EFFECTS OF QUERCETIN ON CYTOKINES AND PULMONARY CAPILLARY CELLS IN PULMONARY ARTERIAL HYPERTENSION RATS

This study aimed to investigate the effects of quercetin in the treatment of pulmonary arterial hypertension (PAH) in a murine model. Thirty-six adult male rats were randomly divided into three groups: the control group (saline), monocrotaline (MCT) - induced PAH group (MCT group) and quercetin treatment group (prevention group). After modelling, the animals from prevention group received 100 mg/(kg bw/day quercetin by gavage and the gavage for 20 days, while the animals from the other two groups received the same amount of 0.9% sodium chloride saline solution. The mean pulmonary artery pressure, right ventricular index and relative expression levels of HIF-1 (hypoxia-inducible factor 1), ET-1(vascular endothelin-1), TGF-beta 1 (transforming growth factor-beta 1), VEGF (vascular endothelial growth factor), IL-1 (interleukin-1), IL-6 (interleukin-6) and TNF-alpha (tumour necrosis factor alpha) in lung tissues significantly increased in MCT group compared with the control group, 21 days after modelling. The levels of HGF (hepatocyte growth factor) and NAC (N-acetyl-L-cysteine) significantly increased compared with the control group. The treatment with quercetin significantly decreased the level of mean PAH, right ventricular index and relative expression levels of H1F-1, ET-1, TGF-beta 1, VEGF, IL-1, IL-6 and TNF-alpha in lung tissues compared with MCT group and significantly decreased the levels of HGF and NAC. In vitro experiment with PCEC (pulmonary capillary endothelial cells) from the three groups showed that in the MCT group the cell proliferation was significantly decreased and the apoptosis was significantly increased compared with the control group, while the quercetin treatment inhibited the MCT-induced cell apoptosis and promoted cell proliferation. In conclusion, quercetin can alleviate PAH by regulating the inflammatory cytokines, promoting cell proliferation and inhibition of cell apoptosis.