Aortic dissection (AD) is a life-threatening vascular disease characterized by progressive vascular remodeling, oxidative stress, and inflammation. Among them, severe oxidative stress and systemic inflammation are important driving factors causing vascular integrity damage. Cistanche deserticola polysaccharides (CTPs) have definite deserticola anti-inflammatory and antioxidant properties. However, their influence on the progression of AD remains to be studied. In this study, we investigated the protective effects of CTP in a BAPN-induced mouse model of aortic dissection and explored the underlying mechanisms. CTP administration significantly attenuated aortic dilation and reduced the incidence of aortic dissection, accompanied by suppression of oxidative stress and inflammatory responses, preservation of extracellular matrix integrity, and maintenance of the contractile phenotype of vascular smooth muscle cells. Most importantly, CTP inhibits oxidative stress responses, as evidenced by the recovery of endogenous antioxidant enzyme activity and the reduction in lipid peroxidation. At the same time, CTP also suppresses systemic inflammatory responses. In addition, CTP markedly reshaped gut microbiota composition, characterized by enrichment of Akkermansia and Lachnospiraceae and reduction in Desulfovibrio and Escherichia-Shigella. Correlation analyses revealed close associations between gut microbial alterations and antioxidant, vascular remodeling, and smooth muscle cell phenotypic modulation. Collectively, these findings suggest that CTP confers vascular protection against aortic dissection through coordinated regulation of oxidative stress, inflammation, and vascular remodeling. The observed changes in gut microbiota composition may represent an additional mechanism associated with the beneficial effects of CTP and warrant further investigation.

Background: Sarcopenia is an age-related disorder characterized by loss of muscle mass, strength, and function, driven by oxidative stress, chronic inflammation, and protein imbalance. Broccoli-derived peptides (BDP) exert anti-inflammatory and myofiber-protective effects, while leucine regulates energy metabolism and redox balance. Methods: We established a D-galactose aging mouse model and treated mice with BDP alone, leucine alone, or their combination for 8 weeks. Lean mass, muscle index, grip strength, endurance, and treadmill capacity were detected, and atrophic, disorganized myofibers were observed through histology. RNA-seq was applied to screen differential signaling pathways, and qPCR was used to verify related gene expression levels. Results: D-galactose caused marked deficits in lean mass, muscle index, grip strength, endurance, and treadmill capacity, accompanied by atrophic and disorganized myofibers. Single BDP or leucine partially reversed these deficits, but the combination produced the most robust improvements. RNA-seq revealed that BDP enriched actin, chemokine, and TNF pathways; leucine enriched Apelin and ECM pathways; while the combination uniquely regulated MAPK signaling. qPCR confirmed that co-administration optimally upregulated myogenic drivers (Myod1, Myog, Mef2c), suppressed catabolic/inflammatory mediators (Mstn, Tnf, Cxcl10), and restored metabolic/adhesive regulators (Sirt3, Aplnr, Icam1). Conclusions: BDP and leucine show superior efficacy in ameliorating sarcopenia, through multimodal regulation of multiple signaling pathways, offering a promising plant-based nutritional strategy against age-related muscle decline.

Doxorubicin-induced cardiotoxicity remains a major limitation of anthracycline chemotherapy and is closely associated with oxidative stress and mitochondrial dysfunction. Here, we investigated whether a commercial Codonopsis pilosula polysaccharide preparation (CPP) could attenuate Dox-induced cardiac injury in mice. The preparation was characterized as a glucose-dominant heteropolysaccharide with a broad and heterogeneous molecular-weight distribution dominated by a lower-molecular-weight fraction (89.25% of the integrated chromatographic area; Mw = 1.64 kDa). CPP administration improved ejection fraction and fractional shortening and attenuated myocardial fibrosis and serum markers of cardiac injury. Histological and ultrastructural analyses showed preservation of myocardial architecture and mitochondrial integrity. CPP treatment was accompanied by increased SOD and GSH-PX activities, reduced MDA accumulation, partial recovery of mitochondrial respiratory-chain-related transcripts, and restoration of cardiac ATP content. In addition, 16S rRNA gene sequencing showed that high-dose CPP treatment was associated with partial reversal of Dox-induced gut-microbiota alterations, including increased microbial diversity, reduced Escherichia-Shigella, and increased norank_f__Muribaculaceae and Ligilactobacillus. Collectively, the tested heterogeneous CPP preparation attenuated Dox-induced cardiac injury and was accompanied by improved oxidative-stress indices, preserved mitochondrial structure and function, and changes in gut-microbiota composition.