Protective Effect of Coriander (Coriandrum sativum L.) on High-Fructose and High-Salt Diet-Induced Hypertension: Relevant to Improvement of Renal and Intestinal Function

Hypertension has become a leading cardiovascular risk factor worldwide. In this study, we explored the salutary effects and relevant mechanisms of coriander (Coriandrum sativum L.), an herbal plant with culinary and medicinal values, on high-fructose and high-salt diet (HFSD)-induced hypertension in SD rats. Our results showed that oral administration of coriander (1.0 or 2.0 g/kg·bw) effectively attenuated HFSD-induced elevation of systolic blood pressure, diastolic blood pressure, and mean arterial pressure. Coriander also increased the serum levels of vasodilator factors (PGI2, NO, and eNOS), decreased Na+ retention and serum uric acid (UA) level, and ameliorated glucolipid profiles. qPCR results revealed that coriander downregulated the mRNA expression of NHE3, a Na+/H+ exchanger responsible for Na+ absorption, in kidney and small intestine. 16S rDNA sequencing showed that coriander altered the gut microbiota composition with the beneficial bacteria Bifidobacterium and Oscillibacter significantly enriched. Correlation analysis indicated that the abundance of Bifidobacterium was evidently correlated with levels of NHE3, NO, eNOS, and UA. LC-MS/MS analysis revealed that coriander contained a variety of flavonoids including rutin and quercetin. Conclusively, long-term consumption of coriander may ameliorate HFSD-induced hypertension by mitigating HFSD-caused abnormal changes in vascular endothelial function, renal and intestinal sodium absorption, glucolipid homeostasis, and gut microbiota in rats.