Traumatic central nervous system injury, including traumatic brain injury and spinal cord injury, has extremely high disability and mortality rates. The huge medical expenses and sequelae further aggravate the economic and psychological burden of patients and their families. Current treatments for traumatic central nervous system injury include surgical therapy, physical therapy, medication and post-rehabilitation treatment, but none of them can achieve ideal efficacy, and more effective treatment is urgently needed. Ferroptosis, as one of the newly discovered modes of programmed cell death, has been shown to play a crucial role in secondary injury to the traumatic central nervous system, but its clinical transformation is limited. This article summarizes the research results of ferroptosis inhibitors, points out the types and effects of them, to provide new ideas for clinical treatment of traumatic central nervous system injury and drug development.

Objective:To explore the mechanism of dexmedetomidine (DEX) regulating microglial (MG) polarization and neuroinflammation after traumatic brain injury (TBI) in rats.Methods:Forty-two adult male SD rats were randomly (random number) divided into the sham group, TBI group, TBI+DEX group (further divided into 1 d, 3 d and 7 d subgroups), TBI+NF-κB inhibitor (pyrrolidine dithiocarbamate, PDTC) group and TBI+DEX+PDTC group, with 6 animals in each group. The rat TBI model was established according to the modified Feeney free fall method. PDTC was intraperitoneally injected 1 h after modeling with a dose of 100 mg/kg, and DEX was intraperitoneally injected 2 h after modeling with a dose of 100 μg/kg. Modified neurological severity score (mNSS) was used to evaluate rat neurological function, ELISA was used to detect serum inflammatory factors, and rats’ damaged cortex was collected to detect the phenotype markers of MG and protein expressions of MyD88 and NF-κB p65, and immunofluorescence staining was used to observe the expression and nuclear entry of NF-κB p65 in MG in injured cortex. One-way and two-way ANOVA were used to compare the measurement data among multiple groups.Results:Compared with the sham group, the mNSS score was significantly higher in the TBI group, and DEX treatment significantly decreased the mNSS score of TBI rats ( P<0.05). ELISA and Western blot results showed that in the TBI group, the tumor necrosis factor-α (TNF-α), interleukin (IL)-1β in serum and M1 phenotype marker (TNF-α, IL-1β) in brain were increased, the expression of anti-inflammatory factor IL-10 in serum and M2 phenotype markers (arginase-1 and IL-10) in brain were decreased ( P<0.05), and DEX downregulated the expression of TNF-α, IL-1β in serum and M1 phenotype markers in brain, while upregulated the level of L-10 in serum and the M2 phenotype marker in brain ( P<0.05). In addition, the expression of MyD88 and the nuclear translocation of NF-κB p65 were inhibited in the DEX group, and this effect could be enhanced by PDTC. Conclusions:DEX modulates MG activation in TBI rats by inhibiting NF-κB nuclear translocation and reduces neuroinflammation.

凡是能引起心房结构、构型、电生理的病理生理学改变,并因此导致心房重构、传导异常、收缩、舒张功能障碍的疾病,如房性快速性心律失常性心肌病、心房纤维化性心肌病、房性淀粉样变性心肌病及心衰、高血压、瓣膜病、心肌梗死等引起的房性扩张性心肌病即为心房性心肌病.超声检查技术、延迟增强心脏磁共振技术、心脏CT等影像学检查以及血清心钠肽、高敏C反应蛋白、氨基末端脑钠肽前体、胶原蛋白合成代谢产物与Ⅲ型前胶原氨基末端肽等分子生物学指标检测是心房性心肌病比较常用的诊断技术,心房肌电压检测、心房肌活检、基因检测等是较为新颖的诊断技术,均可为心房性心肌病的诊断提供依据.