Objective: To explore the preventive and therapeutic effects of pulmonary hypertension model rats.
Method: A PAH rat model was established by left lobectomy combined with monochromatic subcutaneous injection of MCT into the abdominal wall, and 100 adult male Wistar rats were randomly selected from the blank control group (group A) DIZE. Divide them into control group (group B) and PAH. Model group (C group), DIZE treatment PAH model group (D group) and (DIZE + C-16) treatment PAH model group (E group), active fluorescence resonance energy transfer (FRET) and enzyme binding immunosorbent assay (ELISA) Use) Angiotensin converting enzyme 2 (ACE2), serum IL-6 and IL-8 levels, mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index (RVHI), medial thickness and external pulmonary artery diameter ratio calculated by elastic fiber staining (WT), intimal hyperplasia fraction and methods of analyzing pulmonary vascular disease.
Results: Comparison of RVHI, ACE2 enzyme activity, WT and intimal hyperplasia scores: The difference between group C, D and E was statistically significant compared with group A (P\u003c0.05). The difference between group D and group E was statistically significant. Academic significance (P\u003c0.05). The five groups have statistically significant differences in the overall analysis of each index (P\u003c0.05).
Conclusion: Elmidin enhances the activity of ACE2 enzyme, effectively reduces mPAP, RVHI and WT, while reducing lung mesenteric hypertrophy and inhibiting lung intimal hyperplasia. The conclusion of this study provides an experimental basis for the treatment of human PAH with Elmidin.