Acetyl-L-carnitine and/or liposomal co-enzyme Q10 prevent propionic acid-induced neurotoxicity by modulating oxidative tissue injury, inflammation, and ALDH1A1-RA-RARα signaling in rats

Alhusaini, Ahlam; Sarawi, Wedad S.; Mattar, Dareen; Abo-Hamad, Amjad; Almogren, Renad; Alhumaidan, Sara; Alsultan, Ebtesam; Alsaif, Shaikha; Hasan, Iman H.; Hassanein, Emad H.M.; Mahmoud, Ayman M.

doi:10.1016/j.biopha.2022.113360

Cited by 7 publications

(5 citation statements)

References 64 publications

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“…In contrast, the concomitant administration of A-CAR and L-CoQ 10 significantly attenuated the expression levels of these proteins. The findings of the current study support our previous study that revealed the antioxidant and antiapoptotic properties of A-CAR and L-CoQ 10 in the brain tissue in a rat model of autism [40]. To the best of our knowledge, this is the first study investigating the effect of PRA, A-CAR, and L-CoQ 10 on CK18 expression levels.…”

Section: Discussionsupporting

confidence: 90%

Acetyl-L-Carnitine and Liposomal Co-Enzyme Q10 Attenuate Hepatic Inflammation, Apoptosis, and Fibrosis Induced by Propionic Acid

Alhusaini

Alsoghayer

Alhushan

et al. 2023

IJMS

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Propionic acid (PRA) is a metabolic end-product of enteric bacteria in the gut, and it is commonly used as a food preservative. Despite the necessity of PRA for immunity in the body, excessive exposure to this product may result in disruptive effects. The purpose of this study is to examine the hepatoprotective effects of acetyl-L-carnitine (A-CAR) and liposomal-coenzyme Q10 (L-CoQ10) against PRA-induced injury. Liver injury in rats was induced by oral administration of PRA, and A-CAR and L-CoQ10 were administered concurrently with PRA for 5 days. Oxidative stress, inflammatory, apoptotic, and fibrotic biomarkers were analyzed; the histology of liver tissue was assessed as well to further explore any pathological alterations. PRA caused significant increases in the levels of serum liver enzymes and hepatic oxidative stress, inflammatory, and apoptotic biomarker levels, along with histopathological alterations. Concurrent treatment with A-CAR and/or L-CoQ10 with PRA prevented tissue injury and decreased the levels of oxidative stress, proinflammatory cytokines, and apoptotic markers. Additionally, A-CAR and/or L-CoQ10 modulated the expression of high-mobility group box-1, cytokeratin-18, transforming growth factor-beta1, and SMAD3 in liver tissue. In conclusion, A-CAR and/or L-CoQ10 showed hepatoprotective efficacy by reducing oxidative stress, the inflammatory response, apoptosis, and fibrosis in liver tissue.

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Section: Discussionsupporting

confidence: 90%

Acetyl-L-Carnitine and Liposomal Co-Enzyme Q10 Attenuate Hepatic Inflammation, Apoptosis, and Fibrosis Induced by Propionic Acid

Alhusaini

Alsoghayer

Alhushan

et al. 2023

IJMS

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“…Generally, The neuroprotective efficacy of Co-Q10 has been demonstrated by suppressing mitochondrial dysfunction and oxidative stress as shown in disease models of cognitive dysfunction [30] .…”

Section: Discussionmentioning

confidence: 99%

Calcium voltage-gated channel subunit alpha 1 C and glial fibrillary acidic protein signaling pathways as a selective biomarker in predicting the efficacy of liposomal loaded co-enzyme Q in the autistic rat model

et al. 2023

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“…Another study examined how CoQ10 affected rats with induced diabetic neuropathy and discovered that it reduced peripheral neuropathy [80]. In an experimental study on diabetic rabbits with polyneuropathy, CoQ10 showed a significant neuroprotective effect against harmful alterations in the sciatic nerve [81]. Another study examined the neuroprotective effect of liposomal CoQ10 on propionic acid-induced oxidative stress, inflammation, and apoptosis in a rat model further supporting these neuroprotective properties.…”

Section: Effects Of Coq10 On the Regeneration Of Peripheral Nerve Injurymentioning

confidence: 96%

The potential positive effects of coenzyme Q10 on the regeneration of peripheral nerve injury

Mead,

Delibaş,

Önger

et al. 2024

Explor Neuroprot Ther

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Peripheral nerve injuries (PNIs) constitute a significant concern as they predominantly affect young and productive age groups of the population, causing social and economic pressure on patients. PNIs are a global problem that can result in disability because of the disruption of nerve function. PNI leads to a reduction in nerve conduction velocity, which worsens or impairs the mobility of the innervated area. Managing PNI remains a major clinical challenge. Coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant first identified in 1957. It is an important antioxidant necessary for the organs to maintain their normal function and the body’s chemical processes. It scavenges free radicals and reduces oxidative stress. Studies showed that antioxidants such as CoQ10 a potent antioxidant, help the regeneration of PNIs. It has been observed to increase the myelination process in nerve fibres and promote nerve regeneration in rats after injury. Therefore, this review handles the current positive effects of CoQ10 on peripheral nerve regeneration following injury.

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Acetyl-L-carnitine and/or liposomal co-enzyme Q10 prevent propionic acid-induced neurotoxicity by modulating oxidative tissue injury, inflammation, and ALDH1A1-RA-RARα signaling in rats

Cited by 7 publications

References 64 publications

Acetyl-L-Carnitine and Liposomal Co-Enzyme Q10 Attenuate Hepatic Inflammation, Apoptosis, and Fibrosis Induced by Propionic Acid

Acetyl-L-Carnitine and Liposomal Co-Enzyme Q10 Attenuate Hepatic Inflammation, Apoptosis, and Fibrosis Induced by Propionic Acid

Calcium voltage-gated channel subunit alpha 1 C and glial fibrillary acidic protein signaling pathways as a selective biomarker in predicting the efficacy of liposomal loaded co-enzyme Q in the autistic rat model

The potential positive effects of coenzyme Q10 on the regeneration of peripheral nerve injury

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