Effect of puerarin on monocrotaline-induced pulmonary hypertension and expression of chemokine CX3CL1/fractalkine

AIM: To observe the change of CX₃CL1/fractalkine (FKN) in the rats with monocrotaline-induced pulmonary hypertension, and to study the intervention of puerarin. METHODS: The pulmonary hypertension model was established in vivo by intraperitoneal injection of monocrotaline. Thirty male Sprague-Dawley rats (270-310 g) were randomly divided into 3 groups: control group (C), monocrotaline model group (M)and puerarin treatment group (M+P). The mean pulmonary arterial pressure (mPAP), mean right ventricular pressure (mRVP), mean carotid arterial pressure (mCAP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) were also detected. The structural changes of pulmonary arterioles were observed under optical microscope. Remodeling of lung blood vessels was determined by measuring the ratio of vessel wall area to total area (WA/TA) and the medium thickness of pulmonary artery (PAMT). The concentration of soluble fractalkine(sFKN) in plasma was measured by ELISA. The expression of FKN in the pulmonary artery wall was measured by immunohistochemistry. The mRNA level of FKN in the lung tissues was detected by RT-PCR.RESULTS: mPAP, mRVP, RV/(LV+S), WA/TA and PAMT in M group were higher than those in C group (P<0.01). RV/(LV+S), WA/TA and PAMT in M+P group were significantly lower than those in M group (P<0.01). No significant difference of mCAP among the 3 groups was observed. The levels of sFKN, FKN mRNA and FKN protein in M group were higher than those in C group (P<0.01), and the above data in M+P group were lower than those in M group(P<0.05). The serum level of sFKN had a positive correlation with PAMT and RV/(LV+S) (r＝0.719, r=0.685,respectively, P<0.01).CONCLUSION: Puerarin down-regulates the expression of FKN and suppresses the development of pulmonary hypertension and pulmonary vessel remodeling.