Interference Effect of Tanshinoneⅱa on Myocardial Fibrosis in Spontaneously Hypertensive Rats
|School||Huazhong University of Science and Technology|
|Keywords||Tanshinone Ⅱ A Spontaneously hypertensive rats Myocardial fibrosis Matrix metalloproteinase Tissue inhibitor of matrix metalloproteinase|
The purpose of research tanshinone Ⅱ A (TSN) myocardial fibrosis in spontaneously hypertensive rats (SHR) and its possible mechanism of action. Methods 24 8-week-old SHR rats were randomly divided into three groups: SHR control group, tanshinone group, valsartan group; each group of eight. Another eight weeks of age WISTAR rats as normal control group. Were given the drug after four weeks of treatment, the rat tail artery systolic pressure measurement using the rat tail artery blood pressure measuring device and RM6240BD multi-channel physiological signal acquisition and processing system supporting electronic balance to measure the body weight of rats myocardial mass, calculated myocardial VG staining myocardial collagen content and collagen volume fraction (CVF), and reverse transcription polymerase chain reaction (RT-PCR) was used to detect myocardial matrix metalloproteinase protease (MMP) -2, MMP-9 and matrix metalloproteinase tissue inhibitor factor -2 (TIMP-2) mRNA expression. Results (1) Compared with Wistar rats SHR control rats, the growth of the blood pressure increase as the age increased (P lt; 0.01), tanshinone group and valsartan group after four weeks of treatment, blood pressure than SHR decline in the control group (P lt; 0.01), Wistar rats blood pressure remained unchanged. (2) 12 weeks, SHR control group ventricular mass, ventricular mass index were significantly higher than the other groups (P lt; 0.01); compared with SHR control group, tanshinone group and valsartan group treated for 4 weeks, ventricular Quality ventricular mass index decreased (P lt; 0.05). (3) VG staining can be clearly displayed the myocardial collagen stained red, located in the myocardium, mainly gathered in the perivascular. Normal control cardiomyocytes in WISTAR between cells, perivascular small amount of collagen fibers. SHR control rats significantly increased myocardial interstitial and perivascular collagen fibers, and disarranged. Tanshinone group and valsartan rats myocardial interstitial and perivascular collagen accumulation significantly reduced, arrangement also tends rules. Contained CVF determine the extent of myocardial fibrosis, compared with the control group, SHR control group there are significant myocardial fibrosis (P lt; 0.01), tanshinone group and valsartan group myocardial fibrosis compared with SHR control group was significantly reduced (P lt; 0.01). (4) compared with the normal control group, SHR control group, TIMP-2, MMP-2 and MMP-9 were increased, with a statistically significant (P lt; 0.05). Compared with SHR control group, of Tanshinone and valsartan group TIMP-2, MMP-2 and MMP-9 were reduced, with a statistically significant (P lt; 0.05). Conclusion TSN able to lower blood pressure, cardiac hypertrophy and fibrosis, its mechanism of action may be related to reduced myocardial tissue of MMP-2, MMP-9, TIMP-2 expression and improve related to MMP / TIMP balance.