ENZYME AND MICROBIAL TECHNOLOGY
·
2022
·
IF 3.705
Lei Wang,Kecai Chen,Peng Zheng,Xiang Huo,Fei Liao,Liping Zhu,Meirong Hu,Yong Tao
D -Psicose, a new-generation sugar substitute, has been enzymatically synthesized through D -fructose isomerization. However, isomerization often causes low yields due to unfavorable thermodynamic equilibria, which limited its further industrial application. In this study, we present a redox-driven multi-enzyme cascade, two-step biotransformation system to produce D -psicose from D -fructose. Compared to D -fructose isomerization, this method has a maximized theoretical conversion rate of 100%. D -Psicose-3-epimerase from Clostridiales (CBDPE), ribitol 2-dehydrogenase from Providencia alcalifaciens (PRDH), and formate dehydrogenase from Starkeya (SFDH) were co-expressed in Escherichia coli in the first step to produce D -allitol from D -fructose. Afterward, NADH oxidase from Streptococcus pyogenes (SPNOX), and ribitol 2-dehydrogenase from Rubrivivax sp. (RSRDH) were co-expressed in E. coli to oxidize D -allitol into D -psicose in the second step. The two-step biotransformation system was optimized to maximize the D -fructose-to- D -psicose conversion rate (up to 90%), corresponding to a concentration of 450 mM. This study suggests that this redox-driven multi-enzyme cascade strategy through a sugar-to-alcohol-to-sugar pathway has the advantage of great application for enhanced production of D -psicose and other rare sugars.
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PubMed
高影响因子
Neural Regeneration Research
·
2025
·Vol. 21
·期 6
·2658
·
IF 6.7
Chen Xiaokun,Xu Jihai,Yang Ziyuan,Zhou Jiahua,Qin Feng,Li Xueyuan,Yu Miao,Wang Yanhua,Li Ming,Wang Xin
Peripheral nerve injury is a complex condition presenting significant clinical treatment challenges due to the limited regenerative capacity of peripheral nerves. Nerve conduits have been seen as a promising strategy to overcome the shortage of other treatment options (e.g., nerve graft). However, nerve regeneration occurs within a complex environment, and elaborate modulation is needed to meet repair requirements. The aim of this study was to investigate and explore a multifunctional nerve conduit with reactive oxygen species clearing, immune modulation to reshape the regenerative environment, and topographic cues and electrical signals to guide nerve growth. We developed an electroactive nerve guidance conduit composed of polylactic-glycolic acid and carbon nanotubes with an oriented structure using electrospinning and modified it with mussel-inspired polydopamine combining neurotrophin-3. The resulting nerve scaffold exhibited favorable orientation, electrical conductivity, and mechanical properties. Continuous release of neurotrophin-3 from the nerve conduit supported nerve regeneration throughout the repair process. In vitro assessments confirmed the cytocompatibility, reactive oxygen species scavenging, and immune regulation capabilities of the nerve scaffolds. In a rat sciatic nerve defect model, the nerve scaffolds effectively prevented muscle atrophy and promoted nerve regeneration and functional recovery over a 12-week period. These findings suggest that polydopamine-modified, electroactive, oriented nerve guidance conduits with multiple bioactive functions hold great promise for the repair of peripheral nerve injuries.
研究领域:
生物医学工程
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神经组织工程
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再生医学
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生物材料
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神经科学
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PubMed
高影响因子
Neural Regeneration Research
·
2026
·
IF 8.5
Zhou Yiyang,Chen Zihao,Chen Keyang,Xiong Fen,Gao Hongchang
Post-stroke cognitive impairment is a severe sequela of cerebral ischemia, with its underlying mechanisms remaining elusive and specific diagnostic biomarkers currently lacking. Growing evidence suggests that secondary neurodegeneration is closely associated with post-stroke cognitive impairment, although its metabolic basis has not been fully elucidated. Therefore, this study aimed to investigate the spatiotemporal changes and metabolic characteristics of secondary neurodegeneration and cognitive function after cortical stroke. We established a photothrombotic mouse model for post-stroke cognitive impairment research and conducted longitudinal assessments with final endpoints at 14, 32, and 84 days postsurgery. Voxel-based morphometry analysis of whole-brain regions using magnetic resonance imaging revealed that only the hippocampus exhibited gray matter alterations consistent with secondary neurodegeneration pathology. Morris water maze and open field tests demonstrated persistent impairments in recent and remote memory, along with anxietylike behaviors in photothrombotic mice. Untargeted metabolomic and lipidomic analyses were established to comprehensively characterize secondary neurodegeneration-related metabolic disturbances in the hippocampus, highlighting pathophysiological mechanisms involving oxidative stress, lipid peroxidation, neurotransmitter dysregulation, and disrupted energy metabolism. These important mechanisms were verified by immunohistochemistry, immunofluorescence staining, and real-time polymerase chain reaction. The screened potential biomarker, N -acetylneuraminic acid, was validated via targeted metabolomics in both photothrombotic mouse serum and 148 clinical samples, showing significant elevation in both cohorts. Receiver operating characteristic curve analysis and decision curve analysis confirmed the clinical utility of N -acetylneuraminic acid in diagnosing post-stroke cognitive impairment (area under the curve = 0.951, 95% confidence interval: 0.903–0.980). Flow cytometry and immunofluorescence staining revealed that N -acetylneuraminic acid activates microglia-driven neuroinflammation and oxidative stress. Our findings elucidate a potential pathological mechanism of post-stroke cognitive impairment: cortical stroke induces hippocampal accumulation of N -acetylneuraminic acid, which promotes microglial oxidative stress and inflammation, thereby triggering hippocampal secondary neurodegeneration and leading to persistent cognitive deficits. Importantly, N -acetylneuraminic acid serves as a dual-functional biomarker capable of predicting post-stroke cognitive impairment progression while dynamically tracking secondary neurodegeneration.
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PubMed
高影响因子
WEED SCIENCE
·
2017
·Vol. 64
·期 4
·634-641
·
IF 1.862
Hongchun Wang,Bing Zhang,Liyao Dong,Yuanlai Lou
The influence of temperature, light, solution pH, water stress, salt stress, and burial depth on seed germination and seedling emergence of catchweed bedstraw and the sensitivity of that weed to commonly available herbicides in China were studied in laboratory and greenhouse. Germination occurred at day/night temperatures from 5/0 C to 30/25 C, with optimum germination at 15/10 C. Catchweed bedstraw germinated equally well under a 12-h photoperiod and continuous darkness; however, a 24-h photoperiod inhibited seed germination. Catchweed bedstraw seed is moderately sensitive to osmotic potential and salt stress, with 15 and 3% germination rates at an osmotic potential of −0.5 Mpa and salinity level of 120 mM, respectively. Maximum seed germination was observed in near neutral pH; germination was greater than 80% over a broad pH range from 5 to 8. Seedling emergence of the seeds buried at a depth of 1 cm was higher (74%) than those placed on the soil surface (20%), but declined with burial depth increasing. Few (10%) seedlings emerged when seeds were placed at a depth of 5 cm. Bensulfuron-methyl, and ethametsulfuron-methyl applied PRE and tribenuron-methyl, fluroxypyr, and florasulam applied POST can be used to provide greater than 80% control of catchweed bedstraw. The results of this study have contributed to more complete understanding of the germination and emergence of catchweed bedstraw.
研究领域:
植物学
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杂草科学
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生态生理学
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农业生态学
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高影响因子
Journal of Physiological Investigation
·
2024
·Vol. 67
·期 2
·69
·
IF 0
Wang Chunli,Xu Mingzhi,Bai Yafei,Pan Mingjiao,Qi Yonghui,Chen Ruman
Vascular calcification (VC), a major complication in chronic kidney disease (CKD), is predominantly driven by osteoblastic differentiation. Recent studies have highlighted the crucial role of microRNAs in CKD’s pathogenesis. Here, our research focused on the effects of miR-204-5p and its molecular mechanisms within VC. We initially found a notable decrease in miR-204-5p levels in human aortic vascular smooth muscle cells stimulated with inorganic phosphate, using this as a VC model in vitro. Following the overexpression of miR-204-5p, a decrease in VC was observed, as indicated by alizarin red S staining and measurements of calcium content. This decrease was accompanied by lower levels of the osteogenic marker, runt-related transcription factor 2, and higher levels of α-smooth muscle actin, a marker of contractility. Further investigation showed that calcium/calmodulin-dependent protein kinase 1 (CAMK1), which is a predicted target of miR-204-5p, promotes VC. Conversely, overexpressing miR-204-5p reduced VC by suppressing CAMK1 activity. Overexpressing miR-204-5p also effectively mitigated aortic calcification in an in vivo rat model. In summary, our research indicated that targeting the miR-204-5p/CAMK1 pathway could be a viable strategy for mitigating VC in CKD patients.
研究领域:
分子生物学
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病理学
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心血管科学
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遗传学
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DOI
AVIAN DISEASES
·
2025
·
IF 1.3
Du Xiaowen,Zeng Mengting,Yang Wenzhuo,Jiang Yuting,Huang Guangyu,Ding Shiping,Jiang Danli,Yuan Zhaoxia
For decades, infectious bronchitis (IB), caused by the infectious bronchitis virus (IBV), has posed a significant threat to poultry health and is mainly controlled by vaccines. However, the currently available commercial vaccines do not provide adequate protection against new IBV strains that emerge due to ongoing evolution. Therefore, new antiviral strategies need to be explored. Cepharanthine (CEP), tetrandrine (TET), and berbamine hydrochloride (BBM) are natural plant-derived bis-benzylisoquinoline alkaloids (BBAs) with proven antiviral activities against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), porcine epidemic diarrhea virus (PEDV), and other viruses. Despite this, their potential antiviral activities against IBV remain unknown. As a proof-of-concept study, we aimed to investigate the inhibitory effects of CEP, TET, and BBM on the laboratory-adapted IBV Beaudette strain in Vero cells and of CEP in chicken embryos. Our research demonstrated that CEP, TET, and BBM effectively suppressed IBV infection in Vero cells, with CEP showing a particularly high selective index of 309.6. These compounds dose-dependently decreased IBV RNA levels and N protein expression and lowered intracellular and extracellular viral titers. Notably, CEP also exhibited antiviral activity against IBV infection in chicken embryos, resulting in reduced mortality and fewer lesions. While these findings highlight the potential of CEP, TET, and BBM as candidates for further development, further studies are required to evaluate their efficacy against field-prevalent IBV strains (e.g., Massachusetts, QX-like) and clarify the specific antiviral mechanisms.
研究领域:
病毒学
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药物开发
·
兽医学
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DOI
PubMed
高影响因子
Neural Regeneration Research
·
2026
·
IF 8.5
Cao Kai,Xie Jun,Liang Xiaohan,Li Yanqing,Gong Hui,Luo Haiming
Hyperphosphorylation of tau is a key pathological hallmark of Alzheimer's disease and is closely associated with cognitive impairment. Passive immunotherapy targeting hyperphosphorylated tau is a promising approach to inhibit tau pathology. However, the blood-brain barrier restricts antibodies from reaching the central nervous system and exerting their therapeutic effects. Here, we developed an intranasal biomacromolecule delivery strategy for the treatment of Alzheimer's disease using dendritic mesoporous silica nanoparticles modified with hyaluronic acid as a drug carrier. Ten-month-old C57BL/6J mice, htau mice, and 5×FAD mice were intranasally administered 100 μg of hyaluronic acid-dendritic mesoporous silica nanoparticles@4B1 (antibody dose), and brain tissues were collected to evaluate antibody delivery efficiency. Using this delivery system, the anti-p-tau 396,404 antibody 4B1 was efficiently delivered to the brains of 5×FAD mice, with an enrichment of 7.31% ± 0.18% ID/g. Entry of the 4B1 antibody into the brain ameliorated tauopathy in Alzheimer's disease model mice, reduced neuronal loss and neuroinflammation caused by tau pathology, and reversed cognitive dysfunction. These findings suggest that the nasal delivery strategy based on hyaluronic acid-responsive release is an effective method for delivering antibody biomacromolecules to the central nervous system, showing high efficiency of antibody entry into brain tissue and intracellular delivery. Our findings also demonstrate the role of p-tau 396,404 in passive immunotherapy for Alzheimer's disease, suggesting that immunotherapy targeting p-tau 396,404 is a promising strategy for ameliorating Alzheimer's disease pathology, inhibiting the aggregation of hyperphosphorylated tau, and alleviating neurological damage and cognitive dysfunction.
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高影响因子
Neural Regeneration Research
·
2025
·Vol. 21
·期 7
·3122
·
IF 6.7
Liang Yu,Xi Deshuang,Teng Yilin,Liu Pan,Feng Yanbing,Huang Qiumei,Gao Ming,Zong Shaohui
Export Rat nerve growth factor and total flavonoids from hawthorn leaf contribute to the recovery of neurological function after spinal cord injury, including traumatic, non-traumatic spinal cord injuries. However, it remains challenging to efficiently deliver nerve growth factor and total flavonoids from hawthorn leaf to spinal cord injury sites, ensure their sustained release, and minimize further damage. In the present study, we chose a biocompatible and biodegradable gelatin as the substrate, which was crosslinked with the natural biological crosslinker genipin to form a gelatin–genipin hydrogel carrier for the slow release of nerve growth factor and total flavonoids from hawthorn leaf in spinal cord injury sites. The prepared gelatin–genipin hydrogel had good injectable properties and photothermal effects. Furthermore, when the hydrogel with 2% genipin, 200 ng/mL nerve growth factor, and 320 μg/mL total flavonoids from hawthorn leaf was combined with near infrared irradiation, there was a slow release of total flavonoids from hawthorn leaf and nerve growth factor, reduced oxidative stress, an improved inflammatory microenvironment, and accelerated angiogenesis and axonal regeneration via inhibition of the nuclear factor kappa-B signaling pathway, thereby promoting recovery from spinal cord injury. Collectively, our results indicate that this new hydrogel may improve the prognosis of spinal cord injury, and may represent a new strategy for treating spinal cord injury.
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高影响因子
Neural Regeneration Research
·
2025
·
IF 6.7
Ma Yangguang,Liu Yi,Pan Dongsheng,Zhang Jiawei,Liang Zhuowen,Wang Yi,Hu Xueyu,Wang Zhe,Ding Tan
The blood–spinal cord barrier is crucial for preserving homeostasis of the central nervous system. After spinal cord injury, autophagic flux within endothelial cells is disrupted, compromising the integrity of the blood–spinal cord barrier. This disruption facilitates extensive infiltration of inflammatory cells, resulting in exacerbated neuroinflammatory responses, neuronal death, and impaired neuronal regeneration. Previous research has demonstrated that photobiomodulation promotes the regeneration of damaged nerves following spinal cord injury by inhibiting the recruitment of inflammatory cells to the injured site and restoring neuronal mitochondrial function. However, the precise mechanisms by which photobiomodulation regulates neuroinflammation remain incompletely elucidated. In this study, we established a mouse model of spinal cord injury and assessed the effects of photobiomodulation treatment. Photobiomodulation effectively cleared damaged mitochondria from endothelial cells in mice, promoting recovery of hindlimb motor function. Using microvascular endothelial bEnd.3 cells subjected to oxygen–glucose deprivation, we found that the effects of photobiomodulation were mediated through activation of the PINK1/Parkin pathway. Additionally, photobiomodulation reduced mitochondrial oxidative stress levels and increased the expression of tight junction proteins within the blood–spinal cord barrier. Our findings suggest that photobiomodulation activates mitochondrial autophagy in endothelial cells through the PINK1/Parkin pathway, thereby promoting repair of the blood–spinal cord barrier following spinal cord injury.
研究领域:
神经科学
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再生医学
·
细胞生物学
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PubMed
高影响因子
Neural Regeneration Research
·
2024
·Vol. 19
·期 12
·2708
·
IF 5.9
Fang He,Li Mengjie,Yang Jingchen,Ma Shunping,Zhang Li,Yang Hongqi,Tang Qiongyan,Cao Jing,Yang Weimin
Thalamic hemorrhage can lead to the development of central post-stroke pain. Changes in histone acetylation levels, which are regulated by histone deacetylases, affect the excitability of neurons surrounding the hemorrhagic area. However, the regulatory mechanism of histone deacetylases in central post-stroke pain remains unclear. Here, we show that iron overload leads to an increase in histone deacetylase 2 expression in damaged ventral posterolateral nucleus neurons. Inhibiting this increase restored histone H3 acetylation in the Kcna2 promoter region of the voltage-dependent potassium (Kv) channel subunit gene in a rat model of central post-stroke pain, thereby increasing Kcna2 expression and relieving central pain. However, in the absence of nerve injury, increasing histone deacetylase 2 expression decreased Kcna2 expression, decreased Kv current, increased the excitability of neurons in the ventral posterolateral nucleus area, and led to neuropathic pain symptoms. Moreover, treatment with the iron chelator deferiprone effectively reduced iron overload in the ventral posterolateral nucleus after intracerebral hemorrhage, reversed histone deacetylase 2 upregulation and Kv1.2 downregulation, and alleviated mechanical hypersensitivity in central post-stroke pain rats. These results suggest that histone deacetylase 2 upregulation and Kv1.2 downregulation, mediated by iron overload, are important factors in central post-stroke pain pathogenesis and could serve as new targets for central post-stroke pain treatment.
研究领域:
神经科学
·
药理学
·
分子生物学
·
神经病学
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PubMed
高影响因子
Neural Regeneration Research
·
2024
·
IF 5.9
Li Tong,Xing Hui-Min,Qian Hai-Dong,Gao Qiao,Xu Sheng-Lan,Ma Hua,Chi Zai-Long
Several studies have found that transplantation of neural progenitor cells (NPCs) promotes the survival of injured neurons. However, a poor integration rate and high risk of tumorigenicity after cell transplantation limits their clinical application. Small extracellular vesicles (sEVs) contain bioactive molecules for neuronal protection and regeneration. Previous studies have shown that stem/progenitor cell-derived sEVs can promote neuronal survival and recovery of neurological function in neurodegenerative eye diseases and other eye diseases. In this study, we intravitreally transplanted sEVs derived from human induced pluripotent stem cells (hiPSCs) and hiPSCs-differentiated NPCs (hiPSC-NPC) in a mouse model of optic nerve crush. Our results show that these intravitreally injected sEVs were ingested by retinal cells, especially those localized in the ganglion cell layer. Treatment with hiPSC-NPC derived sEVs mitigated optic nerve crush-induced retinal ganglion cell degeneration, and regulated the retinal microenvironment by inhibiting excessive activation of microglia. Component analysis further revealed that hiPSC-NPC derived sEVs transported neuroprotective and anti-inflammatory miRNA cargos to target cells, which had protective effects on RGCs after optic nerve injury. These findings suggest that sEVs derived from hiPSC-NPC are a promising cell-free therapeutic strategy for optic neuropathy.
研究领域:
神经科学
·
干细胞生物学
·
眼科学
·
分子生物学
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DOI
PubMed
高影响因子
AVIAN DISEASES
·
2024
·
IF 1.3
Pang Xiaoyue,Qiu Wenyue,Zhang Xinting,Huang Jianjia,Zhou Shuilian,Wang Rongmei,Tang Zhaoxin,Su Rongsheng
Acute myocardial injury (AMI) induced by lipopolysaccharide (LPS) can cause cardiovascular dysfunction and lead to death in poultry. Traditional antibiotic therapy has been found to have many limitations and negative effects. Asiatic acid (AA) is a naturally occurring pentacyclic triterpenoid that is extracted from Centella asiatica and has anti-inflammatory, antioxidant, and anticancer pharmacological properties. Previously, we studied the effect of AA on LPS-induced liver and kidney injury; however, the impact of AA on LPS-induced AMI remained unclear. Sixty 1-day-old broilers were randomly divided into control group, LPS group, LPS + AA 15 mg/kg group, LPS + AA 30 mg/kg group, LPS + AA 60 mg/kg group, and control + AA 60 mg/kg group. The histopathology of cardiac tissues was detected by hematoxylin and eosin (H&E) staining. The mRNA and protein expressions related to mitochondrial dynamics and mitophagy were detected by quantitative real-time PCR, western blot, immunofluorescence, and immunohistochemistry. Disorganized myocardial cells and fractured myocardial fibers were found in the LPS group, and obvious red-blood-cell filling can be seen in the gaps between the myocardial fibers in the low-dose AA group. Nevertheless, the medium and high dose of AA obviously attenuated these changes. Our results showed that AA significantly restored the mRNA and protein expressions related to mitochondrial dynamic through further promoting mitophagy. This study revealed the effect of AA on LPS-induced AMI in broilers. Mechanically, AA regulated mitochondrial dynamic homeostasis and further promoted mitophagy. These novel findings indicate that AA may be a potential drug for LPS-induced AMI in broilers.
研究领域:
药理学
·
心脏病学
·
兽医学
·
分子生物学
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PubMed
高影响因子
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