Myocardial Protective Effect of Xuebijing Injection on Extracorporeal Membrane Oxygenation Perfused Isolated Langendorff Heart Based on the PI3K/AKT Pathway
DOI:
https://doi.org/10.59958/hsf.7869Keywords:
Xuebijing injection, bama miniature pig, extracorporeal membrane oxygenation (ECMO), PI3K/AKT pathway, preservation of the heart, myocardial protectionAbstract
Objective: This study aimed to investigate the myocardial protective effect of Xuebijing injection in a model of extracorporeal membrane oxygenation (ECMO) isolated heart perfusion and determine the role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway. Methods: To establish an ECMO isolated heart perfusion model, Guangxi Bama miniature pigs were randomly divided into two groups: (1) a normal saline group (NS group), in which 50 mL of normal saline was added to the perfusion solution; and (2) a Xuebijing injection group (XBJI group), in which 10 mL of XBJI was added to the perfusion solution and then continuously pumped at 5 mL/h. Perfusion was maintained for 8 h. The hemodynamic changes, inflammatory response, and myocardial enzyme levels at T0, T2, T4, T6, and T8 were evaluated. The protein expression level of the PI3K/AKT pathway was analyzed by Western blot analysis and Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR). Hematoxylin and eosin staining and transmission electron microscopy were used to observe the pathological morphology and ultrastructure of T8 cardiomyopathy. Results: There was no significant difference in hemodynamics between the two groups. XBJI could reduce serum inflammatory factors and myocardial enzyme levels. XBJI also upregulated the expression of PI3K and AKT mRNA and the phosphorylation levels of PI3K and AKT proteins. The results of pathological and electron microscopy showed that XBJI effectively reduced myocardial cell and mitochondrial damage. Conclusion: XBJI can reduce myocardial inflammation and myocardial cell and mitochondrial damage in isolated heart perfusion. XBJI may play a role in the myocardial protection of ECMO isolated heart perfusion by activating the PI3K/AKT pathway.
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