About: Platycodin D is a research topic. Over the lifetime, 244 publications have been published within this topic receiving 4042 citations. The topic is also known as: Olean-12-en-28-oic acid, 3-(beta-D-glucopyranosyloxy)-2,16,23,24-tetrahydroxy-, O-D-apio-beta-D-furanosyl-(1->3)-O-beta-D-xylopyranosyl-(1->4)-O-6-deoxy-alpha-L-mannopyranosyl-(1->2)-L-arabinopyranosyl ester, (2beta,3beta,16alpha)-.
TL;DR: The results suggest that the main inhibitory mechanism of the platycodin saponins may be the reduction of iNOS and COX-2 gene expression through blocking of NF-κB activation.
TL;DR: The antiobesity effect of the crude saponins in mice fed a high fat diet may be due to the inhibition of intestinal absorption of dietary fat by platycodin D.
Abstract: We examined the effects of crude saponins isolated from Platycodi radix on the degree on fat storage induced in mice by feeding a high fat diet for 9 wk. We reported previously that feeding mice a high fat diet for a longer time caused obesity and fatty liver compared with those fed a low fat diet, nonpurified diet. Feeding a high fat diet containing 10 or 30 g/kg crude saponins prevented the body and parametrial adipose tissue weight increases and hepatic steatosis of mice fed the high fat diet alone. Furthermore, crude saponins (375 mg/kg) inhibited the elevations in blood triacylglycerol in rats orally administered a lipid emulsion compared with that of rats given the lipid emulsion alone. Previously, we reported that crude saponins inhibited pancreatic lipase activity in vitro. To identify the active substance(s) of crude saponins, we examined the effects of purified platycodin D, the primary saponin in the crude mixture, on pancreatic lipase activity and on the blood triacylglycerol elevation in rats administered the oral lipid emulsion tolerance test. Platycodin D (0.5 and 1.0 g/L) inhibited pancreatic lipase activity in vitro and at a dose of 244 mg/kg, inhibited the elevation of blood triacylglycerol. Therefore, the antiobesity effect of the crude saponins in mice fed a high fat diet may be due to the inhibition of intestinal absorption of dietary fat by platycodin D.
TL;DR: As one of the most popular traditional herbal medicines, clinical studies of the main therapeutic aspects, toxicity and adverse effects of Platycodon grandiflorus will also undoubtedly be the focus of future investigation.
TL;DR: A dichotomous regulation of these important proinflammatory mediators by PD and PD3 is suggested, suggesting that PD may stimulate TNF-alpha synthesis or inhibit degradation of T NF-alpha mRNA.
TL;DR: Platycodin D, isolated from the root of Platycodon grandiflorum A. DC.
Abstract: Platycodin D, isolated from the root of Platycodon grandiflorum A. DC. (Campanulaceae) suppressed prostaglandin E2 production at 10 and 30 microM in rat peritoneal macrophages stimulated by the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate (TPA). Platycodin D3 and oleanolic acid showed no effect at these concentrations. Western blot analysis revealed that the induction of COX-2 protein by TPA was inhibited by platycodin D in parallel with the inhibition of prostaglandin E2 production. Platycodin D showed no direct effect on COX-1 and COX-2 activities. TPA-induced release of [3H]arachidonic acid from pre-labeled macrophages was also not inhibited by platycodin D.