[Effects of Jiji decoction on the cognitive function and oxidative stress in mice with vascular dementia induced by cerebral ischemia/reperfusion].

OBJECTIVE: To determine the effects of Jiji decoction (Traditional Chinese Medicine) on the cognitive function and oxidative stress in mice with vascular dementia (VD) induced by cerebral ischemia/reperfusion. METHODS: Thirty-two mice were randomly divided into nonnal group (n = 8), sham group (operation, but no cerebral ischemia/reperfusi6n, n = 8), model group (vascular dementia model induced by cerebral ischemia/reperfusion, n = 8), and Jiji decoction-treated group (vascular dementia model plus treatment with Jiji decoction, n = 8). Fourteen days of treatment after operation, the cognitive behavior was measured in step-through test, spatial probe test and platform test. Afterwards, to assess the levels of oxidative stress, the activity of superoxide dismutase(SOD) and content of malonaldehyde (MDA) in brain of these mice were measured. RESULTS: Data from step-through test indicated that the escaping latency of Jiji decoction-treated group was prolonged and the error counts were decreased significantly ( P <0.01) compared with those of model group. Data from spatial probe test indicated that the time of entering darkroom, the time of climbing height and the time of entering bright room in Jiji decoction-treated group were shortened and the counts of climbing height were increased (P < 0.05-0.01) significantly compared with those of model group. Data from platform test showed that the escaping latency of Jiji decoction-treated group was prolonged significantly (P < 0.01) compared with that of model group. Compared with normal and sham group, the activity of SOD was decreased and the content of MDA was increased in model group significantly (P < 0.01). Compared with those of model group, the levels of SOD and MDA in Jiji decoction-treated group were improved significantly (P < 0.01). CONCLUSION: Jiji decoction could improve cognitive function of VD mice. Its mechanism might be related with the inhibition of oxidative stiess in the brain.

[Preparation process of rutacarpine-hydroxypropyl-beta-cyclodextrin inclusion complex].

Rutaecarpine (Rut) is a type of indole quinazoline alkaloid exracted from Ruticarpum. Studies showed that Rut has a wide range of pharmacological effects, such as anti-hypertension, anticancer, anti-inflammation, anti-thrombus formation. Currently, many scholars are committed to developing it into a new antihypertensive and anti-inflammatory drug with all new mechanisms. But studies found that Rut is a highly fat-soluble drug with low water and oil solubility. Its high insolubility is the main obstacle in its oral absorption and application, which greatly reduced its bioavailability. Therefore, hydroxypropyl-beta-cyclodextrin (HP-beta-CD) was used as the inclusion material to prepare Rut-HP-beta-CD inclusion complex in this experiment, in order to increase its water solubility and bioavailability. In this experiment, the inclusion complex was prepared by the stirring-freeze-dry method. The preparation process was optimized by the orthogonal test, with the inclusion rate as the index, and molar ratio between host and guest molecules, inclusion temperature, time and stirring speed as the impacting factors. Moreover, the inclusion complex was verified by detecting the apparent solubility, thin layer chromatography, microscopic identification, melting point detection and dissolution study. The results showed that under the conditions of the molar ratio between Rut and HP-beta-CD of 1: 1, temperature at 60 degrees C, inclusion time of 4h and stirring speed at 600 r x min(-1), the inclusion rate of Rut-HP-beta-CD reached 91.04%. Therefore, the preparation process of Rut-HP-beta-CD inclusion under the optimum conditions is simple and feasible, with a highest inclusion rate and reproducibility, and could significantly improve Rut's solubility and bioavailability, and provide a reliable experimental basis for its clinical application.

Chrysophanol attenuates lead exposure-induced injury to hippocampal neurons in neonatal mice.

Previous studies have shown that chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, chrysophanol (0.1, 1.0, 10.0 mg/kg) was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after chrysophanol treatment. Collectively, these findings indicate that chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice.

Neuroprotective effects of rutaecarpine on cerebral ischemia reperfusion injury.

Rutaecarpine, an active component of the traditional Chinese medicine Tetradium ruticarpum, has been shown to improve myocardial ischemia reperfusion injury. Because both cardiovascular and cerebrovascular diseases are forms of ischemic vascular disease, they are closely related. We hypothesized that rutaecarpine also has neuroprotective effects on cerebral ischemia reperfusion injury. A cerebral ischemia reperfusion model was established after 84, 252 and 504 µg/kg carpine were given to mice via intraperitoneal injection, daily for 7 days. Results of the step through test, 2,3,5-triphenyl tetrazolium chloride dyeing and oxidative stress indicators showed that rutaecarpine could improve learning and memory ability, neurological symptoms and reduce infarction volume and cerebral water content in mice with cerebral ischemia reperfusion injury. Rutaecarpine could significantly decrease the malondialdehyde content and increase the activities of superoxide dismutase and glutathione peroxidase in mouse brain. Therefore, rutaecarpine could improve neurological function following injury induced by cerebral ischemia reperfusion, and the mechanism of this improvement may be associated with oxidative stress. These results verify that rutaecarpine has neuroprotective effects on cerebral ischemia reperfusion in mice.

[Effect of osthol on memory impairment of mice in AlCl3-induced acute senile model].

AIM: To study the protective effect and mechanism of osthol on learning and memory impairment of mice with acute senile model induced by AlCl3. METHODS: After s.c. AlCl3 60 mg.kg-1 for 7 d and i.p. osthol 15 and 7.5 mg.kg-1 for 12 d, using step-through test and step-down test, the effect of osthol on learning and memory was observed and the glutathione peroxidase (GSH-PX) activities in blood and superoxide dismutase (SOD) activities in plasma and cerebrum were measured. RESULTS: Osthol 15 and 7.5 mg.kg-1 significantly improved the capability of memory and enhanced the activities of GSH-PX and SOD in AlCl3 treated mice. CONCLUSION: Osthol shows protective effect on brain memory impairment of mice in acute senile model induced by AlCl3. Perhaps the mechanism is involved in enhancing the activities of GSH-PX and SOD, clearing away the free radical, protecting the brain neuron from the harm of lipoperoxide.