| Background:In recent years,due to the continuous adjustment of diet structure and the increasing rate of population aging,the incidence rate of AMI has been increasing year by year.Cardiovascular disease has posed a great threat to people’s health and economy.Acute myocardial infarction is a kind of clinical disease,which is caused by long-term coronary artery occlusion,which leads to the decrease of coronary blood flow and myocardial ischemia.With the maturity of PCI,thrombolysis,CABG,the survival rate of acute myocardial infarction is improved.However,the myocardial cells after the acute myocardial infarction will be damaged to varying degrees,even necrosis.Therefore,it is very easy to accompany with heart failure,heart rupture and other adverse events after acute myocardial infarction.At present,there is no effective drug to protect the myocardial necrosis after acute myocardial infarction,so it is of great significance to find the drugs that can protect the damaged myocardial cells.Chinese medicine is a national treasure in China.In the aspects of reducing myocardial injury,protecting cardiac function and delaying the progress of heart failure after acute myocardial infarction,TCM plays an important role in improving the long-term prognosis of patients with acute myocardial infarction.As a traditional Chinese medicine,Scorzonera autriaca will is widely distributed,which has the functions of clearing heat,detoxifying toxin,activating blood circulation and removing blood stasis.With the further research of pharmacology,flavonoids have been proved to be the main active component of Allium vulgaris.The flavonoids of S.austrriaca(FSA)has been widely used in the treatment of coronary heart disease,tumor,and brain insufficiency in recent years.Objective:To observe the protective effect of total flavonoids from Allium Scorzoneri L.on AMI in rats by ligating the LAD and to explore its mechanism.Method:100 Wistar rats were randomly divided into sham operation group(sham,n=25),model group(n=25),Low-dose group(100mg/kg,n=25),and High-dose group(400mg/kg,n=25).The rats in the groups of 100mg/kg and 400mg/kg were given 10ml/kg of FSA,once a day,and the same volume of 0.5% CMC-Na 10ml/kg was given to the Sham group and Model group,and all rats were given for 5 days.In this study,the model of Acute Myocardial Infarction was established by ligating the left anterior descending branch(LAD)of the coronary artery and ischemia.Detection of myocardial infarct area after NBT staining The activity of CK,AST,LDH,MDA and SOD were measured by spectrophotometry.The heart tissues of each group were fixed with 10% formaldehyde,and the pathological changes of myocardial tissue were detected by HE staining;Western Blot was used to detect the expression of relevant specific proteins and the phosphorylation level in myocardial tissue.Results:(1)Compared with sham group,the MIS in model group(34.08 ± 8.04%)was significantly increased(P < 0.01),and CK,AST and LDH activity in serum were significantly increased(P < 0.01 or P < 0.05),indicating that the model was successful in the rats.The area of Acute Myocardial Infarction decreased in the two groups after intervention of FSA,among which,the death surface of myocardial infarction in High-dose group was decreased and the activity of CK,AST and LDH in serum was significantly decreased(P <0.01 or P < 0.05);(2)Compared with the Sham group,SOD and MDA activity in model group decreased significantly(P < 0.01);MDA activity in serum and SOD activity increased in the two groups of rats treated with FSA,and the difference between High-dose group was statistically significant(P < 0.05),suggesting that the FSA had strong antioxidant ability,which could improve SOD level in rats with Acute Myocardial Infarction The activity of the cells can inhibit the oxidative stress reaction and reduce MDA production;(3)The histopathological results showed that the myocardial fibers in Sham group were arranged in order and red stained,and the nucleus of the myocardium was large and oval,and the color was dark blue.In Model group,a large number of myocardium in model group showed loose arrangement of fibers,irregular shape,irregular twist and fracture,uneven thickness,light color,wider spacing between myocardial fibers,and a large number of inflammatory cells infiltrated and leaked red cells.The myocardial fibers of High-dose group were slightly loose,the infarct range was limited to small size,interstitial edema and bleeding were not obvious,and there were a few inflammatory cells infiltrated occasionally between the myocardial fibers.The ischemic myocardial fibers in low dose group were not significantly improved;(4)Compared with sham group,BAX protein expression increased in model group(P <0.05),Bcl-2 protein decreased significantly(P < 0.01),and the difference was statistically significant.After dealing with FSA,the expression level of BAX protein in rat cardiac cells was decreased,Bcl-2,cleaved-caspase-3 and cleaved-caspase-9 were increased,among which,the high dose group had an effect on the expression of Bax protein The results showed that the results were significantly higher than those in other groups(P < 0.01 or P <0.05).It was suggested that the FSA could effectively reduce the number of myocardial cell apoptosis,protect the area of myocardial infarction and improve prognosis by regulating the mitochondrial apoptosis pathway;(5)The expression of PI3K/Akt pathway and Nrf-2/HO-1 pathway were significantly increased by FSA.It suggested that the protection of FSAmight be closely related to activation of two signal pathways.ConclusionFSA can significantly reduce the area of Acute Myocardial Infarction,reduce the activity of LDH,AST and CK,improve the pathological changes of myocardial tissue injury and inhibit oxidative stress in vivo.The mechanism may be to increase the signal pathways of PI3K/Akt and Nrf-2/HO-1,which can reduce oxidative stress and inhibit apoptosis,thus reducing the damaged area of myocardial infarction. |
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