SHI Zhao-ping, ZHOU Xiao-hui, XU Qian, et al. Effect and Mechanism of Paeonol on Myocardial Fibrosis Induced by Myocardial Infarction in Rats[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(9): 150-155.
DOI:
SHI Zhao-ping, ZHOU Xiao-hui, XU Qian, et al. Effect and Mechanism of Paeonol on Myocardial Fibrosis Induced by Myocardial Infarction in Rats[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(9): 150-155. DOI: 10.13422/j.cnki.syfjx.2015090150.
Effect and Mechanism of Paeonol on Myocardial Fibrosis Induced by Myocardial Infarction in Rats
Objective: To study the effect of paeonol (Pae) on myocardial fibrosis in rats with acute myocardial infarction (AMI) and to investigate whether its mechanism is related to the expression of transforming growth factor-β1(TGF-β1)
Smad2 mRNA and protein. Method: In vivo model of AMI was made using the ligation of left anterior descending coronary branch.The successful myocardial infarction(MI) modeling was based on the following changes like electrocardiogram(ECG) ST segment level downward or upward shift ≥0.1 mV and T wave towering over with R wave of 1/2
left ventricular anterior turned pale. The rats were randomly divided into the model group
the sham group
the low-
high-dose Pae groups (8.0
12.0 mg·kg-1). The sham group and model group were given ip volume of saline daily. The left ventricular indexed were measured after 4 weeks. The pathology of myocardial tissue was observed by HE staining
the level of myocardial interstitial fibrosiswas observed by Masson staining. The mRNA expression levels of TGF-β1
Smad 2 in myocardial tissues were detected using real-time quantitative PCR(RT-PCR) technique. Result: Compared with the sham group
he left cardiac index was significantly higher(P< 0.01) in the model group. Compared with the model group
the left cardiac index was decreased(P< 0.01
P< 0.05)in all does Pae groups. HE staining showed that compared with the sham group pathological changes were significantly in the model group
there were cardiac hypertrophy
elongation and coagulation necrosis in injured myocardial hypertrophy edge part
while some loose edema occurred in left ventricular myocardial wall portion. Compared with the model group
the pathological changes were decreased. Masson staining showed that compared with the sham group
collagen fibers increased significantly in model group
and there appeared fiber epilepsy marks
and also severe myocardial fibrosis
Compared with the model group
the level of myocardial fibrosis in all dose Pae groups were decreased. Compared with the sham group
TGF-β1
Smad 2 mRNA and protein expression levels were significantly increased(P< 0.05);compared with the model group
the TGF-β1
Smad 2 mRNA and protein expression level were decreased(P< 0.01)in all dose Pae groups. Conclusion: Pae has anti-myocardial fibrosis effect in AMI rats. Its mechanism may be related to the intervention of TGF-β1/Smad2 signaling pathways.
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