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| Experimental study on Qingyi Decoction targeting the Bcl-2/Bax/Caspase-3 pathway to mediate mitochondrial apoptosis and alleviate severe acute pancreatitis-associated myocardial injury |
| Hits 2 Download times 0 Received:April 29, 2026 |
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| DOI
10.11656/j.issn.1672-1519.2026.09.12 |
| Key Words
SAP-induced myocardial injury;Qingyi Decoction;apoptosis;Caspase-3;Bcl-2/Bax |
| Author Name | Affiliation | E-mail | | LI Xiao | Department of Ultrasound, Tianjin Hospital of ITCWM Nankai Hospital(Tianjin Nankai Hospital), Tianjin 300100, China | | | LI Caixia | Tianjin Hospital of ITCWM Nankai Hospital(Tianjin Nankai Hospital), Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin 300100, China | | | CUI Lihua | Tianjin Hospital of ITCWM Nankai Hospital(Tianjin Nankai Hospital), Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin 300100, China | | | QIAO Yuanyuan | Department of Ultrasound, Tianjin Hospital of ITCWM Nankai Hospital(Tianjin Nankai Hospital), Tianjin 300100, China | | | LI Jing | Department of Ultrasound, Tianjin Hospital of ITCWM Nankai Hospital(Tianjin Nankai Hospital), Tianjin 300100, China | | | PAN Jianhong | Department of Ultrasound, Tianjin Hospital of ITCWM Nankai Hospital(Tianjin Nankai Hospital), Tianjin 300100, China | nankaiyiyuanxgn@126.com |
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| Abstract
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| [Objective] This study aims to examine the role of apoptosis in myocardial injury caused by severe acute pancreatitis（SAP） and to elucidate the mechanism by which Qingyi Decoction（QYD）intervenes in SAP-induced myocardial injury in rats. [Methods] Twenty-four male SD rats were randomly assigned to four groups：a sham-operated group，a model group，a low-dose QYD group（QYD- L），and a high-dose QYD group（QYD-H），with six rats in each group. Tissue and blood samples were collected for analysis. Pathological alterations in pancreatic and myocardial tissues were identified through HE staining. Biochemical measurements were conducted to assess serum amylase and lipase activities. The activities of Lactate Dehydrogenase（LDH），Creatine Kinase（CK），and Creatine Kinase-MB（CK-MB）were measured utilizing an automatic biochemical analyzer. Serum concentrations of the inflammatory cytokines IL-6，TNF-α，and IL-1β were quantified using enzyme-linked immunosorbent assay（ELISA）. The assessment of cardiac cell apoptosis was conducted utilizing the TUNEL assay. The ultrastructure of myocardial mitochondria was examined using transmission electron microscopy. RT-PCR was utilized to detect the mRNA expression levels of B-cell lymphoma-2（Bcl-2）and Bcl-2-associated X （Bax）protein. [Results] In comparison to the sham-operated group，the model group demonstrated significant damage to pancreatic and myocardial tissues，elevated serum levels of amylase，lipase，and myocardial injury markers（CK-MB，CK，LDH，P<0.05）， increased levels of inflammatory cytokines（IL-6，TNF-α，IL-1β，P<0.05），pronounced mitochondrial pathological damage，heightened myocardial apoptosis，upregulated mRNA and protein expression of Bax，and significantly increased protein expression of cleaved Caspase-3. The expression levels of Bcl-2 mRNA and protein were significantly decreased（P<0.05）. In comparison to the model group， the QYD intervention groups exhibited enhanced myocardial tissue integrity，a significant reduction in serum amylase and lipase activities，decreased levels of CK-MB，CK，and LDH，as well as markedly lower concentrations of inflammatory cytokines（IL-6，TNF-α， IL-1β）. Mitochondrial pathological damage was mitigated，myocardial apoptosis was markedly reduced，and there was a downregulation in the mRNA and protein expression of Bax，alongside a significant decrease in the protein expression of cleaved Caspase-3. Simultaneously，there was a significant increase in the mRNA and protein expression of Bcl-2（P<0.05）. [Conclusion] QYD can improve myocardial injury induced by SAP，and its mechanism may be related to regulating Bcl-2/Bax/Caspase-3 signaling pathway and inhibiting apoptosis. |
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