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Bi A.-L.,Shandong University | Bi A.-L.,Shandong University of Traditional Chinese Medicine | Wang Y.,Shandong University | Zhang S.,Shandong University | And 6 more authors.
Brain Structure and Function | Year: 2013

Similar to memory formation, memory extinction is also a new learning process that requires synaptic plasticity. Actin rearrangement is fundamental for synaptic plasticity, however, whether actin rearrangement in the infralimbic cortex (IL) plays a role in memory extinction, as well as the mechanisms underlying it, remains unclear. Here, using a conditioned taste aversion (CTA) paradigm, we demonstrated increased synaptic density and actin rearrangement in the IL during the extinction of CTA. Targeted infusion of an actin rearrangement inhibitor, cytochalasin D, into the IL impaired memory extinction and de novo synapse formation. Notably, we also found increased myosin II phosphorylation in the IL during the extinction of CTA. Microinfusion of a specific inhibitor of the myosin II ATPase, blebbistatin (Blebb), into the IL impaired memory extinction as well as the related actin rearrangement and changes in synaptic density. Moreover, the extinction deficit and the reduction of synaptic density induced by Blebb could be rescued by the actin polymerization stabilizer jasplakinolide (Jasp), suggesting that myosin II acts via actin filament polymerization to stabilize synaptic plasticity during the extinction of CTA. Taken together, we conclude that myosin II may regulate the plasticity of actin-related synaptic structure during memory extinction. Our studies provide a molecular mechanism for understanding the plasticity of actin rearrangement-associated synaptic structure during memory extinction. © 2013 Springer-Verlag Berlin Heidelberg. Source

Zhang Z.,Shandong University | Zhang Z.,Shandong Institute of Otolaryngology | Shi L.,Shandong University | Pang W.,Fudan University | And 8 more authors.
PLoS ONE | Year: 2016

Background: Recently, academic studies suggest that global growth of airway allergic disease has a close association with dietary changes including reduced consumption of fiber. Therefore, appropriate dietary fiber supplementation might be potential to prevent airway allergic disease (AAD). Objective: We investigated whether dietary fiber intake suppressed the induction of AAD and tried to elucidate the possible underlying mechanisms. Methods: The control mice and AAD model mice fed with 4% standard-fiber chow, while low-fiber group of mice fed with a 1.75%low-fiber chow. The two fiber-intervened groups including mice, apart froma standard-fiber diet, were also intragastric (i.g.) administrated daily with poorly fermentable cellulose or readily fermentable pectin (0.4% of daily body weight), respectively. All animals except normal mice were sensitized and challenged with ovalbumin (OVA) to induce airway allergic inflammation. Hallmarks of AAD were examined by histological analysis and ELISA. The variation in intestinal bacterial composition was assessed by qualitative analysis of 16S ribosomal DNA (rDNA) content in fecal samples using real-time PCR. Results: Low-fiber diet aggravated inflammatory response in ovalbumin-induced allergic mice, whereas dietary fiber intake significantly suppressed the allergic responses, attenuated allergic symptoms of nasal rubbing and sneezing, decreased the pathology of eosinophil infiltration and goblet cell metaplasia in the nasal mucosa and lung, inhibited serum OVAspecific IgE levels, and lowered the levels of Th2 cytokines in NALF and BALF, but, increased Th1 (IFN-γ) cytokines. Additionally, dietary fiber intake also increased the proportion of Bacteroidetes and Actinobacteria, and decreased Firmicutes and Proteobacteria. Levels of probiotic bacteria, such as Lactobacillus and Bifidobacterium, were upgraded significantly. Conclusion: Long-term deficiency of dietary fiber intake increases the susceptibility to AAD, whereas proper fiber supplementation promotes effectively the balance of Th1/Th2 immunity and then attenuates allergic inflammatory responses significantly, as well as optimizes the structure of intestinal microbiota, which suggests potential for novel preventive and therapeutic intervention. © 2016 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Source

Yan W.,Shandong University | Yan W.,Shandong Institute of Otolaryngology | Li J.,Shandong University | Li J.,Shandong Institute of Otolaryngology | And 11 more authors.
PLoS ONE | Year: 2014

Objectives: In this study, using an Streptococcus pneumoniae-induced tympanosclerosis (TS) model, we explored the effects of captopril and losartan in the treatment of TS and the possible mechanisms. Study Design: A prospective experimental animal study. Methods: We set up the TS models in both guinea pig and wistar rat by inoculation of type-3 Streptococcus pneumoniae microorganisms and then treated the animals with the combining use of captopril and losartan. Otomicroscopy was employed to observe the development of TS. Auditory brainstem response was used to test the hearing function of animals. Hematoxylin-eosin and von Kossa staining were performed to determine the morphological changes and calcium depositions. The protein expressions of transforming growth factor β1 (TGF-β1) were assessed by western blot and immunohistochemistry staining, and the mRNA level of TGF-β1 was measured by quantitative reverse transcription-polymerase chain reaction. Results: The combining use of captopril and losartan attenuated TS responses in terms of a decrease in the TS incidence and the ABR threshold, a reduction of hyalinization and calcification in the middle ear mucosa and the thickness of the mucosa. In addition, the TGF-β1 expression was decreased at both protein and mRNA levels. Conclusion: Our data indicate, for the first time, that the combining use of captopril and losartan obviously attenuates TS progress through inhibiting the overexpressing of TGF-β1. © 2014 Yan et al. Source

Li L.,Shandong University | Li L.,Shandong Institute of Otolaryngology | Li L.,Shandong Provincial Key Laboratory of Otology | Guo X.,Shandong University | And 21 more authors.
Otolaryngology - Head and Neck Surgery (United States) | Year: 2015

Objective The objective of this study was to investigate the expression and role of surfactant protein (SP) in the middle ear throughout lipopolysaccharide (LPS)-induced otitis media with effusion (OME). Study Design Randomized case-controlled animal model. Setting Shandong University, Jinan, China. Subjects and Methods SP expression was monitored using reverse transcription polymerase chain reaction (PCR) in normal mice (n = 5). Two groups, control phosphate-buffered saline-injected mice (n = 5) and LPS-injected mice (n = 5), were euthanized 5 days following injection. RNA was extracted for reverse transcription PCR and real-time PCR, and temporal bone samples were used for hematoxylin and eosin staining. LPS was injected into mice, and 5 mice per test were euthanized at 0, 12, 24, 48, 72, and 96 hours following injection. For mRNA expression quantification, reverse transcription PCR and real-time PCR were performed, and proinflammatory cytokine levels were measured by enzyme-linked immunosorbent assay. Results SP-A and SP-D expression was detected in normal murine Eustachian tubes. SP-A expression was up-regulated after LPS-induced OME (P =.01). At various time points after LPS injection, concentrations of proinflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin (IL)-1β, and IL-6) in the middle ear increased significantly (P <.05) and correlated with changes in SP-A expression. Conclusion SP-A and SP-D exist in the murine middle ear. The expression of SP-A and TNF-α, IL-1β, and IL-6 was up-regulated in the middle ear of the LPS-induced OME animal model. © Official journal of the American Academy of Otolaryngology-Head and Neck Surgery Foundation 2015. Source

Chao X.,Shandong University | Chao X.,Shandong Institute of Otolaryngology | Xu L.,Shandong University | Xu L.,Shandong Institute of Otolaryngology | And 11 more authors.
Acta Oto-Laryngologica | Year: 2016

Conclusion: C/GP hydrogel was demonstrated to be an ideal drug delivery vehicle and scaffold in the vein conduit. Combined use autologous vein and NGF continuously delivered by C/GP-NGF hydrogel can improve the recovery of facial nerve defects. Objective: This study investigated the effects of chitosan-β-glycerophosphate-nerve growth factor (C/GP-NGF) hydrogel combined with autologous vein conduit on the recovery of damaged facial nerve in a rat model. Methods: A 5 mm gap in the buccal branch of a rat facial nerve was reconstructed with an autologous vein. Next, C/GP-NGF hydrogel was injected into the vein conduit. In negative control groups, NGF solution or phosphate-buffered saline (PBS) was injected into the vein conduits, respectively. Autologous implantation was used as a positive control group. Vibrissae movement, electrophysiological assessment, and morphological analysis of regenerated nerves were performed to assess nerve regeneration. Results: NGF continuously released from C/GP-NGF hydrogel in vitro. The recovery rate of vibrissae movement and the compound muscle action potentials of regenerated facial nerve in the C/GP-NGF group were similar to those in the Auto group, and significantly better than those in the NGF group. Furthermore, larger regenerated axons and thicker myelin sheaths were obtained in the C/GP-NGF group than those in the NGF group. © 2016 Taylor & Francis. Source

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