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Puerarin is an isoflavonoid isolated from the Chinese herb, Kudzu roots (also known as Gegen), which has been widely used for the treatment of hypertensive diseases and diabetic mellitus in traditional Chinese medicine. Dahl salt-sensitive (DS) rat is a genetic model of salt-sensitive hypertension with cardiovascular injury and vascular insulin resistance. Here, we investigated whether puerarin improved vascular insulin resistance and attenuated cardiac and aortic remodeling in salt-sensitive hypertension. DS rats were given a normal (NS) or high salt diet (HS) for five weeks. An additional group of DS rats was pretreated with puerarin and NS for 10 days, then switched to HS plus puerarin for five weeks. HS for five weeks increased systolic blood pressure (SBP), cardiac hypertrophy and fibrosis, and aortic hypertrophy with increased the expression of phosphor-ERK1/2 in the aorta and heart; puerarin attenuated cardiac and aortic hypertrophy, cardiac fibrosis and phosphor-ERK1/2 with a mild reduction in SBP. Hypertensive rats also manifested impairment of acetylcholine- and insulin-mediated vasorelaxation and insulin-mediated Akt and eNOS phosphorylation associated with the activation of NFB/TNF/JNK pathway. Puerarin improved acetylcholine- and insulin-mediated vasorelaxation and insulin-stimulated Akt/NO signaling with the inhibition of the NFB inflammatory pathway. Our results demonstrated that in salt-sensitive hypertension, puerarin improved vascular insulin action with cardiovascular beneficial effects. Our results found that the underlying mechanisms may involve its inhibition of NFB/JNK and ERK1/2 pathway. These results suggest that puerarin could be used as a new antihypertensive agent to expand our armamentarium for the prevention and treatment of end-organ damage in individuals with hypertension and metabolic diseases. [ABSTRACT FROM AUTHOR]

Puerarin, a major isoflavonoid compound from Chinese herb Kudzu roots, has been widely used for the treatment of hypertensive and cardiovascular diseases in China. Here, we investigated puerarin’s beneficial effects on the cardiovascular system in angiotensin (Ang) II-induced hypertensive rats. Sprague–Dawley rats were treated with Ang II for 5 days or with puerarin for 10 days followed by Ang II and puerarin for 5 days. Endothelium-dependent relaxation (EDR) to acetylcholine was determined using an organ chamber bath. Ang II increased the systolic blood pressure (SBP: 178 ± 5 mmHg vs. 112 ± 3 mmHg in control,p< 0.05), aortic (30%,p< 0.05), and left ventricular (LV) weight (23%); puerarin reduced SBP (160 ± 2 mmHg,p< 0.05), aortic, and left ventricular weight in Ang II-infused rats. Puerarin also reduced aortic medial thickness and myocardial cell surface area in Ang II-infused rats. Compared with control rats, Ang II infused rats exhibited an impaired EDR with reduction in the protein expression of phosphor-eNOS at Ser 1177 and an increase in the expression of gp91phox (85%), p22phox (113%), transforming growth factor β1 (145%) and vascular cell adhesion molecule 1 (82%). Puerarin improved EDR and reversed the changes in Ang II-induced protein expression of above molecules. Our results demonstrate that in Ang II-induced hypertensive rats, puerarin protects against endothelial dysfunction and end organ damage with a mild reduction in SBP, and that the cardiovascular beneficial effects of puerarin may be in part attributed to its anti-oxidant and upregulation of phosphor-eNOS. [ABSTRACT FROM AUTHOR]

All these compounds investigated cytotoxic activity on the growth of HepG-2 cells. The results showed that compounds B 4 b and B 7 b exhibited high adenylate deaminase activities with an inhibition ratio of 89.6 and 90.9%, respectively. Adenylate deaminase activity assays of these compounds were performed using spectrophotometry [[18]]. The EtOAc fraction (57 g) was chromatographed on a macroporous resin (AB-8) column eluting with water and ethanol gradually to yield four fractions (Frs. [Extracted from the article]

The present study elucidates the underlying mechanism through which PUE confers protection against CDDP-induced ototoxicity. PUE effectively regulates Calcium overload and suppresses the production of Reactive Oxygen Species (ROS) through the regulation of TRPV1 expression, thereby mitigating damage to the auditory system. To illustrate this mechanism, a schematic diagram has been presented. [Display omitted] Puerarin (PUE), a flavonoid derivative with vasodilatory effects found in the traditional Chinese medicine kudzu, has anti-sensorineural hearing loss properties. However, the mechanism of its protective effect against ototoxicity is not well understood. In this study, we used in vitro and in vivo methods to investigate the protective mechanism of puerarin against cisplatin (CDDP)-induced ototoxicity. We established an ototoxicity model of CDDP in BALB/c mice and assessed the degree of hearing loss and cochlear cell damage. We used bioinformatics analysis, molecular docking, histological analysis, and biochemical and molecular biology to detect the expression of relevant factors. Our results show that puerarin improved CDDP-induced hearing loss and reduced hair cell loss. It also blocked CDDP-induced activation of TRPV1 and inhibited activation of IP3R1 to prevent intracellular calcium overload. Additionally, puerarin blocked CDDP-stimulated p65 activation, reduced excessive ROS production, and alleviated cochlear cell apoptosis. Our study provides new evidence and potential targets for the protective effect of puerarin against drug-induced hearing loss. Puerarin ameliorates cisplatin-induced ototoxicity and blocks cellular apoptosis by inhibiting CDDP activated TRPV1/IP3R1/p65 pathway, blocking induction of calcium overload and excessive ROS expression. [ABSTRACT FROM AUTHOR]

The total extract was suspended in hot distilled water (60°C, 1.5 L) and sequentially partitioned with petroleum ether (1.5 L × 4), ethyl acetate (1.5 L × 4), and I n i -butanol (1.5 L × 4), then concentrated under reduced pressure to obtain the petroleum ether extract (60 g), the ethyl acetate extract (66 g), and the I n i -butanol extract (150 g). The I n i -butanol fraction (150 g) was chromatographed on D101 macroporous resin column and eluted with water-ethanol (1:0-0:1) to obtain three fractions: Fr. 1, 30% ethanol eluent (43 g); Fr. 2, 60% ethanol eluent (60 g); and Fr. 3, 95% ethanol eluent (13 g). Fraction 3 (13 g) was chromatographed on a silica gel column (300-400 mesh) eluted with chloroform-methanol (150:1-0:1) repeatedly to yield five compounds. [Extracted from the article]