Cholic acid mitigates osteoarthritis by inhibiting the NF-κB/PERK/ SIRT1 signaling pathway

Introduction:Cholic acid(CA)is a natural steroid useful in treating chronic bronchitis and cholecystitis.On the other hand,its potential impact on osteoarthritis(OA)is unknown.Objective:Using an in vitro and in vivo osteoarthritis model,we sought to assess the chondroprotective properties of CA.Methods:We employed the Cell Counting Kit-8 to measure the impact of CA on chondrocyte activity to assess the toxicity of the cells.Multiple molecular biology experimental techniques were used to investigate potential signaling pathways that CA may use to prevent inflammation and give chondrocytes protection.Furthermore,how CA affects the OA model in Sprague-Dawley(SD)rats was evaluated.Results:CA significantly suppressed the up-regulation of the interleukin-1β(IL-1β),cyclooxygenase-2(COX-2),and matrix metalloproteinase 13(MMP-13)and the downregulation of aggrecan and type II collagen A1(COL2A)in chondrocytes treated tumor necrosis factor-alpha(TNF-α).Differentially expressed genes(DEG)enrichment revealed IL-17,TNF,chemokine,cytokine-cytokine receptor,toll-like receptor,and nucleotide oligomerization domain-like receptor were the primary signaling pathways.The enriched DEGs included CXCL6,CCL20,MMP3,CXCL3,CXCL11,CCL5,CXCL10,MMP9,MMP13,and CXCL2;these DEGs are involved in inflammatory responses and their expression induced by TNF-αwas reversed by CA treatment.CA inhibits p65 nuclear translocation and inhibitory subunit kappa B alpha(IκBα)phosphorylation induced by TNF-α.Furthermore,CA attenuated protein expression of protein kinase RNA-like endoplasmic reticulum kinase(PERK),inositol-requiring transmembrane kinase/endoribonuclease 1α(IRE1α),glucose regulatory protein 78(GRP78),and sirtuin 1(SIRT1),and down-regulation of phosphorylation of AMP-activated protein kinase-α(p-AMPKα)in TNF-α-treated chondrocytes.Conclusions:CA significantly ameliorated cartilage degradation in the OA rat model.CA alleviated the inflammatory response through the nuclear factor kappa B/PERK/SIRT1 axis and ameliorated cartilage degradation.

绿色人力资源管理与绿色组织绩效:理论机制与未来研究方向

绿色发展是高质量发展的核心组成部分,人作为第一资源是推动企业绿色转型最为活跃的因素。因此,绿色人力资源管理对绿色组织绩效的作用成为近期热点研究领域。近年来,尽管两者关系的研究逐步增多,但尚无系统性文献综述聚焦其间机制。这不利于系统、深入地思考和澄清为何,乃至是否绿色人力资源管理对绿色组织绩效至关重要的问题。本文通过系统回顾文献,从行为论、资源与能力、社会心理视角归纳了现有理论机制的三大脉络。总体而言,现有研究要么假定绿色人力资源管理能提升个体的绿色动机、态度或知识能力,进而转化为组织层面的绩效;要么依赖绿色文化、绿色创新、绿色领导等组织层面的中介变量进行“从宏观到宏观”的解释。基于此,本文认为,在新质生产力发展背景下,未来研究应以可续管理原理为核心驱动力,深化对绿色人力资源管理如何驱动特定的集体互动行为,以及由此带来的绿色实践积累、绿色增长临界点的形成,以及组织绿色涌现状态的显现,最终形成宏观结果的过程性、动态性和复杂性的理论认知。文章最后讨论了相关研究对绿色人力资源管理实践的启示。

员工知识求取:概念、测量、前因与后效

在以创新驱动为核心的知识经济时代,激励员工间开展广泛、高效的知识交流活动,促进知识资源整合,发挥知识协同作用和价值,成为当前组织知识管理实践的关键问题。具有前瞻性特征的知识求取是员工知识交流互动过程中知识需求方行为的重要研究议题之一。知识求取是指个体有意获取他人专业经验、见解和意见等知识成果的行为。基于文献梳理,首先阐明了员工知识求取的起源,并对与其相近的若干概念进行了辨析。其次,从知识来源、知识性质、求取目的与求取方式等视角总结了员工知识求取的主要测量工具。接着,从个体、人际、团队与组织等层面梳理了员工知识求取的影响因素和作用结果。最后,本文对员工知识求取的未来研究方向提出了展望,以期能够完善国内知识需求方行为研究理论“版图”,启发知识拥有方行为理论研究。