Microglia cells are immune cells in the central nervous system.When the microenvironment of brain has changed,microglia will respond rapidly.ATP,UTP,or other nucleotide signals released by neurons from damaged site and their metabolites such as ADP,adenosine,UDP and so on will bind with the purinergic receptors on microglia to regulate the morphology and function of microglia,then the microglial cells activated by nucleotide signals are to regulate neural cells by phagocytosis or releasing cytokines.In this article,the function and corresponding mechanisms of nucleotide signals on chemotaxis,phagocytosis,and process retraction are reviewed.

Larvae of Schistosoma japonicum could be blocked in Oncomelania hupensis with pre-infection by larval Exorchis trematodes (Tang et al., 2008, 2009). The present manuscript reports the result of comparison between the two different developments of larval S.japonicum in O.hupensis snails with and without pre-infection by larval Exorchis trematodes. Of 300 (invader rate 26.74%) abnormal larvae of S.japonicum for 4-82 days old were found from 28 (73.7%) O.hupensis snails which were pre-infected with Exorchis eggs, their body structure were unusual and developed astray at early mother sporocyst stage. From 25 (69.4%) O.hupensis snails without pre- infection by larval Exorchis, 67 (invader rate 13.96%) normal mother sporocysts of S.japonicum for 5-61 days old in different development stages and many early or middle stage daughter sporocysts were found, in the 75th day after infection many mature daughter sporocysts and cercariae of S.japonicum were found. Different increase of lymphocyte in body tissues of snails were found from the two experimental O.hupensis snail groups.

The aim of the study is to investigate the effect of salvianolic acid B (SalB) on blood-brain barrier (BBB) in rats after cerebral ischemia-reperfusion, and to illustrate its possible mechanisms. Cerebral ischemia-reperfusion was induced by middle cerebral artery occlusion in rats. The break-down of BBB was indicated by extravasations of immunoglobulin (IgG) monitored with immunohistochemistry. The expression of MMP-9 and NOS2 in the brain was determined by immunohistochemistry, and the expression of p-p38 and p-ERK1/2 was detected by Western blotting. It was shown that on day 2 after ischemia-reperfusion the IgG accumulated around the vascular boundary zone, suggesting the break-down of BBB, and the expression of MMP-9 and NOS2 up-regulated at the same time. The result of Western blotting suggested that the expression of p-p38 and p-ERK1/2 increased. On day 7 after ischemia-reperfusion the. expression of MMP-9 and NOS2 was about the same level as day 2, the expression of p-p38 was higher than that on day 2 and the expression of p-ERK1/2 was slightly lower than that on day 2. SalB (1 and 10 mg x kg(-1)) significantly alleviated the extravasations of immunoglobulin induced by cerebral ischemia-reperfusion (P < 0.05). On day 2 and day 7 SalB attenuated the expression of MMP-9 and NOS2 (P < 0.05). SalB (10 mg x kg(-1)) reduced the expression of p-p38 and p-ERK1/2 apparently on day 2 and 7 after ischemia-reperfusion (P < 0.05). SalB (1 mg x kg(-1)) inhibited the expression of p-p38 on day 7 after ischemia-reperfusion (P < 0.05). The results indicate that SalB protects blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting the MAPK pathway.

The aim of the study is to investigate the effect of nardosinone (Nar) on neuronal injury induced by oxygen-glucose deprivation (OGD) in primary cortical cultures isolated from embryos at gestational day 14. MTT method was used to determine the dosage regimen of Nar in primary neuronal cultures and observe the influence of Nar on the neurons suffering OGD; Western blotting analysis was used to detect expressions of protein kinase A (PKA), Ras related protein 1 (Rap1), mitogen-activated protein kinase kinase 1 (MEK1) and phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2) of OGD-injured or uninjured primary cultured neurons after Nar treatment. Results showed that Nar (50 and 100 micromol x L(-1)) improved the cell viability during OGD damage (P < 0.01) and increased the expression of PKA, Rap1, MEK1 and p-ERK1/2 in injured neurons. Additionally, elevations of PKA, Rapl, MEK1 and p-ERK1/2 in uninjured neurons were caused by Nar (50, 100 and 200 micromol x L(-1)) with a dose-dependent tenclency as well (P < 0.01). In conclusion, Nar could protect against the neuronal injury exposed to OGD, which may be relevant to the promotion of PKA and ERK signaling pathway.

Rooibos, Aspalathus linearis (Barm.f.) R. Dahlgren, is a South African endemic plant. Modern researches have shown that its leaves and branches are rich in polyphenols and specific flavonoids, aspalathin and nothofagin, which have many pharmacological effects on improving oxidative stress and inflammation, reducing blood sugar, protecting liver, resisting cancer and mutagenesis. In this paper, the research progress of Rooibos is summarized which could provide reference for further research and development.

ObjectiveTo observe the neuroprotective effects of ginsenoside Rb₁ on lipopolysaccharide （LPS）-induced neuroinflammation in mice and to preliminarily investigate its mechanism of action. MethodSeventy ICR mice were randomly divided into blank group， model group， dexamethasone sodium phosphate injection group， and low-dose， high-dose ginsenoside Rb₁ groups， with 14 mice in each group. A mouse brain neuroinflammation model was prepared using the LPS dose escalation method， starting with a dose of 1 mg·kg^-1 and administered via intraperitoneal injection every 48 h （every other morning）. Each subsequent dose increased by 2 mg·kg^-1， for a total of 7 injections， culminating in a final dose of 13 mg·kg^-1. The dexamethasone sodium phosphate injection group received an intraperitoneal injection at 5 mg·kg^-1·d^-1. The low-dose and high-dose ginsenoside Rb₁ groups were given intraperitoneal injections at 10 mg·kg^-1·d^-1 and 20 mg·kg^-1·d^-1， respectively， while the blank and model groups received the same volume of normal saline for 14 days. The behavioral activity of LPS mice was observed， anxiety-like behavior was assessed using the Y-maze and elevated plus maze， and brain levels of monocyte chemoattractant protein-1 （MCP-1）， tumor necrosis factor-α （TNF-α）， and interleukin-1β （IL-1β） were measured by enzyme-linked immunosorbent assay （ELISA）. Neuronal damage of microglia， and the activation status of microglia and astrocytes in the brain were assessed using immunofluorescence staining. The protein expression of phosphatidylinositol-3-kinase （PI3K）， protein kinase B （Akt）， and nuclear factor-κB （NF-κB） in mouse brain were detected by Western blot. ResultCompared with the blank group， the model group showed significantly increased anxiety-like behavior in the Y-maze and elevated plus maze （P<0.05， P<0.01）， significantly elevated levels of MCP-1， TNF-α， and IL-1β in the brain （P<0.01）， a significant decrease in the number of neuronal positive cells in the somatosensory cortex and hippocampus CA1 region （P<0.01）， significant activation of microglia and astrocytes （P<0.01）， and a significant increase in the expression of phosphorylated PI3K， Akt， and NF-κB proteins （P<0.01）. Compared with the model group， the ginsenoside Rb₁ low-dose and high-dose groups showed significantly reduced anxiety-like behavior in the Y-maze and elevated plus maze （P<0.05， P<0.01）， significantly decreased levels of MCP-1， TNF-α， and IL-1β in the brain （P<0.01）， a significant increase in the number of neuronal positive cells in the somatosensory cortex and hippocampus CA1 region （P<0.01）， significant inhibition of microglia and astrocyte activation （P<0.05， P<0.01）， and a significant decrease in the expression of phosphorylated PI3K， Akt， and NF-κB proteins （P<0.05， P<0.01）. ConclusionGinsenoside Rb₁ has neuroprotective effects on LPS-induced inflammation in mice， which may involve the regulation of the PI3K/Akt signaling pathway.

ObjectiveTo observe the effect of intranasal ginsenoside Rb₁ against epilepsy and preliminarily explore the mechanism. MethodThe mouse model of chronic epilepsy was established by intraperitoneal injection of pentylenetetrazole （PTZ）. After successful modeling （21 d）， the epileptic mice were randomly divided into PTZ group， sodium valproate （VPA） group， and low-dose （20 mg·kg^-1） and high-dose （40 mg·kg^-1） ginsenoside Rb₁ groups. Mice in each group were given corresponding drugs intranasally for 30 days， twice a day， and the control group was given the equal volume of normal saline. During the intranasal administration， the weight change， epilepsy latency， and epilepsy stage of the mice were recorded， and the changes in the electroencephalography （EEG） were recorded wirelessly. Neuronal Nuclei （NeuN） was used to observe the damage of neurons in cerebral cortex and hippocampus. The activation of microglia and astrocytes was observed with ionized calcium binding adapter molecule-1 （IBA-1） and glial fibrillary acidic protein （GFAP）， respectively. Glutamate （Glu） transporter-1 （GLT-1） and glutamine synthetase （GS） were used to observe the key molecular changes in Glu regulation. ResultCompared with the control group， the PTZ group decreased body weight （P<0.05，P<0.01）， shortened the epilepsy latency （P<0.01）， and increased the epilepsy stage （P<0.01）. The epileptic EEG waves were increased in the PTZ group. Compared with the PTZ group， the low and high-dose ginsenoside Rb₁ groups increased body weight （P<0.05，P<0.01）， prolonged the epilepsy latency （P<0.05，P<0.01）， decreased the epilepsy stage （P<0.05，P<0.01）， and decreased epileptiform EEG waves. Immunofluorescence staining （IF） showed that ginsenoside Rb₁ significantly ameliorated PTZ-induced neuronal damage （P<0.05，P<0.01） in the motor sensory area of the cerebral cortex and hippocampal CA1 area， and significantly inhibited PTZ-induced activation of microglia （P<0.05，P<0.01） and astrocytes. Further research found that ginsenoside Rb₁ significantly improved the expressions of astrocytic GLT-1 （P<0.01） and GS （P<0.01） in the brains of epileptic mice. ConclusionIntranasal ginsenoside Rb₁ can significantly improve the symptoms of epilepsy caused by PTZ in mice， which has a clear protective effect on neuronal damage in the brains of epileptic mice and significantly inhibits the activation of brain microglia and astrocyte activation. Its anti-epileptic mechanism may be related to the regulation of GLT-1 and GS of the key molecules of astrocyte Glu metabolism.