A Study on the Preventive Mechanism of Salidroside on PAH Syndrome in Broilers

ABSTRACT This study explored how salidroside alleviates pulmonary arterial hypertension (PAH) and ascites in broilers exposed to high-altitude hypoxia. Three groups of broilers (n = 80 each) were kept for 42 d under hypoxic (14.0-16.0 % O2), normoxic (20.8-21.5 % O2) or hypoxic + salidroside (50 mg kg-1 diet) conditions. On days 21, 35 and 42, mortality was recorded; serum SOD, GSH-Px and CAT activities, and MDA levels were quantified, and the right ventricular hypertrophy (RV/TV) index was calculated. At day 42, pulmonary arteries were sampled for histopathology, immunohistochemistry (Caspase-3, Ki67, PCNA), Western blot, RT-qPCR, and immunohistochemistry for CaSR. Compared with the hypoxic group, salidroside and normoxic broilers showed higher antioxidant enzyme activities, lower MDA, lower RV/TV index, and reduced total and ascites-related mortality (all p<0.05). Hypoxia-induced thickening of the arterial wall, decrease in Caspase-3, and increases in Ki67 and PCNA were all reversed by salidroside or normoxia. CaSR mRNA and protein levels were also downregulated in both non-hypoxic groups (p<0.05), with no difference between them (p>0.05). Salidroside thus mitigates hypoxic PAH and ascites by preserving right-heart function, suppressing pulmonary arterial remodeling, enhancing antioxidant capacity, and inhibiting CaSR signalling. In conclusion, salidroside mitigated PAH and ascites under high-altitude conditions by maintaining normal right heart function, reducing pulmonary artery pressure, enhancing antioxidant capacity, and modulating CaSR expression.