Abstract: AIM: To investigate the changes of calreticulin precursor in the normal, pulmonary hypertensive induced by monocrotaline and puerarin rats, and to explore the mechanism of the inhibition of puerarin on the pulmonary hypertension and pneumoangiogram rebuilding.METHODS: The pulmonary hypertensive rat model was established and the mean pulmonary arterial pressure, mean carotid arterial pressure, weight ratio of right ventricle to left ventricle plus septum, thickness of pulmonary arterial media smooth cell layer were measured.The two-dimensional gel electrophoresis was used to detect the total proteins from these five groups.The MALDI-TOF-TOF-MS was used to identify the differential protein and the retrieval databank in NCBInr was searched.RESULTS: The mean pulmonary artery pressure (mPAP), right ventricle proportion by weight ([RV/(LV+S) ] %) and pulmonary artery media thickness(PAMT) of 3-week-monocrotaline group were highly significant than those of normal group (P<0.01), indicated that the rat model of pulmonary hypertention formed.The mPAP, [RV/(LV+S) %] and PAMT of puerarin group were lowly significant than those of 3-week-monocrotaline group, indicated that the pulmonary hypertention, pneumoangiogram rebuilding, the right ventricle hypertrophy could be inhibited by puerarin.The MALDI-TOF-TOF-MS discovered that the calreticulin precursor expressed almost 0 in normal group and expressed a great quantity in 3-week-monocrotaline group, but down-expressed quickly in puerarin group, almost 0 level.CONCLUSION: The puerarin could inhibit the form of pulmonary hypertension by interfering with calreticulin precursor, it is worth further studies.

Key words: calreticulin precursor, puerarin, pulmonary hypertension, two-dimensional gel electrophoresis, MALDI-TOF-TOF-MS