Experimental study on the relationship between tumor necrosis factor α and pulmonary vascular remodeling in rats with chronic thromboembolic pulmonary hypertension / 中国基层医药

ABSTRACT

Objective:To investigate the relationship between tumor necrosis factor α (TNF-α) and pulmonary vascular remodeling in rats with chronic thromboembolic pulmonary hypertension (CTEPH).Methods:A total of 104 Wister rats were provided by Laboratory Animal Center, Harbin Medical University between January 2020 and June 2020 and included in this study. They were randomly divided into CTEPH group ( n = 52) and sham-operation group ( n = 52). Rats in the CTEPH group were injected with an embolus via the left external jugular vein to establish rat models of CTEPH. Rats in the sham-operation group were injected with the same amount of 0.9% sodium chloride injection. Relevant indicators were measured after 7 days and 1 month of embolization. Results:After embolization for 7 days and 1 month, plasma TNF-α level in the sham-operation group was (45.62 ± 1.65) ng/L and (46.24 ± 2.82) ng/L, respectively, which were significantly lower than those in the CTEPH group [(47.15 ± 1.58) ng/L, (48.85 ± 2.96) ng/L, t = 3.48, 3.31, both P < 0.05). Mean pulmonary artery pressure in the sham-operation group was significantly lower than that in the CTEPH group ( t = 1.89, 3.11, both P < 0.05). TNF-α mRNA expression in the sham-operation group was significantly lower than that in the CTEPH group ( t = 3.06, 3.36, both P < 0.05). The area/total area of pulmonary artery wall in the sham-operation group was significantly lower than that in the CTEPH group ( t = 1.73, 4.17, both P < 0.05). Plasma TNF-α level was positively correlated with pulmonary artery TNF-α mRNA expression ( r = 0.82, P < 0.05). Plasma TNF-α level and pulmonary artery TNF-α mRNA expression were positively correlated with mean pulmonary artery pressure ( r = 0.62, 0.73, both P < 0.05) and area/total area of pulmonary artery wall ( r = 0.61, 0.63, both P < 0.05). Conclusion:TNF-α may be involved in the pathogenesis of CTEPH by increasing pulmonary artery pressure and vascular remodeling.