In Vitro and In Vivo Effects of Norathyriol and Mangiferin on α-Glucosidase.

Norathyriol is a metabolite of mangiferin. Mangiferin has been reported to inhibit α-glucosidase. To the best of our knowledge, no study has been conducted to determine or compare those two compounds on inhibiting α-glucosidase in vitro and in vivo by far. In this study, we determined the inhibitory activity of norathyriol and mangiferin on α-glucosidase in vitro and evaluated their antidiabetic effect in diabetic mice. The results showed that norathyriol inhibited α-glucosidase in a noncompetitive manner with an IC50 value of 3.12 µM, which is more potent than mangiferin (IC50 = 358.54 µM) and positive drug acarbose (IC50 = 479.2 µM) in the zymological experiment. Both of norathyriol and mangiferin caused significant (p < 0.05) reduction in fasting blood glucose and the blood glucose levels at two hours after carbohydrate loading and it was interesting that mangiferin and norathyriol can make the decline of the blood glucose earlier than other groups ever including normal group in the starch tolerance test. However, norathyriol and mangiferin did not significantly influence carbohydrate absorption in the glucose tolerance test. Therefore, the antidiabetic effects of norathyriol and mangiferin might be associated with α-glucosidase, and norathyriol was more potent than mangiferin.

Comparative analysis of the neuroprotective effects of ginsenosides Rg1 and Rb1 extracted from Panax notoginseng against cerebral ischemia.

Panax notoginseng, a traditional Chinese medicine, has been used for thousands of years to treat ischemic patients. More than 20 saponin components have been isolated from P. notoginseng root and identified chemically. However, these different chemical components have different roles. In this study we compared the neuroprotective mechanisms of ginsenosides Rg1, Rb1, Rg1/Rb1, and panax notoginsenoside (PNS) against injuries caused by cerebral ischemia-reperfusion (I/R). Our results show that all of these treatments significantly reduced infarction volume and alleviated neurological deficits caused by cerebral I/R. The increase in malondialdehyde (MDA) concentration was inhibited by these treatments in the hippocampus. The decreased expressions of thioredoxin-1 (Trx-1), copper-zinc superoxide dismutase (SOD-1), protein kinase B (PKB/Akt), and nuclear factor-kappa B (NF-κB) caused by cerebral I/R were restored by these treatments. The expression of heat shock protein 70 (HSP70) was enhanced in the middle cerebral artery occlusion (MCAO) group, as well as in all of the treatment groups. These results suggest that Rg1 and Rb1 have similar roles in protecting the brain from ischemic damage; however, neither Rg1/Rb1 nor PNS have synergistic effects, thus either Rg1 or the Rb1 monomer should be considered as a pharmacological neuroprotective strategy for use in the case of ischemic stroke.

[Study on drug release of gastrodin ion-activated nasal in situ gel in vitro].

OBJECTIVE: To study on the drug release characteristics and mechanism of gastrodin ion-activated nasal in situ gel in vitro. METHOD: Regularity and mechanism of the drug release of gastrodin nasal in situ gel were studied by using the diffusion cell model and the membrane-less dissolution model, respectively. A novel kinesis diffusion cell model was designed according to the characteristics of release environment of nasal cavity. It was used to investigate the effect of adhesiveness on the release of the in situ gel. RESULT: Drug release of gastrodin nasal in situ gel followed the one order release model. Erosion rate of the gel was low and not linearly correlated with the release rate. Compared with gastrodin solution, the nasal in situ gel could increase release time and release amount. CONCLUSION: Gastrodin in the nasal in situ gel is released mainly by diffusion rather than erosion. Release amount of the in situ gel in nasal cavity may be obviously increased because of its adhesiveness.

[Brain targeting of gastrodin nasal in situ gel].

OBJECTIVE: To investigate the biodistribution of gastrodin ion-activated nasal in situ gel in rat blood and brain tissues and to evaluate its brain targeting. METHODS: Intravenous administration of gastrodin solution or intranasal administration of gastrodin nasal in situ gel were given to 32 rats, respectively. The concentrations of gastrodin in the plasma and gastrodigenin in the brain tissues of the rats were determined by HPLC. RESULTS: The intranasal administration of the in situ gel of gastrodin produced more significant brain targeting effect than the intravencus administration of gstrodin solution (P < 0.01). The area under curve (AUC) of cerebrum, cerebellum and olfactory bulb increased by 1.16, 0.77 and 3.34 times, with 2.66. 2.18 and 5.34 brain targeting indexes (BTI), respectively. The mean residence time (MRT) increased by nearly four-folds. CONCLUSION: Gastrodin nasal in situ gel can improve the brain targeting of gastrodin and slow its release.