title: 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.
authors.affiliation: Department of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Yu-Feng
authors.initials: YF
authors.lastname: Qiao
authors.affiliation: Department of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Wen-Juan
authors.initials: WJ
authors.lastname: Guo
authors.affiliation: Department of Nephrology, Baoding No. 1 Hospital, Baoding, Hebei 071000, P.R. China.
authors.forename: Lu
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Shan
authors.initials: S
authors.lastname: Shao
authors.affiliation: Department of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Xi
authors.initials: X
authors.lastname: Qiao
authors.affiliation: Department of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Jin-Jin
authors.initials: JJ
authors.lastname: Shao
authors.affiliation: Department of Nephrology, Shanxi People's Hospital, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Department of Nephrology, Shanxi People's Hospital, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Rong-Shan
authors.initials: RS
authors.lastname: Li
authors.affiliation: Department of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Wang
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003404:Creatinine / Q000097:blood; D004487:Edema / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000187:drug effects; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism; D006977:Hypertension, Renal / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D007150:Immunohistochemistry; D007249:Inflammation / Q000097:blood / Q000150:complications / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008550:Melatonin / Q000494:pharmacology*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011507:Proteinuria / Q000097:blood / Q000150:complications / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D003404:Creatinine; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase; D008550:Melatonin