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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: A novel complement C3 inhibitor CP40-KK protects against experimental pulmonary arterial hypertension via an inflammasome NLRP3 associated pathway

Fig. 1

C3a was significantly upregulated in the plasma of MCT-induced PAH rats A–C Right ventricular systolic pressure (RVSP), right ventricular hypertrophy indexes (RV/LV + S), and RV/body weight (BW) increased significantly after MCT treatment (n = 6 per group). D,H–I Representative HE staining images of rat lungs from the two groups (D, upper) and graphs reflecting the percentage of medial wall thickness WT% and vessel wall area WA% (H, I; n = 6 per group). E,F,J,L Pulmonary vascular remodeling was aggravated by MCT. Representative immunohistochemical staining images of α-SMA (E, upper) and graphs summarizing results (J; n = 6 per group). Representative western blots and quantification of PCNA protein levels in lung homogenates (F,L; n = 6 per group). (D, lower and E, lower) representative immunofluorescence and immunohistochemistry staining for Mac-2 of the distal pulmonary arteries exposed to MCT (n = 6 per group). G,M Representative Western blots and quantification of C3a protein levels in the rat plasma (n = 6 per group). Scale bar: 20 μm (D,E); MCT: monocrotaline; RV: right ventricle; LV: left ventricle; S: septum; mean ± SEM; comparisons between the control and MCT groups made by student t test; *P < 0.05, **P < 0.01

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