BackgroundRecent evidence has suggested that peripheral inflammatory responses induced by lipopolysaccharides (LPS) play an important role in neuropsychiatric dysfunction in rodents. Interleukin-1β (IL-1β), a pro-inflammatory cytokine, has been proposed to be a key mediator in a variety of behavioral dysfunction induced by LPS in mice. Thus, inhibition of IL-1β may have a therapeutic benefit in the treatment of neuropsychiatric disorders. However, the precise underlying mechanism of knock-down of IL-1β in repairing behavioral changes by LPS remains unclear.MethodsThe mice were treated with either IL-1β shRNA lentivirus or non-silencing shRNA control (NS shRNA) lentivirus by microinjection into the dentate gyrus (DG) regions of the hippocampus. After 7 days of recovery, LPS (1 mg/kg, i.p.) or saline was administered. The behavioral task for memory deficits was conducted in mice by the novel object recognition test (NORT), the anxiety-like behaviors were evaluated by the elevated zero maze (EZM), and the depression-like behaviors were examined by the sucrose preference test (SPT) and the forced swimming test (FST). Furthermore, the levels of malondialdehyde (MDA), superoxide dismutase (SOD), nuclear factor erythroid-derived 2-like 2 (Nrf2), heme oxygenase 1 (HO1), IL-1β, tumor necrosis factor (TNF-α), neuropeptide VGF (non-acronymic), and brain-derived neurotrophic factor (BDNF) were assayed.ResultsOur results demonstrated that IL-1β knock-down in the hippocampus significantly attenuated the memory deficits and anxiety- and depression-like behaviors induced by LPS in mice. In addition, IL-1β knock-down ameliorated the oxidative and neuroinflammatory responses and abolished the downregulation of VGF and BDNF induced by LPS.ConclusionsCollectively, our findings suggest that IL-1β is necessary for the oxidative and neuroinflammatory responses produced by LPS and offers a novel drug target in the IL-1β/oxidative/neuroinflammatory/neurotrophic pathway for treating neuropsychiatric disorders that are closely associated with neuroinflammation, oxidative stress, and the downregulation of VGF and BDNF.

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Purpose: To introduce a novel localization method in minimally invasive spine surgery, which has the advantages of precise positioning, simple operation, customization and industrialization. Methods: We used localization membrane applied to osteoporotic fracture of spine, including the percutaneous kyphoplasty (PKP) group in 40 cases and the percutaneous internal fixation group in 10 cases. The success rate of one-time fluoroscopy, two-dimensional target acquisition, and the localization time preoperatively were recorded. Results: The success rate of one-time fluoroscopy was 100%. Two-dimensional target acquisition was 100%. The mean localization time of the percutaneous kyphoplasty (PKP) group was 3.53 ± 1.28 minutes. The mean localization time of the percutaneous internal fixation group was 3.78 ± 1.32 minutes. Conclusion: The localization membrane is a simple and practical device that can be customized and industrialized. In the future, we will innovate and transform it, so that it can be applied to other fields.

It is reported that parathyroid hormone 1 receptor (PTH1R) is crucial for intervertebral disc homeostasis maintenance. Annular tear was widely accepted as a common condition to destroy the immune privilege of the disk. To explore whether PTH1R is related to the pathogenesis of annular tear induced-intervertebral disc degeneration (IVDD) in this study, we analyzed the protein content of PTH1R in deteriorated people nucleus pulposus (NP) structure. Moreover, PTH1R activity andextracellular matrix (ECM) metabolism-related factors in the rat nucleus pulposus cells (NPCs) under oxidative stress conditions were evaluated by quantitative real-time polymerase chain reaction (RT-qPCR) in vitro. In addition, a rat IVDD model was constructed by a customized annulus needle puncture (ANP) device to evaluate IVDD grades in vivo. Immunohistochemical staining was used to detect the performance of type II collagen (Col II) and PTH1R. The results displayed that the expression of PTH1R declined in degenerated human NP tissue. The increased PTH1R activity were observed in rat NPCs with low concentration Tert-Butyl hydroperoxide (TBHP) treatment in vitro. In the rat IVDD model, the disc height had progressively narrowed and the disc structure was apparently disrupted in the ANP punctured discs. The protein expression of Col II and PTH1R was significantly down-regulated in ANP-punctured disc. This research demonstrated that our previous rat annulus needle puncture model could provide a reliable guide to the study of biologic processes in degenerating disks. Besides PTH1R has an inevitable connection with IVDD disease.