Protective effect of naringin against the LPS-induced apoptosis of PC12 cells: Implications for the treatment of neurodegenerative disorders.

Several studies have demonstrated that increased apoptosis plays an essential role in neurodegenerative disorders. It has been demonstrated that lipopolysaccharide (LPS) induces apoptosis largely through the production of intracellular reactive oxygen species (ROS) and inflammatory mediators. In this study, we investigated the potential protective mechanisms of naringin (Nar), a pummelo peel extract, on LPS-induced PC12 cell apoptosis. Nar pre-conditioning prior to stimulation with LPS for 18 h was a prerequisite for evaluating PC12 cell viability and the protective mechanisms of Nar. Nar significantly improved cell survival in a time- and concentration-dependent manner. On the one hand, Nar downregulated cytochrome P450 2E1 (CYP2E1), inhibited the release of ROS, mitigated the stimulation of oxidative stress, and rectified the antioxidant protein contents of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), superoxide dismutase (SOD)2 and glutathione synthetase (GSS). On the other hand, Nar downregulated inflammatory gene and protein expression, including interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, HMGB1, high mobility group box 1 protein (HMGB1), cyclooxygenase-2 (COX-2), the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-TNF receptor­associated factor 6 (TRAF6) path-way and downstream mitogen activated protein kinase (MAPK) phosphorylation, activator protein transcription factor-1 (AP-1) and nuclear factor (NF)-κB. Moroever, Nar markedly attenuated the cytochrome c shift from the mitochondria to the cytosol and regulated caspase-3-related protein expression. To the best of our knowledge, this is the first study to report the antioxidant, anti-inflammatory and anti-apoptotic effects of Nar in neuronal-like PC12 cells. These results suggest that Nar can be utilized as a potential drug for the treatment of neurodegenerative disorders.

Synergistic anti-glioma effect of Hydroxygenkwanin and Apigenin in vitro.

Apigenin (AP) and Hydroxygenkwanin (HGK) are two natural flavonoid compounds. Previous studies have already demonstrated the anti-tumor capability of AP. However, it is not clear whether HGK has such property. In the current study, the anti-glioma activities of HGK and its synergistic anti-glioma effects with AP on C6 glioma cells were investigated. In addition, the possible mechanisms were also studied. MTT assay and morphologic analysis including acridine orange/ethidium bromide (AO/EB) and 4',6-diamidino-2-phenylindole (DAPI) staining were used in the research, and the results indicated that the treatment with AP or HGK could inhibit C6 glioma cell proliferation respectively. Moreover, when AP was administrated simultaneously, the anti-glioma effect of HGK was dramatically enhanced in a dose-dependent manner, which is obviously better than that of carmustine (BCNU) at the concentration 25µM for treating of 24h. Compared with control, mitochondrial membrane potential (MPP) loss and mitochondrion damage were detected by JC-1 fluorescence probes (JC-1) and transmission electron microscopy (TEM) after treatment. Obvious DNA damage and cell cycle S phase arrest were detected by alkaline comet assay and flow cytometric analysis (FCM). Additionally, up regulation of TNF-α level, activations of caspase-3, -8, over expressions of BID and BAK protein and BCL-XL protein down expression were also observed after treatment by the combination of AP and HGK. The results indicate that HGK may be an effective natural product to treat glioma, and the combination of AP and HGK may be a promising method for glioma chemotherapy.

Microsurgical treatment for parasagittal meningioma in the central gyrus region.

The aim of the present study was to determine the efficacy of microsurgery treatment for parasagittal meningioma in the central gyrus region. A microsurgical technique was used to treat 26 patients with large parasagittal meningioma in the central gyrus region. The Rolandic and draining veins and the peritumoral normal brain tissue were retained, and the associated sagittal sinus was appropriately protected. A Simpson grade I, II or III resection was performed in 8 (30.8%), 12 (46.2%) and 6 (23.1%) patients, respectively, with no post-operative mortalities. Following treatment, 9 patients exhibited hemiparalysis. No tumor recurrence was found in 21 patients during the follow-up examination. The treatment protocol described in the current study included sufficient pre-operative imaging evaluations, a skilled microsurgical technique, improved protection of the Rolandic vein and treatment of the sagittal sinus, and was found to significantly increase the total tumor removal rate and decrease post-operative recurrence.

Plasma copeptin levels in Chinese patients with acute ischemic stroke: a preliminary study.

Copeptin is a stable by-product of arginine-vasopressin synthesis and reflects its secretion. The objective of the study was to evaluate the predictive value of copeptine on functional outcome at 90-day follow-up from stroke onset. We conducted a prospective, observational cohort study in the emergency department of two hospitals and enrolled 125 patients with acute ischemic stroke. Plasma copeptin concentrations, determined by a CT-proAVP-luminescence-immunoassay, were measured. There was a good correlation between levels of plasma copeptin and NIHSS score (r = 0.733, P < 0.01). In the 41 patients (32.8 %) with a poor functional outcome, copeptin levels were higher compared with those in patients with a favorable outcome (27.3; IQR, 14.9-34.8 pmol/L vs. 12.9; IQR, 9.4-21.6 pmol/L; P < 0.0001). Copeptin levels in 18 patients who died were more than two times greater as compared to patients who survived (32.4; IQR, 18.7-38.5 pmol/L vs. 15.1; IQR, 12.4-24.6 pmol/L; P < 0.0001). After adjusting for all other significant outcome predictors, copeptin level remained an independent predictor for poor functional outcome and mortality with an odds ratio of 3.12 (95 % CI 1.54-6.46), 3.16 (95 % CI 0.92-6.15), respectively. Our study suggests that copeptin levels are a useful tool to predict outcome and mortality 3 months after acute ischemic stroke and have a potential to assist clinicians.