Melatonin modulates pulmonary hypertension syndrome through increase of nitric oxide and its enzyme in chickens


Δημοσιευμένα: Feb 11, 2026
S Bahadoran
MR Khoozan-Chermahini
H Hassanpour
N Farhadi
Περίληψη

This study aimed to evaluate the effect of dietary melatonin in pulmonary hypertensive response by measuring nitric oxide and relative gene expression of endothelial and inducible nitric oxide synthases (eNOS and iNOS). A total of 144 one-day-old fast-growing chickens (Ross 308) were divided into three groups, with 48 birds per group. Each group was housed in one room and randomly split into three replicates, with 16 chickens per pen. The chicks were raised for 6 weeks under programmed cold stress. In experimental groups, cold stress was induced to study pulmonary hypertension syndrome (PHS), with melatonin supplemented at 0, 0.2, and 0.4 % diets. Post-experiment, serum total nitric oxide metabolites were measured and also heart (right ventricle) and lung tissues were analyzed for eNOS and iNOS gene expression by quantitative real-time PCR. Mortality rates were highest in the control group at 33.3%, followed by a decrement to 22.2% in the melatonin-0.2% treatment group, and further reduction to 13.9% in the melatonin-0.4% treatment group of chickens. The ratio of the right to total ventricular weight of heart as an indication of PHS was decreased in the melatonin-0.4% group of chickens at 42 days of age. A significant increase was revealed in the relative abundance of eNOS and iNOS genes within both the melatonin-0.2% and melatonin-0.4% groups of chickens compared to the control group (P < 0.05). However, no significant disparities in the expression levels of these genes were noted between the melatonin-0.2% and melatonin-0.4% groups (P > 0.05). There were no significant alterations in the relative quantities of these genes in both the melatonin-0.2% and melatonin-0.4% groups of chickens when compared to the control group (P > 0.05). It is concluded that melatonin may improve the cardiovascular system and decrease pulmonary hypertensive response through eNOS upregulation and the production of nitric oxide as a vasodilator.

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Αναφορές
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