BackgroundMicroglial polarization with M1/M2 phenotype shifts and the subsequent neuroinflammatory responses are vital contributing factors for spinal cord injury (SCI)-induced secondary injury. Nuclear factor-κB (NF-κB) is considered the central transcription factor of inflammatory mediators, which plays a crucial role in microglial activation. Lysine acetylation of STAT1 seems necessary for NF-kB pathway activity, as it is regulated by histone deacetylases (HDACs). There have been no studies that have explained if HDAC inhibition by valproic acid (VPA) affects the NF-κB pathway via acetylation of STAT1 dependent of HDAC activity in the microglia-mediated central inflammation following SCI. We investigated the potential molecular mechanisms that focus on the phenotypic transition of microglia and the STAT1-mediated NF-κB acetylation after a VPA treatment.MethodsThe Basso-Beattie-Bresnahan locomotion scale, the inclined plane test, the blood-spinal cord barrier, and Nissl staining were employed to determine the neuroprotective effects of VPA treatment after SCI. Assessment of microglia polarization and pro-inflammatory markers, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and interferon (INF)-γ was used to evaluate the neuroinflammatory responses and the anti-inflammatory effects of VPA treatment. Immunofluorescent staining and Western blot analysis were used to detect HDAC3 nuclear translocation, activity, and NF-κB signaling pathway activation to evaluate the effects of VPA treatment. The impact of STAT1 acetylation on NF-kB pathway and the interaction between STAT1 and NF-kB were assessed to evaluate anti-inflammation effects of VPA treatment and also whether these effects were dependent on a STAT1/NF-κB pathway to gain further insight into the mechanisms underlying the development of the neuroinflammatory response after SCI.ResultsThe results showed that the VPA treatment promoted the phenotypic shift of microglia from M1 to M2 phenotype and inhibited microglial activation, thus reducing the SCI-induced inflammatory factors. The VPA treatment upregulation of the acetylation of STAT1/NF-κB pathway was likely caused by the HDAC3 translocation to the nucleus and activity. These results indicated that the treatment with the VPA suppressed the expression and the activity of HDAC3 and enhanced STAT1, as well as NF-κB p65 acetylation following a SCI. The acetylation status of NF-kB p65 and the complex with NF-κB p65 and STAT1 inhibited the NF-kB p65 transcriptional activity and attenuated the microglia-mediated central inflammatory response following SCI.ConclusionsThese results suggested that the VPA treatment attenuated the inflammatory response by modulating microglia polarization through STAT1-mediated acetylation of the NF-κB pathway, dependent of HDAC3 activity. These effects led to neuroprotective effects following SCI.

In a DC microgrid (DC-MG), the dc bus voltage is vulnerable to power fluctuation derived from the intermittent distributed energy or local loads variation. In this paper, a virtual inertia control strategy for DC-MG through bidirectional grid-connected converters (BGCs) analogized with virtual synchronous machine (VSM) is proposed to enhance the inertia of the DC-MG, and to restrain the dc bus voltage fluctuation. The small-signal model of the BGC system is established, and the smallsignal transfer function between the dc bus voltage and the dc output current of the BGC is deduced. The dynamic characteristic of the dc bus voltage with power fluctuation in the DC-MG is analyzed in detail. As a result, the dc output current of the BGC is equivalent to a disturbance, which affects the dynamic response of the dc bus voltage. For this reason, a dc output current feed-forward disturbance suppressing method for the BGC is introduced to smooth the dynamic response of the dc bus voltage. By analyzing the control system stability, the appropriate virtual inertia control parameters are selected. Finally, simulations and experiments verified the validity of the proposed control strategy.

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Traditional grid-connected inverters (TGCI) could suffer from small-signal instability owing to the dynamic interactions among inverters and a weak grid. In this letter, the small-signal sequence impedance model of the virtual synchronous generator (VSG) is built, and the sequence impedance characteristics of the VSG and the TGCI are compared and analyzed. The sequence impedance of the TGCI is mainly capacitive in the middle-frequency area, and the impedance amplitude is quite high. By contrast, the sequence impedance of the VSG, being consistent with the grid impedance characteristics, is generally inductive, and the impedance amplitude is quite low. Based on the sequence impedance model and the Nyquist stability criterion, the influence of the grid stiffness, number of paralleled inverters, and phase-locked loop (PLL) bandwidth on the stability of the VSG and the TGCI grid-connected system is analyzed. The stability analysis results show that the TGCI loses stability easily whereas the VSG still works well without PLL restrictions under an ultraweak grid or with a large number of inverters connected to the grid. Therefore, the VSG is more suitable than the TGCI for achieving high penetration of renewable energy generation in an ultra-weak grid from a system stability viewpoint. Finally, experimental results validate the sequence impedance model and the stability analysis.

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