is well documented ( Chang et al, 2012 , Okamoto et al, 1995 ), its effect on classical and non-classical RAS system is not revealed yet.…”

Section: Discussionmentioning

confidence: 99%

CoQ10 augments candesartan protective effect against tourniquet-induced hind limb ischemia-reperfusion: Involvement of non-classical RAS and ROS pathways

Awad

El-Din

Kamel

2021

Saudi Pharmaceutical Journal

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Tourniquet is a well-established model of hind limb ischemia–reperfusion (HLI/R) in rats. Nevertheless, measures should be taken to alleviate the expected injury from ischemia/ reperfusion (I/R). In the present study, 30 adult male Sprague-Dawley rats were randomly divided into 5 groups (n = 6): control, HLI/R, HLI/R given candesartan (1 mg/kg, P.O); HLI/R given Coenzyme Q10 (CoQ10) (10 mg/kg, P.O); HLI/R given candesartan (0.5 mg/kg) and CoQ10 (5 mg/kg). The drugs were administered for 7 days starting one hour after reperfusion. Candesartan and CoQ10 as well as their combination suppressed gastrocnemius content of angiotensin II while they raised angiotensin-converting enzyme 2 (ACE2) activity, angiotensin (1–7) expression, and Mas receptor mRNA level. Consequently, candesartan and/or CoQ10 reversed the oxidative stress and inflammatory changes that occurred following HLI/R as demonstrated by the rise of SOD activity and the decline of MDA, TNF-α, and IL-6 skeletal muscle content. Additionally, candesartan and/or CoQ10 diminished gastrocnemius active caspase-3 level and phospho-p38 MAPK protein expression. Our study proved that CoQ10 enhanced the beneficial effect of candesartan in a model of tourniquet-induced HLI/R by affecting classical and non-classical renin-angiotensin system (RAS) pathway. To our knowledge, this is the first study showing the impact of CoQ10 on skeletal muscle RAS in rats.

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Coenzyme Q10 protects skeletal muscle from ischemia-reperfusion through the NF-kappa B pathway

Abstract: It seems that CoQ10 has inhibitory effects on NF-κB and TNF-α activation.

Cited by 12 publications

References 27 publications

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

CoenzymeQ10 and Ischemic Preconditioning Potentially Prevent Tourniquet-Induced Ischemia/Reperfusion in Knee Arthroplasty, but Combined Pretreatment Possibly Neutralizes Their Beneficial Effects

CoQ10 augments candesartan protective effect against tourniquet-induced hind limb ischemia-reperfusion: Involvement of non-classical RAS and ROS pathways

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