Melatonin attenuates hypertension-induced renal injury partially through inhibiting oxidative stress in rats

Abstract

The aim of the present study was to investigate the protective effects of melatonin (MLT) on hypertension-induced renal injury and identify its mechanism of action. Twenty-four healthy male Wistar rats were divided into a sham control group (n=8), which was subjected to sham operation and received vehicle treatment (physiological saline intraperitoneally at 0.1 ml/100 g), a vehicle group (n=8), which was subjected to occlusion of the left renal artery and vehicle treatment, and the MLT group (n=8), which was subjected to occlusion of the left renal artery and treated with MLT (10 mg/kg/day). Pathological features of the renal tissues were determined using hematoxylin and eosin staining and Masson staining. Urine protein, serum creatinine (Scr), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined. Immunohistochemical analysis was performed to determine the expression of heme oxygenase-1 (HO-1), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS). Furthermore, reverse transcription polymerase chain reaction was conducted to determine the mRNA expression of HO-1, ICAM-1, eNOS and iNOS. A marked decrease in blood pressure was noticed in the MLT group at week 4 compared with that of the vehicle group (P<0.01). Furthermore, MLT treatment attenuated the infiltration of inflammatory cells and oedema/atrophy of renal tubules. MLT attenuated hypertension-induced increases in urine protein excretion, serum creatinine and MDA as well as decreases in SOD activity in renal tissues. Furthermore, MLT attenuated hypertension-induced increases in iNOS and ICAM-1 as well as decreases in eNOS and HO-1 expression at the mRNA and protein level. In conclusion, the results of the present study indicated that MLT had protective roles in hypertension-induced renal injury. Its mechanism of action is, at least in part, associated with the inhibition of oxidative stress.

Thymoquinone Upregulates Catalase Gene Expression and Preserves the Structure of the Renal Cortex of Propylthiouracil-Induced Hypothyroid Rats

“…In favor with that hypothesis, Masson's trichrome stain revealed extensive collagen deposition in cortical interstitium and in the glomeruli of the hypothyroid group versus few collagen fibers detected in the control group. These results were in line with those of Qiao et al [35]. In the same context, the current immunohistochemical findings of the hypothyroid group showed strong expression of ASMA in the glomeruli and numerous peritubular ASMA-positive cells supporting the findings of Masson's stain.…”

“…Under normal conditions, eNOS is the major source of nitric oxide; however, in renal tissues with pathological lesions, a decoupling process of eNOS is induced, resulting in the generation of O 2-. Reactive oxygen species are able to induce cellular injury and contribute to fibrosis [34,35]. In favor with that hypothesis, Masson's trichrome stain revealed extensive collagen deposition in cortical interstitium and in the glomeruli of the hypothyroid group versus few collagen fibers detected in the control group.…”

Influence of Synbiotics on Selected Oxidative Stress Parameters

“…Modrzewiowa 37, Poland) was used. This method is based on the reaction of free MDA (present in the sample) with thiobarbituric acid (TBA) to generate a MDA-TBA adduct [ 21 ].…”

Rescue effects of prenatal melatonin administration against bisphenol A- induced perturbations of reproductive and thyroid activities in male rat offsprings

“…The collected serum samples were used to evaluate the levels of T and triiodotyrosine (T3) using competitive enzyme immunoassay (TYPE7 &5) according to Tietz (1995). Also, malondialdehyde (MDA) and total antioxidant activities (TAC) were analyzed using commercial kits (Sigma-Aldrich, USA) according to Valko et al (2006) and Qiao et al (2016).…”