Editors-in-Chief

Shu-Min DUAN

Zhi-Hong LIU

ISSN 1673-1581

CN 33-1356/Q

Published by

Zhejiang University Press

2022 JIF 4.7

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  • Review

    Abstract：Inflammation is a key physiological process in the regeneration of bone tissue following injury. The acute inflammatory response, along with the timely resolution of inflammation, is essential for effective bone tissue repair. Exacerbation of either acute or chronic inflammation can lead to impaired bone regeneration, which is closely associated with interactions between immune cells and bone-related cells, as well as the regulatory roles of various inflammatory cytokines. In this review, we discuss the role of the immune microenvironment in bone regeneration and the negative impact of dysregulated inflammation on bone regeneration, and highlight on the need for timely elimination of inflammation. Additionally, the application of nanobiomaterials with immunomodulatory function in the treatment of inflammatory bone defects is discussed to clarify its current challenges and the future direction of its development.  

    Rong’an LI, Jiakang YANG, Wenjun DUAN, Kexin YANG, Katong LO, Qianming CHEN, Baixiang WANG

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  • Review

    Abstract：This review summarizes progress made in research on hydrogel wound dressings in promoting scarless skin healing. Wound healing is a complex biological process that involves four stages: hemostasis, inflammation, proliferation, and remodeling. Scar formation is a common issue during this process, especially pathological scars such as hypertrophic scars and keloids, which severely affect aesthetics and function. In recent years, hydrogel dressings have become a research hotspot for promoting scarless healing due to their unique physicochemical and biological properties. Hydrogels promote wound healing and reduce scar formation through multiple mechanisms, including providing a moist environment, antimicrobial activity, anti-inflammatory effects, promoting tissue regeneration, and regulating the wound microenvironment. This review details the concept and mechanisms of scarless healing and explores the application of hydrogel dressings loaded with anti-scarring drugs, stem cells, and extracellular vesicles (EVs) in scarless wound healing. Additionally, it summarizes progress in research on hydrogel dressings that regulate mechanical signals and innovative multifunctional hydrogel dressings, such as photo-responsive, organic biopolymer, and nanoparticle hydrogels. These hydrogel dressings show great potential for clinical application but still face challenges such as drug delivery efficiency, biocompatibility, and long-term safety. Future research needs to further optimize the composition and functionality of hydrogels and explore their potential applications in clinical settings.  

    Xian HU, Fawei XU, Minxia ZHANG, Yiqing CHEN, Jiaqin CAI, Jingjing MA, Weiqiang TAN, Qingqing FANG

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  • Research Article

    Abstract：Acute myocardial infarction (AMI) remains a major global health burden and is characterized by profound cardiac inflammation, apoptotic cell death, and impaired myocardial function. While interleukin-15 (IL-15) has been implicated in immune regulation, its precise role in the pathogenesis of AMI has not been clarified. Therefore, this study sought to delineate the functional role of IL-15 in the progression of AMI, with a particular focus on its influence on macrophage-driven inflammation, efferocytosis, and metabolic reprogramming. IL-15 levels were assessed in AMI patients and murine models. To evaluate the impact of IL-15 on cardiac inflammation, apoptosis, and functional outcomes following AMI, IL-15 and IL-15 receptor α (IL-15Rα) knockout (KO) mouse models were employed. Mechanistic studies were conducted to investigate IL-15-mediated effects on macrophage efferocytosis, polarization, and metabolic remodeling, with an emphasis on nuclear factor-κB (NF-κB) signaling and glycolytic flux. Elevated IL-15 levels were detected in both the plasma of AMI patients and the cardiac tissues of murine AMI models, correlating with increased disease severity. The genetic deletion of IL-15 or IL-15Rα significantly ameliorated cardiac injury by reducing inflammation and apoptosis while preserving myocardial function. Mechanistic analyses revealed that IL-15 impaired macrophage efferocytosis via Mer tyrosine kinase (MERTK) downregulation and promoted M1 polarization via NF-κB pathway activation. Furthermore, IL-15 reprogrammed macrophage metabolism by enhancing glycolytic activity. Ultimately, IL-15 restoration exacerbated cardiac ischemic injury following AMI, serving as a critical regulator of macrophage-mediated inflammation in AMI. These findings highlight the role of IL-15 as a potential therapeutic and prognostic target for mitigating cardiac inflammation and improving myocardial recovery in AMI.  

    Lei GUO, Zhehui YIN, Ning ZHANG, Han CHEN, Zhuo WANG, Yuxue HUANG, Jiniu HUANG, Yayu YOU, Chenyun ZHANG, Qinyi BAO, Shuxin LEI, Jun JIANG, Xiaojie XIE

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  • Research Article

    Abstract：Parkinson’s disease (PD) is a prevalent neurodegenerative disorder with limited therapeutic options and no cure, underscoring the urgent need for novel treatment strategies. Our previous work demonstrated that an engineered strain of Clostridium butyricum-pMTL007-glucagon-like peptide-1 (C. butyricum-pMTL007-GLP-1) alleviated PD symptoms by enhancing mitophagy, though the exact molecular mechanisms remained incompletely understood. In this study, we further investigated the neuroprotective effects and underlying mechanisms of this engineered strain using an A53T α-synuclein (α-syn) transgenic mouse model of PD. Specifically, we evaluated its impact on motor function, gut α-syn expression, intestinal barrier function, gut microbial composition, and neuropathological changes, with a focus on the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β) signaling pathway. Our findings revealed that C. butyricum-pMTL007-GLP-1 ameliorated motor deficits in PD mice by reducing intestinal α-syn accumulation, restoring gut barrier function, and modulating microbial diversity—notably increasing the relative abundance of Prevotella at the genus level. Furthermore, the engineered strain attenuated neuropathological alterations by decreasing phosphorylated α-syn (p-α-syn) in the substantia nigra while upregulating tyrosine hydroxylase (TH), dopamine-transporter (DAT), and glucagon-like peptide-1-receptor (GLP-1R) expression. These neuroprotective effects were associated with suppressed proinflammatory responses and enhanced anti-inflammatory and anti-apoptotic signaling, likely mediated through PI3K/AKT/GSK-3β pathway activation. In conclusions, C. butyricum-pMTL007-GLP-1 exerts significant neuroprotective effects in PD mice by reshaping gut microbiota composition and activating the PI3K/AKT/GSK-3β pathway. These findings provide further theoretical support for the potential application of probiotic-based therapies in PD treatment.  

    Xin FANG, Yun WANG, Zhenli LONG, Bin LIAO, Bo WANG, Daojun HONG, Jie LUO, Tingtao CHEN

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  • Research Article

    Abstract：ObjectiveNeuroinflammation may disrupt neurotransmitter signaling. This study investigated whether gut microbiota-induced neuroinflammation can regulate glutamate pathways in bipolar disorder (BD).MethodsFecal microbiota transplantation (FMT) was performed to observe behavioral changes in the antibiotic-treated C57BL/6J male mouse model of bipolar depression. Gut microbial structure, circulating, and prefrontal levels of inflammatory factors, microglial activation, and transcription levels of N-methyl-d-aspartate receptor (NMDAR) and α-amino-3-hydroxy-5-methyl-4 isoxazole receptor (AMPAR) genes were measured in the “BD” and control mice. Furthermore, the effects of interleukin-1 (IL-1) receptor antagonist (IL-1RA) on the glutamate pathways were assessed.ResultsCompared with the control mice, “BD” mice displayed depression-like behaviors, with a lower diversity of gut bacteria and a decreased abundance of certain species. In addition, “BD” mice showed increased levels of inflammatory factors (e.g., IL-1β) in the serum and prefrontal cortex, microglial activation, and changes in the messenger RNA (mRNA) levels of NMDAR and AMPAR. Treatment with IL-1RA partially reversed the behavioral patterns, neuroinflammation, and transcription levels of glutamate receptors.ConclusionsThe findings suggest that gut microbiota may influence glutamate receptor gene expression via an IL-1β-dependent pathway in a mouse model of BD, potentially contributing to neuroinflammatory mechanisms relevant to this disorder.  

    Anying TANG, Yi CHEN, Kaijing DING, Jinyu ZHANG, Le XU, Wenhao CHEN, Shaohua HU, Jianbo LAI

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  • Research Article

    Abstract：ObjectiveExcessive frictional heat generated at the drill–bone interface during implant osteotomy can compromise osseointegration and lead to implant failure. This study’s objective was to use a helical milling technique for dental implant osteotomy preparation to mitigate thermal damage to the bone.MethodsThis study introduces a novel helical milling technique designed to minimize thermal damage to bone during dental implant osteotomy preparations. Finite element simulations were conducted to compare the thermal distribution and cutting stress of a conventional twist drill and the newly designed helical drill. The experimental validation was performed ex vivo on animal bone using a robot-assisted osteotomy system.ResultsThe finite element simulations revealed that the helical drill produced a maximum cutting stress of 128.9 MPa, higher than the 121.0 MPa generated by the twist drill, indicating improved cutting efficiency. The ex vivo study demonstrated that the helical milling technique maintained the drilling site temperature below 38.7 ℃, which was significantly lower than the clinically critical threshold of 47 ℃ and the 61 ℃ recorded with the twist drill. Furthermore, the helical milling process facilitated efficient bone chip removal, reducing thermal buildup.ConclusionsThese findings suggest that the helical milling tool and technique optimize robot-assisted osteotomy and effectively mitigate frictional heat generation at the drill–bone interface. This innovation holds promise for enhancing osseointegration success rates in dental implant procedures, offering a clinically viable solution to a long-standing challenge in implantology.  

    Chaofan LI, Kangjie CHENG, Chenhao YU, Russell WANG, Fudong ZHU, Yunfeng LIU

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  • Correspondence

    Abstract：脂肪沉积是影响牛生长发育及肉产量和品质的重要因素。前期发现环状RNA circBDP1可促进牛脂肪细胞的增殖与分化。本研究通过鉴定circBDP1基因（rs454813519）上的A>G突变，采用Sanger测序与Kompetitive Allele-Specific PCR（KASP）技术，在秦川牛及山东黑牛遗传资源群体（Shandong Black Cattle Genetic Resource, SDBCGR）中检测到circBDP1-SNP位点的三种基因型（AA、AG和GG）。关联分析结果表明，该circBDP1-SNP A>G变异与SDBCGR母牛胸肌、上脑、牛肋排等性状和公牛胴体重、秦川牛体长等性状相关。为揭示该突变的相关功能，本研究构建了携带circBDP1-SNP不同等位基因的circBDP1-G/A过表达载体，并转染至牛前体脂肪细胞中。EdU检测、流式细胞术及qRT-PCR等实验结果显示，与circBDP1-G相比，circBDP1-A可显著增强前脂肪细胞的增殖与分化。此外，据已发表的全球牛基因组数据推测，G等位基因可能源自印度瘤牛。综上，circBDP1基因上的circBDP1-SNP A>G突变影响前脂肪细胞增殖与分化，可作为肉牛分子辅助选择的DNA标记。  

    Enhui JIANG, Chiyuan ZHANG, Zhuoyuan HE, Yuli ZHANG, Yuta YANG, Chuanying PAN, Fugui JIANG, Enliang SONG, Sihuan ZHANG, Xianyong LAN

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  • Correspondence

    Abstract：伪狂犬病是由伪狂犬病病毒（PRV）引起的一种严重危害全球养猪业的传染病，由于不同基因型毒株的致病性与流行特征存在差异，临床上需建立一种能够快速、准确区分PRV基因I型和基因II型的分型检测方法。本研究首次以gN基因为靶标，基于其保守区域鉴别稳定差异序列，成功建立了一种TaqMan三重实时荧光定量聚合酶链式反应（PCR）检测方法。该方法不仅可检测PRV感染，而且能有效区分其基因型。该检测方法具有特异性强、灵敏度高、重复性好及操作简便等优点。该检测体系仅需一对引物和三个探针即可完成分型鉴定，极大简化了反应体系，降低了引物错配及非特异性扩增的风险。对实验动物来源样本初步应用的结果显示，该方法能准确检测PRV的感染情况及其基因型。本研究为PRV的分子流行病学监测提供了实用、高效的技术工具，也为猪群中PRV的净化工作提供了有力支持。  

    Yulan JIN, Xuan JI, Weiren DONG, Yanming HUANG, Jiyong ZHOU, Jinyan GU

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