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Investigation of the mechanism of Xuebijing Injection in treating sepsis-induced myocardial injury in rats via the TCTP/AKT/P53 signaling pathway
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DOI   10.11656/j.issn.1672-1519.2026.04.13
Key Words   sepsis-induced cardiomyopathy;Xuebijing Injection;TCTP/AKT/P53 signaling pathway
Author NameAffiliationE-mail
LIU Anbu Department of Emergency Medical, General Hospital of Ningxia Medical University, Yinchuan 750000, China
State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi 830054, China 
 
MA Lei Department of Emergency Medical, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
WU Jiali Department of Emergency Medical, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
ZHANG Junfei Department of Emergency Medical, General Hospital of Ningxia Medical University, Yinchuan 750000, China zhangjunfei007@126.com 
Abstract
    [Objective] To investigate the mechanism by which Xuebijing Injection(XBJ) improves sepsis-induced cardiomyopathy(SICM) through the translationally controlled tumor protein(TCTP)/protein kinase B(AKT)/tumor protein 53(P53) signaling pathway. [Methods] Eighteen SD rats were randomly assigned to the sham group,cecum ligation and puncture(CLP) group,and XBJ group,with 6 rats in each group. After 3 days of continuous treatment,histopathological changes in myocardial tissue were observed using hematoxylin and eosin(HE) staining. left ventricular ejection fraction(LVEF) and left ventricular fractional shortening(LVFS) were assessed by ultrasound. Serum levels of creatine kinase(CK) and lactate dehydrogenase(LDH) were measured using an automated biochemical analyzer. Enzyme-linked immunosorbent assay(ELISA) was performed to measure the expression levels of tumor necrosis factor-α(TNF-α),lnterleukin-6(IL-6),and lnterleukin-1β(IL-1β) in serum. Western blotting was used to detect the protein expression levels of TCTP,p-AKT,P53,B-cell lymphoma 2(Bcl-2),Bcl-2-associated X protein(Bax),and Cleaved Caspase3 in myocardial tissue. Immunohistochemistry was employed to observe the expression of Bax,Bcl-2,and Cleaved Caspase3 proteins. Finally,immunofluorescence was used to examine the expression levels of TCTP,p-AKT,and P53 in cardiac tissue. [Results] XBJ treatment significantly reduced the serum levels of CK,LDH,TNF-α,IL-1β,and IL-6,while improving LVEF and LVFS in CLP rats,with statistically significant differences(P<0.05). Ultrasound,HE staining,and electron microscopy results indicated that XBJ treatment alleviated myocardial injury in SICM rats. Western blot analysis showed that XBJ treatment decreased the expression levels of Bax,Cleaved Caspase3,TCTP,and p-AKT,while increasing the expression of Bcl-2 and P53 compared to the CLP group,with statistically significant differences(P<0.05). Immunohistochemical analysis confirmed that XBJ treatment upregulated Bcl-2 and downregulated Bax and Cleaved Caspase3. Moreover,immunofluorescence results revealed that XBJ treatment decreased the expression of TCTP and p-AKT,while increasing P53 expression in myocardial tissue compared to the CLP group. [Conclusion] XBJ may improve SICM by regulating the TCTP/AKT/P53 signaling pathway,inhibiting myocardial cell apoptosis and inflammatory responses.

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