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Much evidence demonstrates that microglia mediated neuroinflammation is an important contributor to the inflammatory injury in intracerebral hemorrhage (ICH). Therefore, the compounds that can inhibit neuroinflammation are greatly needed. In the current study, we examined whether curcumin, present in a Chinese medicinal plant, could prevent ICH induced microglia activation and confer protection against neurotoxicity. The cytokines of microglia were measured by ELISA, p38MAPK/PKC and NF-κB were measured by Western blot and EMSA. Microglial toxicity was assessed using MTT and FACS assays. And neurological function was evaluated by animal behavioristics. We found that curcumin prevented ICH-induced inflammatory molecules through NF-κB activation via the p38MAPK/PKC pathway in vitro. In addition, curcumin protected hippocampal HT22 cells from indirect toxicity mediated by ICH-treated microglia cells. Further, curcumin also attenuated ICH-induced neurological deficit and cerebral water content in vivo. Together, our findings suggest that curcumin could suppress ICH induced inflammatory injury and represent a novel herbal sources for ICH therapeutical strategy.

This study presents the fabrication and improved properties of an AlGaAs/InGaAs metal-oxide-semiconductor pseudomorphic high-electron-mobility transistor (MOS-PHEMT) using liquid phase deposited titanium dioxide (LPD-TiO2) as a gate dielectric. Sulfur pretreatment and postoxidation rapid thermal annealing (RTA) were consecutively employed before and after the gate dielectric was deposited to fill dangling bonds and therefore release interface trapped charges. Compared with a benchmark PHEMT, the AlGaAs/InGaAs MOS-PHEMT using LPD-TiO2 exhibited larger gate bias operation, higher breakdown voltage, suppressed subthreshold characteristics, and reduced flicker noise. As a result, the device with proposed process and using LPD-TiO2 as a gate dielectric is promising for high-speed applications that demand little noise at low frequencies.

As phagocytic cells of central nervous system, excessive activation or cell death of microglia is involved in a lot of nervous system injury and degenerative disease, such as stroke, epilepsy, Parkinson's disease, Alzheimer's disease. Accumulating evidence indicates that hypoxia upregulates HIF-1α expression leading to cell death of microglia. However, the exact mechanism of cell death induced by hypoxia in microglia is not clear. In the current study, we showed that hypoxia induced cell death and autophagy in microglia. The suppression of autophagy using either pharmacologic inhibitors (3-methyladenine, bafilomycin A1) or RNA interference in essential autophagy genes (BECN1 and ATG5) decreased the cell death induced by hypoxia in microglia cells. Moreover, the suppression of HIF-1α using either pharmacologic inhibitors (3-MA, Baf A1) or RNA interference decreased the microglia death and autophagy in vitro. Taken together, these data indicate that hypoxia contributes to autophagic cell death of microglia through HIF-1α, and provide novel therapeutic interventions for cerebral hypoxic diseases associated with microglia activation.