Background : Oxidative stress and inflammatory response are important features of the brain pathology of Alzheimer's disease. Therefore, the purpose of this study was to the antioxidant activity and biochemical characterization of safflower seed. Moreover, we investigated the impact of Safflower seed on scopolamine-induced memory impairment in mice. Methods and Results : First, in order to determine active ingredient contents of safflower seed extract, we were carried out total phenol content and total flavonoid content analyses. As a result, dried safflower seed were found to contain 35.4 ± 0.4 ㎎·GAE/g dry weight and 45.3 ± 7.5 ㎎·NE/g dry weight in boiling water extraction. Also, the major compounds of safflower seed from HPLC analysis were identified as serotonin and serotonin derivatives [N- (p-coumaroyl)serotonin and N-feruloylserotonin]. In addition, the antioxidant activity of safflower seed showed IC50 values of 331.4 and 168.2, respectively, against DPPH and ABTS in vitro. Finally, with regard to the memory improvement activity, the administration of Safflower seed extract significantly restored memory impairments induced by scopolamine in the behavior tests such as novel object recognition and Morris water maze test. Conclusion : The results of our study suggest that the safflower seed extract possess potent memory improvement activity and are also a good source of natural antioxidants. Further study is needed to identify the mechanism responsible for their memory improvement activity.

Background: Traditional plant drugs, are less toxic and free from side effects compared to general synthetic drugs. They have been used for the treatment of diabetes and associated renal damage. In this study, we evaluated effect of Hachimi-jio-gan against diabetic renal damage in a rat model of type 1 diabetic nephropathy induced by subtotal nephrectomy plus streptozotocin (STZ) injection, and in Otsuka Long-Evans Tokushima Fatty (OLETF) rats and db/db mice as a model of human type 2 diabetes, and its associated complications. To explore the active components of Hachimi-jio-gan, the antidiabetic effect of corni fructus, a consituent of Hachimi-jio-gan, and 7-O-galloyl-D-sedoheptulose, a phenolic compound isolated from corni fructus, were investigated. Methods and Results: We conducted an extensive literature search, and all required data were collected and systematically organized. The findings were reviewed and categorized based on relevance to the topic. A summary of all the therapeutic effects were reported as figures and tables. Conclusions: Hachimi-jio-gan serves as a potential therapeutic agent to against the development of type 1 and type 2 diabetic nephropathy. From the results of characterization active components of corni fructus, 7-O-galloyl-D-sedoheptulose is considered to play an important role in preventing and/or delaying the onset of diabetic renal damage. 7-O-Galloyl-D-sedoheptulose is expected to serve as a novel therapeutic agent against the development of diabetic nephropathy.

Background : We have previously reported that Oligonol, a low-molecular polyphenol derived from lychee fruit, has protective effect on the liver and kidney of diabetic animal model. In this study, we examined whether Oligonol has any beneficial effects on pancreas of diabetic rats. Methods and Results : Oligonol was orally administered at a dose of 10 and 20 mg/kg body weight for 10 days to STZ-induced diabetic rats, and the effects were compared with those of vehicle-treated diabetic control and non-diabetic control rats. The administration of Oligonol reduced hyperglycemia in diabetic rats through an improvement of serum and pancreatic insulin levels. The increased reactive oxygen species levels in pancreas of diabetic control rats was attenuated by the Oligonol administration through inhibiting the expression of NADPH oxidase-related proteins. The enhanced expression of pro-apoptotic proteins in pancreas of diabetic control rats was significantly reduced by Oligonol administration through down-regulation of phosphor-c-Jun N-terminal kinases protein in pancreas. Furthermore, the expressions of cell proliferation-related protein were also augmented in Oligonol treated-diabetic rats. However, Oligonol treatment led to improved histological changes in the pancreas. Conclusion : These pancreatoprotective effects of Oligonol were achieved through attenuation of oxidative stress and its sensitive protein expression associated with apoptosis and cell proliferation in diabetic rats.

Background : In this study, we investigated the renoprotective effects of serotonin and its derivatives, on the renal function and expression of inflammation and apoptosis in cisplatin-induced nephrotoxicity mice. Methods and Results : Serotonin and its derivatives were orally administered at a dose of 7.5 mg/kg body weight for 5 days before the intraperitoneal injection of cisplatin 20 mg/kg body weight, and the effects were compared with those of vehicle-treated nephrotoxicity control and normal groups. In the serum and kidney, renal function parameters, reactive oxygen species and expression of protein related to pro-oxidant, antioxidant, inflammation and apoptosis were examined. As a result, serotonin and its derivatives administrations to nephrotoxicity mice lowered serum BUN and creatinine concentrations. These results were derived, at least in part, from attenuation the expression of antioxidant enzymes-related proteins, SOD and GPx. In the cisplatin-induced renal condition, augmented p-p38, p-ERK and p-JNK (mitogen-activated protein kinase pathway) were reduced with a increase in antioxidant enzymes on serotonin and its derivatives treatment. Moreover, in the serotonin and its derivatives-treated groups, NF- κB-induced inflammatory factors and apoptotic protein expressions were regulated in the kidney. Conclusion : The present study indicates that serotonin and its derivatives exerts a renoprotective effect against cisplatin-induced nephrotoxicity through the recovery of kidney function deterioration and attenuation of renal inflammation and apoptosis by regulating oxidative stress condition.