Propofol and Salvianolic Acid a Synergistically Attenuate LPS-Induced Myocardial Pyroptosis in Diabetic Mice via the SIRT1/HMGB1 Pathway.
A, Z., R, H., K, H., T, L., J, Z., Y, W., J, Z., J, C., W, S., & SSC, W. (2026). Propofol and Salvianolic Acid a Synergistically Attenuate LPS-Induced Myocardial Pyroptosis in Diabetic Mice via the SIRT1/HMGB1 Pathway.. Mediators of inflammation. https://doi.org/10.1155/mi/6298056
A Z, R H, K H, T L, J Z, Y W, et al. Propofol and Salvianolic Acid a Synergistically Attenuate LPS-Induced Myocardial Pyroptosis in Diabetic Mice via the SIRT1/HMGB1 Pathway.. Mediators of inflammation. 2026; doi: 10.1155/mi/6298056
A Z, R H, K H, et al. Propofol and Salvianolic Acid a Synergistically Attenuate LPS-Induced Myocardial Pyroptosis in Diabetic Mice via the SIRT1/HMGB1 Pathway.[J]. Mediators of inflammation. 2026. DOI: 10.1155/mi/6298056.
@article{a2026,
author = {Zhang A and Han R and Han K and Li T and Zhu J and Wang Y and Zhou J and Chen J and Shangguan W and Wong SSC},
title = {Propofol and Salvianolic Acid a Synergistically Attenuate LPS-Induced Myocardial Pyroptosis in Diabetic Mice via the SIRT1/HMGB1 Pathway.},
journal = {Mediators of inflammation},
year = {2026},
doi = {10.1155/mi/6298056},
note = {PMID: 42411292},
}
TY - JOUR AU - Zhang A AU - Han R AU - Han K AU - Li T AU - Zhu J AU - Wang Y AU - Zhou J AU - Chen J AU - Shangguan W AU - Wong SSC TI - Propofol and Salvianolic Acid a Synergistically Attenuate LPS-Induced Myocardial Pyroptosis in Diabetic Mice via the SIRT1/HMGB1 Pathway. T2 - Mediators of inflammation PY - 2026 DO - 10.1155/mi/6298056 AN - PMID:42411292 ER -
BACKGROUND: We investigated whether propofol (PPF) combined with salvianolic acid A (SAA) confers synergistic cardioprotection in diabetic sepsis. METHODS: Diabetic-septic mice and high-glucose/LPS-treated cardiomyocytes were treated with PPF and SAA. Cardiac function, reactive oxygen species (ROS), inflammation, and the SIRT1/HMGB1 pathway were assessed. RESULTS: PPF combined with SAA synergistically attenuated cardiac inflammation, pyroptosis, and dysfunction, accompanied by SIRT1 upregulation and HMGB1 downregulation. Notably, low-dose coadministration of PPF (12.5 µM) and SAA (12.5 µM) achieved protection comparable to high-dose PPF (25 µM), significantly reducing ROS and pyroptosis markers. These protective effects were reversed by SIRT1 inhibition or silencing but enhanced by HMGB1 inhibition. CONCLUSION: PPF and SAA synergistically inhibit LPS-induced myocardial pyroptosis under hyperglycemia by activating the SIRT1/HMGB1 pathway. This combination offers a potential strategy to enhance cardioprotection while minimizing anesthetic dosage.