Yating An, Jia Hao, Jian Li, Wei He, Lei Wang, Yi Zhang
{"title":"The inhibitory effect of lotus leaf extract on hyperuricemia and its potential mechanism","authors":"Yating An, Jia Hao, Jian Li, Wei He, Lei Wang, Yi Zhang","doi":"10.1097/HM9.0000000000000001","DOIUrl":null,"url":null,"abstract":"Abstract Objective: Lotus leaf is a traditional Chinese herb that has been used successfully for centuries for relieving edema by inducing diuresis. Based on its good clinical evidence and anti-hypertensive effectiveness, this study aimed to investigate the potential mechanism of the hyperuricemic inhibitory effects of lotus leaf crude extract (LL) and lotus leaf total alkaloids fraction (LA). Methods: The xanthine oxidase (XOD) inhibitory effect of LL and LA was analyzed in vitro by determining mRNA expression and protein expression levels of hepatic XOD. The hyperuricemic inhibitory effect of the lotus leaf was analyzed in vivo in a potassium oxonate (PO)-induced rat model by determining mRNA expression for renal urate transporters. Results: At a concentration of 40 μg/mL, LL and LA suppressed XOD enzymatic activity by 37.35% ± 9.50% and 47.73% ± 8.32%, respectively. Both LL and LA administration significantly reduced the concentration of uric acid in the serum and liver of PO-induced hyperuricemic rats. Both LL and LA administration could inhibit XOD mRNA and protein expression, activate renal organic anion transporter 1/3 mRNA expression, and inhibit renal urate reabsorption by decreasing renal GLUT9 and renal urate transporter 1. Conclusions: Insight was gained into the mechanism behind the hyperuricemic inhibitory effects of LL and LA. Our results suggest that they act on two targets: decreasing the production of uric acid by inhibiting mRNA and protein expression of XOD in the liver, and regulating the mRNA expression of renal urate transporters in the kidneys.","PeriodicalId":93856,"journal":{"name":"Acupuncture and herbal medicine","volume":"5 1","pages":"122 - 129"},"PeriodicalIF":0.0000,"publicationDate":"2021-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acupuncture and herbal medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/HM9.0000000000000001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
Abstract Objective: Lotus leaf is a traditional Chinese herb that has been used successfully for centuries for relieving edema by inducing diuresis. Based on its good clinical evidence and anti-hypertensive effectiveness, this study aimed to investigate the potential mechanism of the hyperuricemic inhibitory effects of lotus leaf crude extract (LL) and lotus leaf total alkaloids fraction (LA). Methods: The xanthine oxidase (XOD) inhibitory effect of LL and LA was analyzed in vitro by determining mRNA expression and protein expression levels of hepatic XOD. The hyperuricemic inhibitory effect of the lotus leaf was analyzed in vivo in a potassium oxonate (PO)-induced rat model by determining mRNA expression for renal urate transporters. Results: At a concentration of 40 μg/mL, LL and LA suppressed XOD enzymatic activity by 37.35% ± 9.50% and 47.73% ± 8.32%, respectively. Both LL and LA administration significantly reduced the concentration of uric acid in the serum and liver of PO-induced hyperuricemic rats. Both LL and LA administration could inhibit XOD mRNA and protein expression, activate renal organic anion transporter 1/3 mRNA expression, and inhibit renal urate reabsorption by decreasing renal GLUT9 and renal urate transporter 1. Conclusions: Insight was gained into the mechanism behind the hyperuricemic inhibitory effects of LL and LA. Our results suggest that they act on two targets: decreasing the production of uric acid by inhibiting mRNA and protein expression of XOD in the liver, and regulating the mRNA expression of renal urate transporters in the kidneys.