Experimental gerontology · 2026
Astragalus membranaceus and Salvia miltiorrhiza injections confer cardioprotection via SERCA/SIRT1-mediated Ca2+ regulation.
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Xiu Shengyao, Cai Yi, Guo Nan, Zhao Yingkun, Yuan Wenjuan, Chang Peifen, Zhao Mingjing
Аннотация
OBJECTIVE: This study aimed to compare the distinct cardioprotective mechanisms of Astragalus membranaceus (AM) and Salvia miltiorrhiza (SM) injections in myocardial ischemia.
METHODS: Male Sprague-Dawley rats were subjected to left anterior descending (LAD) coronary artery ligation to establish a myocardial ischemia model, followed by daily administration of AM or SM (intraperitoneal injection, 4 g/kg) for 14 days. Cardiac function and remodeling were evaluated via echocardiography and histopathological staining. Platelet aggregation, intracellular Ca2+ dynamics, and sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) and sirtuin 1 (SIRT1) signaling were analyzed using optical aggregometry, calcium assays, flow cytometry, fluorescence imaging, and Western blotting. Endothelial integrity and function were assessed by measuring the expression of zonula occludens-1 (ZO-1), endothelial nitric oxide synthase (eNOS), von Willebrand factor (vWF), and tumor necrosis factor-α (TNF-α) via immunofluorescence and immunohistochemistry. Additionally, lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) were utilized to model endothelial injury in vitro. Pharmacological inhibitors were employed to validate pathway specificity, and molecular docking was performed to predict binding interactions between key bioactive constituents of AM/SM and their SERCA/SIRT1 targets.
RESULTS: Both AM and SM improved cardiac function, reduced fibrosis, inhibited platelet aggregation, and alleviated endothelial dysfunction in ischemic rats. AM primarily enhanced SERCA expression and Ca2+ reuptake, resulting in improved endothelial barrier preservation, whereas SM preferentially activated SIRT1 signaling, with greater anti-inflammatory effects. Both treatments reduced Ca2+ overload in platelets and HUVECs, which were partially reversed by SERCA or SIRT1 inhibition. Molecular docking further supported preferential targeting of SERCA by AM-derived compounds and SIRT1 by SM-derived compounds.
CONCLUSION: AM and SM injections confer cardioprotection by differentially modulating SERCA and SIRT1 to stabilize cytosolic Ca2+.
METHODS: Male Sprague-Dawley rats were subjected to left anterior descending (LAD) coronary artery ligation to establish a myocardial ischemia model, followed by daily administration of AM or SM (intraperitoneal injection, 4 g/kg) for 14 days. Cardiac function and remodeling were evaluated via echocardiography and histopathological staining. Platelet aggregation, intracellular Ca2+ dynamics, and sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) and sirtuin 1 (SIRT1) signaling were analyzed using optical aggregometry, calcium assays, flow cytometry, fluorescence imaging, and Western blotting. Endothelial integrity and function were assessed by measuring the expression of zonula occludens-1 (ZO-1), endothelial nitric oxide synthase (eNOS), von Willebrand factor (vWF), and tumor necrosis factor-α (TNF-α) via immunofluorescence and immunohistochemistry. Additionally, lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) were utilized to model endothelial injury in vitro. Pharmacological inhibitors were employed to validate pathway specificity, and molecular docking was performed to predict binding interactions between key bioactive constituents of AM/SM and their SERCA/SIRT1 targets.
RESULTS: Both AM and SM improved cardiac function, reduced fibrosis, inhibited platelet aggregation, and alleviated endothelial dysfunction in ischemic rats. AM primarily enhanced SERCA expression and Ca2+ reuptake, resulting in improved endothelial barrier preservation, whereas SM preferentially activated SIRT1 signaling, with greater anti-inflammatory effects. Both treatments reduced Ca2+ overload in platelets and HUVECs, which were partially reversed by SERCA or SIRT1 inhibition. Molecular docking further supported preferential targeting of SERCA by AM-derived compounds and SIRT1 by SM-derived compounds.
CONCLUSION: AM and SM injections confer cardioprotection by differentially modulating SERCA and SIRT1 to stabilize cytosolic Ca2+.