CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats

Figure 3

CTRP9 suppresses inflammation in vivo. (a) The interleukin 18 (IL-18), IL-10, monocyte chemoattractant protein-1 (MCP-1), IL-6, F4/80, and tumor necrosis factor alpha mRNA expression levels were analyzed by RT-qPCR. (b, d) Injection of the rats with CTRP9 in the sham and shunt groups reduced the protein expression of MCP-1, IL-6, TNF-α, and IL-18, as assessed by immunoblot analysis of the total lung tissue. (c, e) Representative western blots of the total lung tissues indicating the induction of the inflammatory markers MCP-1, IL-6, TNF-α, and IL-18 following treatment of the rats with CTRP9 in the shunt group (β-actin was used as a loading control) for each group. In (b) and (d), the protein molecular weight of the MCP-1 (18 kDa), IL-6 (21 kDa), TNF-α (26 kDa), and IL-18 (22 kDa) was very similar, so they were all originating from the same gel. After exposure of the MCP-1 or TNF-α, we striped the primary antibody by the striping solution from the membrane and incubated the TNF-α antibody or IL-18 antibody. So, we use the same β-actin blot banding as the corresponding lading control from the same membrane. A total of 6 samples were selected from each group to perform RT-qPCR. The data are expressed as the . , , and vs. the Ad-GFP-sham group. IL: interleukin; MCP-1: monocyte chemoattractant protein-1; TNF-α: tumor necrosis factor alpha; RT-qPCR: reverse transcription-quantitative PCR; CTRP9: C1q/TNF-related protein 9; Ad-GFP: adenovirus-GFP.

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