Key result
Polydatin reduces aortic dilation and medial injury via PPARγ/Nrf2 antioxidant signaling in mice.
Why the study?
Polydatin has cardiovascular protective potential, but its therapeutic mechanism against aortic dissection remained unclear.
Does polydatin protect against aortic dissection and reduce vascular degeneration in a BAPN-induced mouse model?
Does polydatin protect against aortic dissection and reduce vascular degeneration in a BAPN-induced mouse model?
Polydatin alleviates experimental aortic dissection by restoring vascular redox homeostasis via PPARγ and Nrf2-related antioxidant pathways, identifying it as a potential preclinical therapeutic candidate.
Answers are grounded in this paper and cite their sources.
Should not change aortic dissection management; leaves open human translation of PPARγ/Nrf2 pathways.
Aortic dissection (AD) is a life-threatening vascular disease characterized by medial degeneration, extracellular matrix (ECM) destruction, inflammation, and oxidative stress. Polydatin (PD), a natural stilbene glucoside, has cardiovascular protective potential, but its mechanism against AD remains unclear. This study investigated the therapeutic mechanism of PD in AD by integrating network pharmacology, transcriptomic analysis, weighted gene co-expression network analysis (WGCNA), molecular modeling, and in vivo validation. IGF1, PPARG, and KDR were identified as core targets in the PD-AD network, with PPARG prioritized for its association with vascular redox homeostasis, inflammation, and antioxidant defense. Molecular docking and molecular dynamics simulations indicated stable interactions between PD and PPARγ and Keap1, a key regulator of Nrf2 stability. In a β-aminopropionitrile (BAPN)-induced AD mouse model, PD significantly reduced aortic dilation and medial injury, preserved elastic fiber architecture, and attenuated ECM degradation. PD also decreased ROS and MDA levels, restored SOD, GSH-Px, and CAT activities, and upregulated PPARγ, Nrf2, HO-1, and NQO1 expression. These findings suggest that PD alleviates AD by restoring vascular redox homeostasis, potentially involving PPARγ-associated signaling and Nrf2-related antioxidant responses, supporting PD as a potential therapeutic candidate for AD-related vascular degeneration.
No takes yet. Share an insight, caveat, or question.
Yang et al. (2026) studied Aortic dissection. Polydatin was evaluated on Aortic dilation, medial injury, elastic fiber architecture preservation, and extracellular matrix degradation. Polydatin significantly reduced aortic dilation, medial injury, and ECM degradation in a BAPN-induced mouse model via PPARγ/Nrf2 antioxidant signaling.
Synapse has enriched 10 related papers. Consider them for comparative context: