Ameliorative effect of Rutin on sodium fluoride‐induced hypertension through modulation of Kim‐1/NF‐κB/Nrf2 signaling pathway in rats

Oyagbemi, Ademola Adetokunbo; Omóbòwálé, Temidayo Olutayo; Ola‐Davies, Olufunke Eunice; Asenuga, Ebunoluwa Racheal; Ajibade, Temitayo Olabisi; Adejumobi, Olumuyiwa Abiola; Afolabi, Jeremiah; Ogunpolu, Blessing Seun; Falayi, Olufunke Olubunmi; Ayodeji, Fatimah; Hassan, Fasilat Oluwakemi; Saba, Adebowale Benard; Adedapo, Adeolu Alex; Yakubu, Momoh Audu

doi:10.1002/tox.22636

Cited by 20 publications

(13 citation statements)

References 75 publications

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“…Rutin is a flavonol that presents in buckwheat and citrus fruits. In a sodium fluoride-induced hypertensive rats, administration of rutin reduced blood pressure elevation by enhancing NO bioavailability via down-regulation of NFκB expression and up-regulation of Nrf2 (Oyagbemi et al, 2018b).…”

Section: Anti-inflammatory Effects Of Flavonoids In Cvds Via Modulatimentioning

confidence: 99%

Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B (NFκB) Signaling in Cardiovascular Diseases: A Mini Review

et al. 2019

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Cardiovascular diseases (CVDs) such as angina, hypertension, myocardial ischemia, and heart failure are the leading causes of morbidity and mortality worldwide. One of the major transcription factors widely associated with CVDs is nuclear factor-kappa B (NFκB). NFκB activation initiates the canonical and non-conical pathways that promotes activation of transcription factors leading to inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. Flavonoids are bioactive polyphenolic compounds found abundantly in various fruits, vegetables, beverages (tea, coffee), nuts, and cereal products with cardiovascular protective properties. Flavonoids can be classified into six subgroups based on their chemical structures: flavanones, flavones, flavonols, flavan-3-ols, isoflavones, and anthocyanidins. As NFκB inhibitors, these flavonoids may modulate the expression of pro-inflammatory genes leading to the attenuation of the inflammatory responses underlying various cardiovascular pathology. This review presents an update on the anti-inflammatory actions of flavonoids via inhibition of NFκB mechanism supporting the therapeutic potential of these natural compounds in various CVDs.

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Section: Anti-inflammatory Effects Of Flavonoids In Cvds Via Modulatimentioning

confidence: 99%

Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B (NFκB) Signaling in Cardiovascular Diseases: A Mini Review

et al. 2019

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“…Again, several human studies have found that exposure to excessive F is closely associated with hypertension [546,547,548,549,550]. Similar observations have been observed in experimental studies with rodents [551,552,553,554,555,556]. Interestingly, activation of the TRH system, with increased production of TRH and an upregulation of its receptors has also been implicated in the pathogenesis of hypertension [557].…”

Section: Discussionmentioning

confidence: 64%

“…Increasing evidence also suggests that maternal iodine deficiency and hypothyroidism is associated with increased risk of cognitive impairment, neurodevelopmental and neuropsychiatric disorders in offspring including ADHD [511,512,513,514,515,516,517,518,519,520,521,522,523,524,525,526,527,528,529,530,531,532,533,534,535,536,537,538,539,540,541,542,543,544,545,546,547,548,549,550,551,552,553,554,555,556,557,558,559,560,561,562,563,564,565], ASD [566,567,568], behavioural seizures [517] and schizophrenia [516]. Moreover, maternal iodine deficiency and hypothyroidism is also associated with increased risk of asthma [518] and hypertension [569] in offspring.…”

Section: Discussionmentioning

confidence: 99%

Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health

Waugh¹

2019

IJERPH

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In this study, several lines of evidence are provided to show that Na + , K + -ATPase activity exerts vital roles in normal brain development and function and that loss of enzyme activity is implicated in neurodevelopmental, neuropsychiatric and neurodegenerative disorders, as well as increased risk of cancer, metabolic, pulmonary and cardiovascular disease. Evidence is presented to show that fluoride (F) inhibits Na + , K + -ATPase activity by altering biological pathways through modifying the expression of genes and the activity of glycolytic enzymes, metalloenzymes, hormones, proteins, neuropeptides and cytokines, as well as biological interface interactions that rely on the bioavailability of chemical elements magnesium and manganese to modulate ATP and Na + , K + -ATPase enzyme activity. Taken together, the findings of this study provide unprecedented insights into the molecular mechanisms and biological pathways by which F inhibits Na + , K + -ATPase activity and contributes to the etiology and pathophysiology of diseases associated with impairment of this essential enzyme. Moreover, the findings of this study further suggest that there are windows of susceptibility over the life course where chronic F exposure in pregnancy and early infancy may impair Na + , K + -ATPase activity with both short- and long-term implications for disease and inequalities in health. These findings would warrant considerable attention and potential intervention, not to mention additional research on the potential effects of F intake in contributing to chronic disease.

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“…Exercise training can relieve hypertension by targeting NF-κB signaling in the hypothalamic paraventricular nucleus ( 31 ). Rutin has been reported to ameliorate sodium fluoride-induced hypertension by regulating NF-κB/Nrf2 signaling in rats ( 32 ). The present study revealed that the phosphorylation of ERK, p65 and IκBα was stimulated by Ang II, and sinigrin treatment reduced this effect in a concentration-dependent manner in vivo and in vitro .…”

Section: Discussionmentioning

confidence: 99%

Sinigrin attenuates angiotensin II‑induced kidney injury by inactivating nuclear factor‑κB and extracellular signal‑regulated kinase signaling in vivo and in vitro

et al. 2021

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The present study investigated the function of sinigrin in angiotensin II (Ang II)-induced renal damage. The results demonstrated that systolic blood pressure (SBP) and diastolic blood pressure (dBP) were increased in Ang II-challenged rats, and sinigrin treatment inhibited their increase. The levels of blood urea nitrogen (BUN) and serum creatinine (ScR) were increased by Ang II in the rats, and these were reversed by sinigrin in a dose-dependent manner. In addition, the Ang II-induced elevation of urinary protein levels was inhibited by sinigrin treatment. Glomerular basement membrane thickness and EcM degradation markers, such as collagen I, collagen IV and fibronectin, were suppressed by sinigrin in the Ang II-challenged rats. Moreover, the levels of inflammatory regulators, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (McP-1), were reduced following sinigrin treatment of the Ang II-challenged rats and in Ang II-exposed proximal tubule epithelial cells. Furthermore, the superoxide dismutase (SOd) and catalase (cAT) levels were downregulated, whereas the malondialdehyde (MdA) levels were upregulated by Ang II; these effects were reversed by sinigrin treatment in vivo and in vitro. Mechanistically, sinigrin inhibited the Ang II-induced phosphorylation of ERK, p65 and IκBα. Thus, sinigrin attenuated Ang II-induced renal injury by inactivating ERK and NF-κB signaling. Sinigrin may thus prove to be a potential candidate for the treatment of hypertension-induced kidney damage.

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Ameliorative effect of Rutin on sodium fluoride‐induced hypertension through modulation of Kim‐1/NF‐κB/Nrf2 signaling pathway in rats

Cited by 20 publications

References 75 publications

Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B (NFκB) Signaling in Cardiovascular Diseases: A Mini Review

Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B (NFκB) Signaling in Cardiovascular Diseases: A Mini Review

Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health

Sinigrin attenuates angiotensin II‑induced kidney injury by inactivating nuclear factor‑κB and extracellular signal‑regulated kinase signaling in vivo and in vitro

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