Luteolin normalizes blood pressure via its antioxidant activity and down-regulation of renal Angiotensin II receptor and Mineralocorticoid receptor expressions in rats …

T Ajibade, A Akinrinde, M Adetona… - Nigerian Journal of …, 2022 - ojshostng.com
Nigerian Journal of Physiological Sciences, 2022ojshostng.com
This study was designed to investigate the modulatory role of Luteolin (Lut), a flavonoid
phytochemical, on haemodynamic parameters and the potential mechanisms involving renal
Angiotensin II (AT 2 R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-
exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were
administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF
(300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 …
Abstract
This study was designed to investigate the modulatory role of Luteolin (Lut), a flavonoid phytochemical, on haemodynamic parameters and the potential mechanisms involving renal Angiotensin II (AT 2 R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF (300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 mg/kg) along with Dcf and NaF exposures. All treatments lasted 8 days, following which blood pressure indices were measured using tail-cuff plethysmography. Renal expressions of AT 2 R and MCR were studied with immunohistochemistry, while biomarkers of oxidative and antioxidant status were also measured in the kidneys. Systolic, diastolic and mean arterial pressures were significantly (p< 0.05) reduced in Dcf-treated rats, compared to control values. However, co-treatment with NaF or Lut restored these parameters. While the expression of AT 2 R and MCR was high in the Dcf and Dcf+ NaF groups, treatment with Lut caused obvious reduction in the renal expression of these receptors. Increased lipid peroxidation (Malondialdehyde) and protein oxidation (protein carbonyls) with a lowering of reduced glutathione levels contributed to the renal toxicity of Dcf, and these were significantly ameliorated in Lut-treated rats. In conclusion, the preservation of haemodynamic indices by Lutin the experimental ratsprobably included mechanisms involving down-regulation of renal expressions of AT 2 R and MCR, reduction of oxidative stress and an improvement of renal antioxidant status.
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