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Objective: Dietary intake of fruit is associated with lower incidence of hypertension and cardiovascular risk. Papaya is a kind of delicious fruit and reported has dietary therapeutic effects, such as digestive stimulation and hypotensive efficacy. However, the mechanism of pawpaw involved have not been elucidated. Here, we illustrate that the effect of pawpaw on the gut microbiota and the prevention of cardiac remodeling. Methods: Gut microbiome, cardiac structure/function, and blood pressure were examined in SHR and WKY groups. The intestinal barrier was tested with histopathologic; immunostaining and Western blot were used to measure the tight junction protein level; Gpr41 was tested by RT-PCR, and inflammatory factors were detected with ELISA. Results: We observed a significant decrease in microbial richness, diversity, and evenness is the spontaneously hypertensive rat (SHR), in addition to an increased Firmicutes/Bacteroidetes (F/B) ratio. These changes were accompanied by decreased in acetate and butyrate-producing bacteria. Compared with SHR, treatment with pawpaw at the dosage of 10 g/kg for 12 weeks significantly reduced the blood pressure, cardiac fibrosis and cardiac hypertrophy, while the ratio of F/B decreased. We also found that the concentration of short-chain fatty acids (SCFAs) was increased in SHR fed with pawpaw compared with that in control group, while the gut barrier was restored and level of proinflammatory cytokines in the serum were decreased. Conclusions: Pawpaw, rich of high fiber, led to changes in the gut microbiota that played a protective role in the development of cardiac remodeling. The potential mechanism of pawpaw may explained by the generation of one of the main metabolites of the gut microbiota, the short-chain fatty acid acetate, increasing tight junction protein level occluding to enhance the gut barrier for less releasing the inflammation cytokines, and upregulating G-protein-coupled receptor 41 (GPR41) to reduce blood pressure.

Ethnopharmacological relevance: Salvianolic acid D (Sal D) is a natural substance extracted from Radix Salviae that performs a cardiovascular benefit. However, the protective mechanism of Sal-D for heart failure remains uncertain. Aim of the study: In this study, we aim to evaluate the effect of Sal D on heart failure and elucidate its underlying mechanisms. Materials and methods: Using the spontaneously hypertensive rats (SHR) as a cardiac remodelling model, the cardioprotective effect of Sal D was evaluated. Employing bioinformatics analysis, the related mechanisms of Sal D treatment on heart failure were identified and validated by Western blot and polymerase chain reaction. Results: The results showed that Sal D significantly improved cardiac function and attenuated cardiac hypertrophy. Besides, Sal D impaired mitochondrial structure and restored the energy charge of cardiomyocytes managed by angiotensin II. Bioinformatics analysis suggested that Sal D might improve heart failure by modulating the Ras and PI3K/AKT signalling pathways verified in vitro and in vivo. Conclusion: In summary, Sal D can improve the heart function of SHR by inhibiting the Ras signalling pathway and activating the PI3K/AKT signalling pathway.