Fig. 4. Edaravone alleviates pulmonary damage in HPH mice by targeting NOS3.
(A) STITCH analyzed the target proteins of edaravone. (B) Quantitative reverse transcription polymerase chain reaction and western blotting were used to detect the expression of NOS3 mRNA and protein in the lung tissue of HPH mice before and after edaravone treatment. Next, HPH mice were injected with 5 mg/kg edaravone and 40 mg/kg NOS inhibitor L-NMMA. (C) The Griess method was used for detecting the contents of NO in lung tissue. (D) H&E staining was used to reveal the pathological changes of lung tissue and the remodeling of pulmonary vessels (×200); terminal deoxynucleotidyl transferase dUTP nick end labeling was used to reveal pulmonary cell apoptosis (×200). (E, F) WT, RVSP, mPAP, and RV / (LV + S) were measured. (G) Enzyme-linked immunosorbent assay was performed to detect the expression of TNF-α and IL-6 in serum and lung tissue. (H) The expression of MAD and SOD was measured. (I) Immunohistochemistry was used to reveal the expression of α-SMA in pulmonary arterioles (×200). The data were expressed as mean ± SD. n = 10. HPH, hypoxic pulmonary hypertension; NOS3, nitric oxide synthase 3; NO, nitric oxide; WT, wall thickness; RVSP, right ventricular systolic pressure; mPAP, mean pulmonary artery pressure; RV, right ventricle; LV, left ventricle; S, septum; TNF, tumor necrosis factor; IL, interleukin; MAD, malondialdehyde; SOD, superoxide dismutase; α-SMA, α-smooth muscle actin. *p < 0.05, **p < 0.01, and ***p < 0.001, compared with the control group. #p < 0.05, ##p < 0.01, and ###p < 0.001, compared with the HPH group. &p < 0.05, &&p < 0.01, and &&&p < 0.001, compared with the HPH + edaravone group.
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