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2017 ; 18
(6
): ä Nephropedia Template TP
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Melatonin Attenuates Pulmonary Hypertension in Chronically Hypoxic Rats
#MMPMID28538666
Hung MW
; Yeung HM
; Lau CF
; Poon AMS
; Tipoe GL
; Fung ML
Int J Mol Sci
2017[May]; 18
(6
): ä PMID28538666
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Chronic hypoxia induces pulmonary hypertension and vascular remodeling, which are
clinically relevant to patients with chronic obstructive pulmonary disease (COPD)
associated with a decreased level of nitric oxide (NO). Oxidative stress and
inflammation play important roles in the pathophysiological processes in COPD. We
examined the hypothesis that daily administration of melatonin (10 mg/kg)
mitigates the pulmonary hypertension and vascular remodeling in chronically
hypoxic rats. The right ventricular systolic pressure (RVSP) and the thickness of
pulmonary arteriolar wall were measured from normoxic control, vehicle- and
melatonin-treated hypoxic rats exposed to 10% O? for 14 days. Levels of markers
for oxidative stress (malondialdhyde) and inflammation (tumor necrosis factor-?
(TNF?), inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2)) and the
expressions of total endothelial NO synthase (eNOS) and phosphorylated eNOS at
serine1177 (ser1177) were determined in the lung tissue. We found that the RVSP
and the thickness of the arteriolar wall were significantly increased in the
vehicle-treated hypoxic animals with elevated levels of malondialdhyde and mRNA
expressions of the inflammatory mediators, when compared with the normoxic
control. In addition, the phosphorylated eNOS (ser1177) level was significantly
decreased, despite an increased eNOS expression in the vehicle-treated hypoxic
group. Melatonin treatment significantly attenuated the levels of RVSP, thickness
of the arteriolar wall, oxidative and inflammatory markers in the hypoxic animals
with a marked increase in the eNOS phosphorylation in the lung. These results
suggest that melatonin attenuates pulmonary hypertension by antagonizing the
oxidative injury and restoration of NO production.
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