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Sodium houttuyfonate (SH) is a chemical compound synthesized by houttuynin and sodium bisulfite. As it has antinflammatory effects, SH has been widely used to treat autoimmune diseases, including post events following traumatic brain injury (TBI).Meanwhile, NOD-like receptor with pyrin domain containing-3 (NLRP3) inflammasomes in microglia may play a central role in TBI. But to date, the intracellular mechanisms involved in the anti-inflammatory effects of SH in TBI remain unknown, especially whether regulating NLRP3. To gain an insight into this possibility, we conducted cell culture and biochemical studies on the effect of SH on NLRP3 inflammasome in microglia. The results showed that SH inhibited TLR4 and NLRP3 inflammasome activation in the microglia cell. In parallel, phosphorylation of ERK and NF-κB p65, which play a key role in NLRP3 inflammasome formation, was decreased. Intraperitoneal injection of SH into TBI mice significantly reduced the modified neurological severity score (mNSS), as well as the degree of microglia apoptosis post-controlled cortical impact (CCI). Immunohistochemistry, Western blot analysis, and reverse-transcription polymerase chain reaction (RT-PCR) revealed that SH markedly reduced NLRP3 inflammasome activation, TLR4 activity, phosphorylation of ERK and NF-κB. Moreover, SH significantly inhibited microglia activation post-CCI, but effectively promoted the astrocyte activation and angiopoiesis.Taken together, our research provides evidence that SH attenuated neurological deficits post TBI through inhibiting NLRP3 inflammasome activation, via influencing the TLR4/NF-κB signaling pathway. These findings explain the intracellular mechanism of the anti-inflammatory activity caused by SH treatment following TBI.

Background Studies have shown that vagus nerve stimulation (VNS) significantly reduces the frequency of seizures. MicroRNAs (miRNAs) in cerebrospinal fluid are expected to become a new biomarker of epilepsy. Therefore, studying the interaction mechanism between the VNS and miRNAs is hopeful of bringing a new therapeutic direction for the treatment of epilepsy.Methods Kainic acid was used to induce the Sprague-Dawley rat epilepsy model, and the rats were treated with VNS. The miR-210 expression was determined by quantitative reverse transcription PCR (qRT-PCR). Racine score was adopted to evaluate the performance of behavioral seizures, whereas qRT-PCR and ELISA were employed to test inflammatory factors. Western blotting was implemented to testify the inflammatory and apoptotic proteins.Results Kainic acid-induced the Sprague-Dawley rat epilepsy model and upregulated the expression of miR-210, inflammatory response, inflammation and apoptosis-related proteins in brain tissues. In addition, compared with the epilepsy model group, miR-210 in the hippocampus of the epilepsy model rats treated with VNS was downregulated, and the expression of apoptosisrelated proteins and inflammatory factors was reduced. Moreover, after further inhibiting the expression of miR-210, the inhibition of VNS on epilepsy, inflammation and apoptosis were significantly enhanced.Summary VNS relieves the inflammatory response and apoptosis of epileptic rats via inhibiting miR-210.