Neuroprotective effects of carvacrol against cadmium-induced neurotoxicity in rats: role of oxidative stress, inflammation and apoptosis

Yıldız, Mustafa; Çelik, Hamit; Çağlayan, Cüneyt; Genç, Aydın; Doğan, Tolga; Satıcı, Emine

doi:10.1007/s11011-022-00945-2

Cited by 20 publications

(8 citation statements)

References 57 publications

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“…In an animal study, transmission electron microscopy shows degenerative changes in myelinated bers in cadmium intervention groups, with swollen axons, irregular outlines, disordered arrangement of neuro laments, swelling of many mitochondria, and destruction of cartridges [41]. Although the exact molecular mechanism has not been fully elucidated, the toxic effects of cadmium on nerve cells may rely on in ammation, oxidative stress, sphingolipid disturbance [42], mitochondrial damage, interference with neurotransmitter transmission, and induction of cell autophagy and apoptosis [25,43]. Many chemicals with anti-in ammatory and antioxidant properties can protect against cadmium-induced neurotoxicity [43,44,41].…”

Section: Discussionmentioning

confidence: 98%

The association between cadmium exposure and axonal injury biomarker, serum neurofilament light chain levels in US adults

Luo,

Lin

2024

Preprint

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Background and Aims: Cadmium exposure has been shown a toxic effect on the nervous system, but little is known regarding the link between cadmium exposure and axonal injury. Therefore, we aim to investigate whether there is a relationship between blood cadmium and serum neurofilament light chain (NfL) levels in the general population. Methods and Results: In the National Health and Nutrition Examination Survey 2013–2014, 1,040 participants with a median (IQR) age of 47 (35–60) years are enrolled. Serum NfL levels are measured using a highly sensitive immunoassay. Whole blood cadmium concentrations are detected using inductively coupled plasma mass spectrometry. Linear regression and restricted cubic spline models are used to analyze the strength and shape of the relationship between blood cadmium and serum NfL levels. In full adjusted model, blood cadmium levels are positively associated with serum NfL levels (Q4 vs Q1, β = 3.35, 95%CI: 0.41, 6.30, p for trend = 0.014). A potential linear positive dose-effect relationship is found between blood cadmium and serum NfL levels (p for non-linearity = 0.15), and the potential threshold dose of blood cadmium is 0.7 µg/L. The stratified analysis shows a significant positive relationship between blood cadmium and serum NfL levels is limited to middle-aged and older adults. Conclusion: The present study suggests a positive association between blood cadmium and serum NfL levels in the general US population. This study is expected to provide new ideas for the primary prevention and mechanism exploration of neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 98%

The association between cadmium exposure and axonal injury biomarker, serum neurofilament light chain levels in US adults

Luo,

Lin

2024

Preprint

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“…Zare et al 77 showed that a lead‐induced decrease in antioxidant enzyme activity and an increase in lipid peroxidation products were improved by CRV administration. Yildiz et al 78 reported that CRV decreased MDA levels and significantly increased GSH levels and catalase (CAT), SOD and GPx activities in brain tissue against cadmium induced neurotoxicity in rats.…”

Section: Discussionmentioning

confidence: 99%

Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve

Durmus,

Burak,

Goktug

et al. 2024

Clin Exp Pharma Physio

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The study aimed to investigate the harmful effects of acrylamide (AA), which forms in carbohydrate‐rich foods at temperatures above 120°C, on the central and peripheral nervous systems and to evaluate the potential neuroprotective effects of carvacrol (CRV). Male Wistar Albino rats were subjected to AA (40 mg/kg/bw/day) and CRV (50 mg/kg/bw/day) for 15 days. Following the last administration, evaluations revealed disrupted gait, heightened thermal sensitivity and altered paw withdrawal thresholds in AA‐exposed rats. Notably, AA reduced glutathione (GSH) and raised malondialdehyde (MDA) levels in both brain and sciatic nerve tissues. AA raised nuclear factor erythroid 2‐related factor 2 (Nrf2), caspase 3 and nuclear factor κB (NF‐κB) gene expressions while decreasing NR4A2. CRV co‐administration mitigated gait abnormalities, elevated GSH levels and lowered MDA levels in both tissues. CRV also modulated gene expression, reducing Nrf2 and NF‐κB while increasing NR4A2. Histopathological signs of AA‐induced neurodegeneration and elevated glial fibrillary acidic protein levels observed in brain and sciatic nerve tissues were rectified with simultaneous administration of CRV, thereby demonstrating neuroprotective efficacy in both regions. This study is pioneering in demonstrating CRV's neuroprotective potential against AA‐induced neurotoxicity in both central and peripheral nervous systems, effectively addressing limitations in the literature. In conclusion, the study revealed AA‐induced neurodegeneration in the brain and sciatic nerve, with CRV significantly mitigating this neurotoxicity. This novel research underscores CRV's promise as a neuroprotective agent against AA‐induced adverse effects in both the central and peripheral nervous systems.

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“…According to our study, Cd is capable reduce the amounts of DA and NE in the brain tissue. Following Cd intoxication, the monoaminergic disturbance has been observed in animal models (Yıldız et al, 2022;Omairi et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Neurotherapeutic effects of prodigiosin conjugated with silver-nanoparticles in rats exposed to cadmium chloride-induced neurotoxicity

et al. 2022

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Prodigiosin is a red pigment produced by Serratia marcescens strain. Bacterial prodigiosin and its synthetic derivatives are efficacious antioxidants and proapoptotic agents. This study illustrates a new approach for use of prodigiosin conjugated silver nanoparticles (PG-AgNP 2 ) against cadmium chloride (CdCl 2 ) induced neurotoxicity in rats. Rats were (ip) injected with Cd (6.5 mg/kg) for 7 days with or without PG-AgNP 2 (3 mg/kg). The concentration of Cd, DA, NE, 5-HT, amino acids, NO, MDA, SOD, GSH, catalase, TNF-α, IL-6, Bax, Bcl 2 and Caspase-3. The Cd-intoxicated group showed a significant increase in Cd concentration in brain tissue, in addition, to an increase in MDA and NO and a decrease in the content of neurotransmitters (DA, NE, and 5-HT), inhibitory amino acids, and level of all studied antioxidant enzymes. PG-AgNP 2 treatment, significantly reduced Cd-induced brain tissue injury as indicated by increased antioxidant molecules, neurotransmitters (DA, NE, and 5-HT), and inhibitory amino acids accompanied by lower oxidative stress indices (MDA and NO) and excitatory amino acids in brain tissue. PG-AgNP 2 decreased inflammatory mediators including pro-inflammatory cytokines and prevented the development of apoptosis in the brain tissue. Our findings suggest that PG-AgNP 2 can act as a therapeutic agent against neuronal impairments associated with Cd exposure.

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Neuroprotective effects of carvacrol against cadmium-induced neurotoxicity in rats: role of oxidative stress, inflammation and apoptosis

Cited by 20 publications

References 57 publications

The association between cadmium exposure and axonal injury biomarker, serum neurofilament light chain levels in US adults

The association between cadmium exposure and axonal injury biomarker, serum neurofilament light chain levels in US adults

Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve

Neurotherapeutic effects of prodigiosin conjugated with silver-nanoparticles in rats exposed to cadmium chloride-induced neurotoxicity

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