Depression is a pervasive mental disorder and a significant contributor to the global burden of disease,characterized by enduring sadness,loss of interest or pleasure,decreased energy or feelings of tiredness,feelings...
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Depression is a pervasive mental disorder and a significant contributor to the global burden of disease,characterized by enduring sadness,loss of interest or pleasure,decreased energy or feelings of tiredness,feelings of low self-worth,disturbed sleep or appetite,and poor *** studies of antidepressants,depression-specific psychotherapies and new somatic treatments have made clear advances,there were still no fully satisfactory treatments for *** imbalance and up-regulation of pro-inflammatory cytokines have been proposed to be associated with the pathogenesis of depression.A multi-protein complex of the innate immune system,the NLRP3 inflammasome regulates cleavage and secretion of pro-inflammatory cytokines interleukin-1βand *** can detect a bunch of pathogen-associated molecule patterns and damage-associated molecule patterns and lead to a series of immune-inflammatory *** explore the the role of inflammasome activation in depression and some of its underlying biological mechanisms,we established depression mouse model with lipopolysaccharide or unpredictable chronic mild ***-inflammatory cytokine interleukin-1βprotein significantly increased in serum and hippocampi in LPS or chronic stress induced depression ***,increased activation and expression of the NLRP3 inflammasome in hippocampi was also *** with the NLRP3 inflammasome inhibitor Ac-YVAD-CMK or Vx765significantly abrogated the depressive-like *** data suggest that the NLRP3 inflammasome is a central mediator between immune activation and *** critical role of early phase inflammatory mediators in the pathogenesis of depression,such as inflammasome,IL-1 and tumor-necrosis factor alpha(TNF-α),were ***,in our experiments,high mobility group box 1(HMGB1),a late phase inflammatory mediator which can be mediated by inflammasome and secreted actively by various immune cells in res
Aims:Reversible adrenal insufficiency has frequently been diagnosed in critically ill patients with sepsis,however the mechanisms underlying down-regulation of GCs production during sepsis remain largely *** play a ce...
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Aims:Reversible adrenal insufficiency has frequently been diagnosed in critically ill patients with sepsis,however the mechanisms underlying down-regulation of GCs production during sepsis remain largely *** play a central role in adrenocortical ***,hydrogen sulfide(H2S),a gaseous transmitter endogenously produced by cystathionine-β-synthase(CBS)andcystathionine-γ-lyase(CSE),has been found to improve mitochondrial *** present study aimed at examining whether CBS and CSE are expressed in adrenal glands,and investigated the role of these enzymes in the maintenance of mitochondrial function and the production of glucocorticoids in adrenocortical ***:Both CBS and CSE are present in murine adrenocortical cells and account for H2S generation in adrenal *** a combination of both in vivo and in vitro approaches,we demonstrated that either CBS/CSE inhibitors or small interfering RNAs led to mitochondrial oxidative stress and dysfunction,which meanwhile resulted in blunted corticosterone responses to adrenocorticotropic hormone(ACTH).These effects were significantly attenuated by the treatment of H2S donor ***(LPS)also caused mitochondrial damage,thereby resulting in adrenal *** mitochondrial superoxide dismutase 2 mimetic Mn TBAP and mitochondrial superoxide scavenger mito-TEMPO which were used to block mitochondria superoxide production could reverse LPS-induced mitochondrial oxidative stress and dysfunction and prevented LPS-induced corticosterone hyporesponsiveness to ***,LPS inhibited CBS/CSE expression and H2S production in adrenal glands and primary adrenocortical cells,while H2S donor GYY4137 protected against LPS-induced mitochondrial damage and hyporesponsiveness to ***:Endogenous H2S is critical for maintaining mitochondrial function and glucocorticoid production in adrenal *** inhibit the expression of H2S-forming enzyme and product
电磁辐射尤其是高功率微波(high power microwave,HPM)是现代信息化战争及HPM武器使用条件下的主要环境作用与致伤因素,而无论平战时,皮肤软组织创伤都是最常见的伤类,研究探讨此条件下创面修复的变化规律及机制具有重要的理论和实践意...
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电磁辐射尤其是高功率微波(high power microwave,HPM)是现代信息化战争及HPM武器使用条件下的主要环境作用与致伤因素,而无论平战时,皮肤软组织创伤都是最常见的伤类,研究探讨此条件下创面修复的变化规律及机制具有重要的理论和实践意义.在观察研究不同功率HPM辐射对在体创面愈合作用存在不同效应:30W/cm2辐射可促进创伤愈合，而90W/cm2及120W/cm2辐射则可延缓创伤愈合的基础上，进一步研究不同效应的HPM辐射对成纤维细胞、血管内皮细胞两种主要修复细胞增殖、迁移、细胞周期及凋亡的影响，以探讨HPM对创面愈合影响的作用及机制。研究表明，30W/cm2辐照对C3H10T1/2细胞早期有促进增殖、迁移及加速进入增殖期作用，但对VE细胞则无明显作用;90W/cm2辐照则明显引起两种细胞G1期阻滞，抑制细胞的增殖、迁移并增加细胞的凋亡率，提示90W/cm2辐射对创面修复细胞具有明显的抑制及损伤作用，表明30W/cm2和90W/cm2HPM辐射对主要修复细胞具有不同的作用，进一步揭示在体研究中它们促进及抑制创面修复效应的发生机制。
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