Objective  To investigate the therapeutic efficacy and mechanism of action of Campsis flos on cardiac injury in mice with heart failure (HF).

Methods  Thirty mice were randomly divided into three groups: sham operation group, model group, and Campsis flos group. HF models were established in the model group and Campsis flos group via aortic arch constriction. After modeling, the Campsis flos group received intragastric administration of Campsis flos total flavonoid extract (10  mg/ kg), while the sham operation group and model group received an equivalent volume of saline. After one month of continuous intragastric administration, comparative analyses were performed on cardiac function, relative protein expression levels, pathological sections, blood biochemical indicators, inflammatory factors, and apoptosis across the three groups.

Results  Compared with the model group, the Campsis flos group showed significant improvement in cardiac function in HF mice. This was evidenced by significantly increased ejection fraction (EF), fractional shortening (FS), and cardiac output (CO), along with significantly decreased left ventricular anterior wall thickness (LVAW), left ventricular posterior wall thickness (LVPW), and heart weight-to-tibia length ratio (HW/TL) (P<0.05). The expression levels of Akt and B-cell lymphoma-2 (Bcl-2) proteins were significantly higher, while the expression levels of Smad and Bcl2-associated X protein (Bax) were significantly lower in the Campsis flos group compared to the model group (P<0.05). The myocardial cells in the Campsis flos group exhibited a more organized arrangement, reduced inflammatory cell infiltration, and significantly attenuated collagen fiber deposition. The expression levels of Notch homolog (NOTCH1), hairy and enhancer of Split 1 (HES1), phosphatase and tensin homolog (PTEN), and transforming growth factor-β (TGF-β) were significantly lower in the Campsis flos group than in the model group (P<0.05). The blood biochemical analysis revealed that the serum levels of malondialdehyde (MDA), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and the pro-inflammatory cytokine interleukin (IL)-6 were significantly reduced in Campsis flos group (P<0.05). Conversely, the activity of superoxide dismutase (SOD), the levels of the anti-inflammatory cytokine IL^-10, and the expression of the endothelial marker CD31 were significantly increased (P<0.05).

Conclusion  Campsis flos inhibits myocardial apoptosis by activating the PTEN/phosphatidylinositol 3-kinase (PI3K)/Akt pathway, blocks the TGF-β/Smad signaling pathway, and alleviates fibrosis, which has the cardioprotective potential and provides experimental evidence supporting its use in traditional Chinese medicine (TCM) for anti-heart failure therapy.

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