Significance of decreased serum interleukin-10 levels in the progression of cerebral infarction.

Anti-inflammatory cytokine and its serological detection may have an important role in the process of cardiovascular and cerebrovascular diseases. We investigated whether serum interleukin-10 (IL-10) is associated with cerebral infarction or not in the general population. Identified comprehensive searching was performed covering PubMed, EMBASE, Web of Science, Cochrane Library, CISCOM, CINAHL, Google Scholar, China BioMedicine, and China National Knowledge Infrastructure databases. Two reviewers extracted data and assessed studies independently. Information was extracted separately and classed into Asians and Caucasians. Summary standardized mean differences (SMDs) with 95 % confidence intervals (CI) were used with the utilization of Z test. Nine studies ranged from 2003 to 2014 were collected for meta-analysis. Results identified a negative association between serum IL-10 levels and cerebral infarction (SMD = 1.80, 95 % CI 0.79-2.81, P < 0.001). Country-subgroup analysis showed that low IL-10 level may be the main risk factor for cerebral infarction in India (SMD = 1.44, 95 % CI 1.13-1.75, P < 0.001) and Croatia (SMD = 2.96, 95 % CI 2.48-3.44, P < 0.001). In the ethnicity-stratified subgroup analysis, serum IL-10 levels were negatively correlated with cerebral infarction in Asians (SMD = 2.52, 95 % CI 0.47-4.57, P = 0.016), while not in Caucasians (P > 0.05). The lower serum IL-10 concentration was significantly associated with an increased likelihood of cerebral infarction in this meta-analysis. More prospective studies should be conducted to provide stronger evidence justifying the use of IL-10 as new biomarker to identify a predisposition toward cerebral infarction.

Inhibitory effect of piperlonguminine/ dihydropiperlonguminine on the production of amyloid beta and APP in SK-N-SH cells.

The study was undertaken to explore whether piperlonguminine/dihydropiperlonguminine could inhibit the production of amyloidbeta (Abeta) in human neuroblastoma cells (SK-N-SH) and to examine the underlying mechanism of this effect. Piperlonguminine/dihydropiperlonguminine components (1:0.8) were extracted from Futokadsura stem, and then used to treat SK-N-SH cells at three different concentrations: 3.13 microg/ml, 6.25 microg/ml and 12.50 microg/ml. Subsequently, the production of Abeta42 and Abeta40 were measured by Western blot analysis and enzyme linked immunosorbent assay (ELISA). On the other hand, the expressions of amyloid precursor protein (APP), Notch1 (Notch intracellular domain) and beta-site amyloid precursor protein cleavage enzyme (BACE-1) were also examined by Western blot assay. The activities of beta-secretase and gamma-secretase were detected at the same time. Furthermore, Abeta42 level was detected by immunocytochemistry staining. We demonstrated that the treatment of piperlonguminine/dihydropiperlonguminine could significantly decrease the levels of APP, Abeta42 and Abeta40 peptide in SK-N-SH cells, despite the fact that the activities of beta-secretase and gamma-secretase were not affected significantly. These data suggest that piperlonguminine/dihydropiperlonguminine components could significantly inhibit the level of APP, Abeta42 and Abeta40 peptide without affecting the activity of beta-secretase and gamma-secretase in SK-N-SH cells.

[Establishment of the organotypic model of amyotrophic lateral sclerosis from the SD rats' spinal cord].

OBJECTIVE: To establish an in vitro model of amyotrophic lateral sclerosis (ALS) from the organotypic culture of SD rats' lumber spinal cord induced by the mitochondrial inhibitor,malonate sodium. METHOD: The lumber spinal cord prepared from the 6-day-old SD rats was cut into 350 microm coronarily, cultured on the Millicell-CM inserts which make the spinal cord culturing on the interface between air and fluid. First, the optimum malonate sodium dose was determined by adding different doses into the medium and counting the living motor neuron numbers by using immuno-histochemistry staining. Second, the ALS model was established as following: the cultures were divided into the malonate groups and the control groups, adding 2 mmol/L sodium malonate into the medium of the malonate groups an the 3rd day, continue culture to 12 days with this concentration; the control groups culturing without malonate. RESULTS: The organotypic characteristics are still kept till the end of the curlturing. After adding the sodium malonate, counting the number of motor neurons and interneurons on the different spinal slices in the different groups, the number of motor neuron in the cultured spinal cord was less than control (11.00+/-2.45 vs 15.29+/-1.70 per semislice at the end of the culturing, P<0.01), but the difference of the interneuron was not significant. CONCLUSION: The amyotrophic lateral sclerosis model is successful with selective injury of motor neuron, and this model can be used for the exploring of the theraptic method and its pathogenesis.