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Coronary artery disease (CAD) is a major public health problem and the chief cause of morbidity and mortality worldwide. Panax notoginseng, a valuable herb in traditional Chinese medicine (TCM) with obvious efficacy and favorable safety, shows a great promise as a novel option for CAD and is increasingly recognized clinically. Firstly, this review introduced recent clinical trials on treatment with PNS either alone or in combination with conventional drugs as novel treatment strategies. Then we discussed the mechanisms of P. notoginseng and Panax notoginseng saponins (PNS), which can regulate signaling pathways associated with inflammation, lipid metabolism, the coagulation system, apoptosis, angiogenesis, atherosclerosis, and myocardial ischaemia.
Previous studies have confirmed the clinical efficacy of sacubitril/valsartan (Sac/Val) for the treatment of heart failure with reduced ejection fraction (HFrEF). However, the role of Sac/Val in heart failure with preserved ejection fraction (HFpEF) remains unclear. Sac/Val is a combination therapeutic medicine comprising sacubitril and valsartan that acts as a first angiotensin receptor blocker and neprilysin inhibitor (angiotensin-receptor neprilysin inhibitor (ARNI)). Here, we investigated the role of Sac/Val in high-salt diet-induced HFpEF coupled with vascular injury as well as the underlying mechanism. Rats were fed with high-salt feed, followed by intragastric administration of Sac/Val (68 mg/kg; i.g.). The results of functional tests revealed that a high-salt diet caused pathological injuries in the heart and vascular endothelium, which were significantly reversed by treatment with Sac/Val. Moreover, Sac/Val significantly decreased the levels of fibrotic factors, including type I collagen and type Ⅲ collagen, thus, reducing the ratio of MMP2/TIMP2 while increasing Smad7 levels. Further investigation suggested that Sac/Val probably reversed the effects of high-salt diet-induced HFpEF by inhibiting the activation of the TGF-β1/Smad3 signaling pathway. Thus, treatment with Sac/Val effectively alleviated the symptoms of high-salt diet-induced HFpEF, probably by inhibiting fibrosis via the TGF-β1/Smad3 signaling pathway, supporting the therapeutic potential of Sac/Val for the treatment of HFpEF.
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