Clofibrate, a Peroxisome Proliferator–Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride–Induced Toxicity

Oyagbemi, Ademola Adetokunbo; Adejumobi, Olumuyiwa Abiola; Jarikre, Theophilus Aghogho; Ajani, Olumide Samuel; Asenuga, Ebunoluwa Racheal; Gbadamosi, Idayat Titilayo; Adedapo, Aduragbenro Deborah; Aro, A.O.; Ogunpolu, Blessing Seun; Hassan, Fasilat Oluwakemi; Falayi, Olufunke Olubunmi; Ogunmiluyi, Iyanuoluwa Omolola; Omóbòwálé, Temidayo Olutayo; Arojojoye, Oluwatosin Adetola; Ola‐Davies, Olufunke Eunice; Saba, Adebowale Benard; Emikpe, Benjamin Obukowho; Oyeyemi, M. O.; Nkadimeng, Sanah Malomile; McGaw, Lyndy Joy; Kayoka-Kabongo, Prudence Ngalula; Oguntibeju, Oluwafemi Omoniyi; Yakubu, Momoh Audu

doi:10.1007/s12011-021-02722-1

Cited by 9 publications

(4 citation statements)

References 96 publications

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“…Significantly increased blood and brain MDA in the F group in our study corroborate earlier reports for experimental animals and children with chronic fluorosis ( 69 , 70 , 71 ). However, unlike some reports of fluoride poisoning resulting in high MDA levels and oxidative stress that disturbed kidney and liver function in different animal species ( 72 , 73 , 74 ), MDA levels in our study remained similar to control in these organs.…”

Section: Resultscontrasting

confidence: 96%

Redox and biometal status in Wistar rats after subacute exposure to fluoride and selenium counter-effects

Radovanović

Antonijević

Baralić

et al. 2022

Archives of Industrial Hygiene and Toxicology

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This study aimed to investigate the effect of 150 mg/L sodium fluoride (NaF) on redox status parameters and essential metals [copper (Cu), iron (Fe), and zinc (Zn)] in the blood, liver, kidney, brain, and spleen of Wistar rats and to determine the protective potential of selenium (Se) against fluoride (F-) toxicity. Male Wistar rats were randomly distributed in groups of five (n=5) receiving tap water (control) or water with NaF 150 mg/L, NaF 150 mg/L + Se 1.5 mg/L, and Se 1.5 mg/L solutions ad libitum for 28 days. Fluorides caused an imbalance in the redox and biometal (Cu, Fe, and Zn) status, leading to high superoxide anion (O2 .-) and malondialdehyde (MDA) levels in the blood and brain and a drop in superoxide dismutase (SOD1) activity in the liver and its increase in the brain and kidneys. Se given with NaF improved MDA, SOD1, and O2 .- in the blood, brain, and kidneys, while alone it decreased SH group levels in the liver and kidney. Biometals both reduced and increased F- toxicity. Further research is needed before Se should be considered as a promising strategy for mitigating F- toxicity.

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Section: Resultscontrasting

confidence: 96%

Redox and biometal status in Wistar rats after subacute exposure to fluoride and selenium counter-effects

Radovanović

Antonijević

Baralić

et al. 2022

Archives of Industrial Hygiene and Toxicology

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“… 28 Clofibrate, peroxisome proliferator-activated receptor-alpha (PPARα) agonist, was reported to reduce oxidative stress, improved antioxidant status. 29 Ikarugamycin was showed anti antibacterial activity against Intracellular Staphylococcus aureus. 30 …”

Section: Resultsmentioning

confidence: 99%

Multi-Transcriptomic Analysis and Experimental Validation Implicate a Central Role of STAT3 in Skin Barrier Dysfunction Induced Aggravation of Rosacea

Wang¹,

Wang²,

Huang³

et al. 2022

JIR

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Objective Rosacea is a chronic inflammatory skin disease with high morbidity. Previous studies have described the contribution of skin barrier dysfunction (SBD) in the progression of rosacea, but the specific mechanism remains unclear. In this study, we aim to investigate the key genes that may involve SBD-mediated rosacea aggravation. Methods In this study, we evaluated the SBD patterns of rosacea based on the expression of 23 skin barrier-related genes (SBRGs) using a consensus clustering analysis, and revealed the SBD-mediated immune cells infiltration in rosacea using GSE65914 dataset. The key genes associated with SBD and rosacea progression were identified using WGCNA analysis and then verified in rosacea mice model. Results Two distinct SBD patterns (moderate- and high-SBD patterns) were determined in rosacea. GO, KEGG and GSEA analysis revealed the differently immune-related signal pathways between two SBD patterns in rosacea. The XCell immune cell assays showed that the increased immune infiltration with SBD. Subsequently, the WGCNA analysis identified STAT3 as the hub gene related to rosacea and SBD, and correlation analysis revealed that STAT3 could contribute to the progression of rosacea partly by dysregulating immune infiltration via activating the cytokine/chemokines signal. Finally, the up-regulated STAT3 was verified in the epidermis of rosacea tissues and correlated with SBRGs expression using IHC and epidermal transcriptome data of rosacea. The vivo experiment showed that tape stripping-induced SBD evidently induced the expression of STAT3 and increased CD4 + T cell infiltration in LL37-induced rosacea-like skin lesion in mice. Conclusion In conclusion, our results showed that the destruction of the skin barrier aggravates the inflammation levels and immune infiltration of rosacea partly by activating STAT3-mediated cytokine signal pathways in keratinocytes.

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“…Sodium uoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals (Oyagbemi et al 2021). NaF is universally present in water, soil and the atmosphere (Oyagbemi et al 2020).…”

Section: Introductionmentioning

confidence: 99%

“…From our laboratory, we have documented organ and non-organ toxicities associated with NaF Omóbòwálé et al 2018;Oyagbemi et al 2021). Cardiovascular and neurodegenerative dysfunctions such as hypertension and motor in-coordination have been reported (Oyagbemi et L-Arginine is one of the most metabolically versatile amino acids (Gad 2010).…”

Section: Introductionmentioning

confidence: 99%

L-arginine and lisinopril supplementation protects against sodium fluoride–induced nephrotoxicity and hypertension by suppressing mineralocorticoid receptor and angiotensin-converting enzyme 3 activity

Ajibade

Awodele²,

Tijani

et al. 2022

Environ Sci Pollut Res

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Sodium uoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals. NaF is universally present in water, soil and the atmosphere.The persistent and alarming rate of increase in cardiovascular and renal diseases and disorders caused by chemicals such as sodium uoride (NaF) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the renoprotective and antihypertensive effects of L-Arginine against NaF-induced nephrotoxicity. Thirty male Wistar rats (150-180 g) were used in this study. The rats were randomly divided into ve groups of six rats each as Control, NaF (300 ppm), NaF + L-Arginine (100 mg/kg), NaF + L-Arginine (200 mg/kg), and NaF + Lisinopril (10 mg/kg), respectively; orally for eight days. Histopathological examination and immunohistochemistry of renal angiotensin converting enzyme (ACE) and mineralocorticoid receptor (MCR) were performed. Markers of renal damage, oxidative stress, antioxidant defence system, and blood pressure parameters were determined. L-Arginine and Lisinopril signi cantly (p < 0.05) ameliorated the hypertensive effects of NaF. The systolic, diastolic and mean arterial blood pressure of the treated groups were signi cantly (p < 0.05) reduced compared with the hypertensive group. This nding was concurrent with signi cantly increased serum bioavailability of nitric oxide in the hypertensive treated with and Lisinopril. Also, there was signi cant reduction in the level of blood urea nitrogen and creatinine in the serum of the hypertensive rats treated with L-arginine and Lisinopril. There was signi cant (p < 0.05) reduction in markers of oxidative stress such as malondialdehyde and protein carbonyl and concurrent increase in the levels of antioxidant enzymes in the kidney of hypertensive rats treated with L arginine and Lisinopril. The results of this study suggest that L-Arginine and and Lisinopril normalized high blood pressure, reduced oxidative stress, reduced the expression of renal angiotensin converting enzyme and mineralocorticoid receptor and improved nitric oxide production. Thus, L-Arginine holds promise as a potential therapy against hypertension and renal damage.

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Clofibrate, a Peroxisome Proliferator–Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride–Induced Toxicity

Cited by 9 publications

References 96 publications

Redox and biometal status in Wistar rats after subacute exposure to fluoride and selenium counter-effects

Redox and biometal status in Wistar rats after subacute exposure to fluoride and selenium counter-effects

Multi-Transcriptomic Analysis and Experimental Validation Implicate a Central Role of STAT3 in Skin Barrier Dysfunction Induced Aggravation of Rosacea

L-arginine and lisinopril supplementation protects against sodium fluoride–induced nephrotoxicity and hypertension by suppressing mineralocorticoid receptor and angiotensin-converting enzyme 3 activity

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