Effect of artemisinin on remodeling of sympathetic nerve and its mechanism of myocardial infarction rats
Zheng Wu-yan
Abstract
Zheng Wu-yan
Abstract
Objective To study the effect of artemisinin on remodeling of sympathetic neural in rats with myocardial infarction and explore its molecular mechanism. Methods 70 SD male rats were randomly divided into three groups,10 rats in sham operation group,30 rats in myocardial infarction group,30 rats in MI administration group. The myocardial infarction model was induced by ligating the left anterior descending coronary artery. After 24 h,the rats in myocardial infarction administration group were gavage with artemisinin of 75 mg /( kg·d),three times a day,meanwhile,MI group received isodose 0. 5% of sodium carboxymethyl cellulose. Sham operation group were only opened chestcoronary artery under wear line but not ligation,while given isodose 0. 5% of sodium carboxymethyl cellulose. Four weeks after treatment,the rats were sacrificed and drawed materials according to the needs. Infarcted size of left ventricular were measured by Masson staining method. The growth associated protein in infarcted border zone( GAP43), distribution and density of tyrosine hydroxylase( TH)-positive nerves, number of macrophages were quantitatively analysed by immunohistochemical method. IKB alpha,GAP43,TH and NGF in infarcted border zone were detected by Western blot. The inflammatory factor of TNF-α and IL-1 β mRNA expression level were detected by RT-PCR. Results There was no difference in myocardial infarction area between MI group and MI administration group. GAP43 and TH positive sympathetic nerve fibers density in MI group were higher than those in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05). TNF-α and IL-1 β mRNA expression levels in MI group were higher than those in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05). IKB α protein in MI group was higher than that in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05).Protein expressions of NGF,GAP43 and TH were higher than those in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05). The number of macrophages was higher than that in sham operation group,and the above index in MI administration group were lower than that in MI group( P 0. 05). Conclusion Artemisinin could inhibit the remodeling of sympathetic nerve after myocardial infarction,and its mechanism may be to inhibit the inflammation after acute myocardial infarction.
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Objective To study the effect of artemisinin on remodeling of sympathetic neural in rats with myocardial infarction and explore its molecular mechanism. Methods 70 SD male rats were randomly divided into three groups,10 rats in sham operation group,30 rats in myocardial infarction group,30 rats in MI administration group. The myocardial infarction model was induced by ligating the left anterior descending coronary artery. After 24 h,the rats in myocardial infarction administration group were gavage with artemisinin of 75 mg /( kg·d),three times a day,meanwhile,MI group received isodose 0. 5% of sodium carboxymethyl cellulose. Sham operation group were only opened chestcoronary artery under wear line but not ligation,while given isodose 0. 5% of sodium carboxymethyl cellulose. Four weeks after treatment,the rats were sacrificed and drawed materials according to the needs. Infarcted size of left ventricular were measured by Masson staining method. The growth associated protein in infarcted border zone( GAP43), distribution and density of tyrosine hydroxylase( TH)-positive nerves, number of macrophages were quantitatively analysed by immunohistochemical method. IKB alpha,GAP43,TH and NGF in infarcted border zone were detected by Western blot. The inflammatory factor of TNF-α and IL-1 β mRNA expression level were detected by RT-PCR. Results There was no difference in myocardial infarction area between MI group and MI administration group. GAP43 and TH positive sympathetic nerve fibers density in MI group were higher than those in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05). TNF-α and IL-1 β mRNA expression levels in MI group were higher than those in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05). IKB α protein in MI group was higher than that in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05).Protein expressions of NGF,GAP43 and TH were higher than those in sham operation group,and the above indexes in MI administration group were lower than those in MI group( P 0. 05). The number of macrophages was higher than that in sham operation group,and the above index in MI administration group were lower than that in MI group( P 0. 05). Conclusion Artemisinin could inhibit the remodeling of sympathetic nerve after myocardial infarction,and its mechanism may be to inhibit the inflammation after acute myocardial infarction.
Key concepts: Myocardial infarction, Medicine, Ligation, Infarction, Gap-43 protein, Internal medicine, Tyrosine hydroxylase, Artery