Melatonin prevents kidney injury in a high salt diet‐induced hypertension model by decreasing oxidative stress. Issue 1 (18th November 2015)

• Record Type: Journal Article
• Authors: Leibowitz, Avshalom; Volkov, Alexander; Voloshin, Konstantin; Shemesh, Chen; Barshack, Iris; Grossman, Ehud
• Is Part Of: Journal of pineal research. Volume 60:Issue 1(2016)
• Page Start: 48
• Page End: 54
• Publication Date: 2015-11-18
• Subjects: blood pressure -- kidney -- melatonin -- oxidative stress -- salt; Pineal gland -- Periodicals; Pineal Gland -- Periodicals; Épiphyse (Glande); Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 612.492
• DOI: 10.1111/jpi.12287
• Languages: English
• ISSNs: 0742-3098

Abstract

Abstract: Melatonin, a potent antioxidant molecule, plays a role in blood pressure regulation. We hypothesized that melatonin may generate a protective effect in a high salt diet (HSD) rodent model mediated by decreasing renal oxidative stress. Dahl salt‐sensitive rats were divided into three groups according to diet: normal chow (control); HSD; HSD with melatonin [30/mg/kg/day]) placed in their water (HSD + Mel) over an 8‐wk period. Blood pressure was measured by the tail cuff method. Kidney injury was evaluated by 24 H urine protein excretion. Glomerular injury index (GII) (fibrotic glomeruli/100 glomeruli) was evaluated from a Masson's trichrome‐stained section. Kidney oxidative stress was determined by superoxide production via dihydroethidium staining. Expression of oxidative stress‐related genes was measured by reverse transcriptase‐qPCR. Melatonin had no effect on blood pressure increase induced by HSD and attenuated proteinuria induced by HSD (HSD – 50.7 ± 12, HSD + Mel – 22.3 ± 4.3, controls – 6.5 ± 1.0 gram protein/gram creatinine, P < 0.001). HSD‐induced glomerular damage was significantly diminished by melatonin (GII in HSD – 24 ± 6, HSD + Mel – 3.6 ± 0.8, controls – 0.8 ± 0.5, P < 0.05). Superoxide production was significantly higher in kidneys of HSD fed rats than the controls (99 ± 9 versus 60 ± 7 relative fluorescent units (RFU)/ μ m 2, respectively, P < 0.05). Melatonin also decreased superoxide production (74 ± 5 RFU/ μ m 2, P < 0.05). The expression of kidney inducible nitric oxide synthase and p67 phox mRNA was significantly higher in HSD than in the controls and HSD + Mel rats. Treatment with melatonin eliminated the deleterious effect of HSD in the kidneys of Dahl salt‐sensitive rats. The beneficial effect of melatonin is not mediated by lowering blood pressure but by a direct antioxidative effect.