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
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心脏病学
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兽医学
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分子生物学
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高影响因子
Neural Regeneration Research
·
2025
·
IF 6.7
Yu Ning,Zhao Yang,Wang Peng,Zhang Fuqiang,Wen Cuili,Wang Shilei
Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus (GEO) database (GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC’ tool. We found that, in response to hypoxia, border- associated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3 (Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment.
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高影响因子
Neural Regeneration Research
·
2024
·
IF 5.9
Li Shiming,Li Jianfeng,Chen Guoliang,Lin Tao,Zhang Penghui,Tong Kuileung,Chen Ningning,Liu Shaoyu
We previously demonstrated that inhibiting neural stem cells necroptosis enhances functional recovery after spinal cord injury. While exosomes are recognized as playing a pivotal role in neural stem cells exocrine function, their precise function in spinal cord injury remains unclear. To investigate the role of exosomes generated following neural stem cells necroptosis after spinal cord injury, we conducted single–cell RNA sequencing and validated that neural stem cells originate from ependymal cells and undergo necroptosis in response to spinal cord injury. Subsequently, we established an in vitro necroptosis model using neural stem cells isolated from embryonic mice aged 16-17 days and extracted exosomes. The results showed that necroptosis did not significantly impact the fundamental characteristics or number of exosomes. Transcriptome sequencing of exosomes in necroptosis group identified 108 differentially expressed messenger RNAs, 104 long non-coding RNAs, 720 circular RNAs, and 14 microRNAs compared with the control group. Construction of a competing endogenous RNA network identified the following hub genes: tuberous sclerosis 2 ( Tsc2 ), solute carrier family 16 member 3 ( Slc16a3 ), and forkhead box protein P1 ( Foxpl ). Notably, a significant elevation in TSC2 expression was observed in spinal cord tissues following spinal cord injury. TSC2-positive cells were localized around SRY-box transcription factor 2-positive cells within the injury zone. Furthermore, in vitro analysis revealed increased TSC2 expression in exosomal receptor cells compared with other cells. Further assessment of cellular communication following spinal cord injury showed that Tsc2 was involved in ependymal cellular communication at 1 and 3 days post-injury through the epidermal growth factor and midkine signaling pathways. In addition, Slc16a3 participated in cellular communication in ependymal cells at 7 days post-injury via the vascular endothelial growth factor and macrophage migration inhibitory factor signaling pathways. Collectively, these findings confirm that exosomes derived from neural stem cells undergoing necroptosis play an important role in cellular communication after spinal cord injury and induce TSC2 upregulation in recipient cells.
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高影响因子
Neural Regeneration Research
·
2024
·
IF 5.9
Ren Chunge,Chen Min,Ren Bangqi,Zeng Yuxiao,Tan Qiang,Li Qiyou,Zhang Xue,Fang Yajie,Zhou Yixiao,Zhang Weitao,Chen Fang,Bian Baishijiao,Liu Yong
Our previous study demonstrated that combined transplantation of bone marrow–derived mesenchymal stem cells and retinal progenitor cells in rats has therapeutic effects on retinal degeneration that are superior to transplantation of retinal progenitor cells alone. Bone marrow- derived mesenchymal stem cells regulate and interact with various cells in the retinal microenvironment by secreting neurotrophic factors and extracellular vesicles. Small extracellular vesicles derived from bone marrow–derived mesenchymal stem cells, which offer low immunogenicity, minimal tumorigenic risk, and ease of transportation, have been utilized in the treatment of various neurological diseases. These vesicles exhibit various activities, including anti-inflammatory actions, promotion of tissue repair, and immune regulation. Therefore, novel strategies using human retinal progenitor cells combined with BMSC-derived small extracellular vesicles may represent an innovation in stem cell therapy for retinal degeneration. In this study, we developed such an approach utilizing retinal progenitor cells combined with bone marrow–derived mesenchymal stem cell-derived small extracellular vesicles to treat retinal degeneration in Royal College of Surgeons rats, a genetic model of retinal degeneration. Our findings revealed that the combination of bone marrow–derived mesenchymal stem cell-derived small extracellular vesicles and retinal progenitor cells significantly improved visual function in these rats. The addition of bone marrow–derived mesenchymal stem cell-derived small extracellular vesicles as adjuvants to stem cell transplantation with retinal progenitor cells enhanced the survival, migration, and differentiation of the exogenous retinal progenitor cells. Concurrently, these small extracellular vesicles inhibited the activation of regional microglia, promoted the migration of transplanted retinal progenitor cells to the inner nuclear layer of the retina, and facilitated their differentiation into photoreceptors and bipolar cells. These findings suggest that bone marrow–derived mesenchymal stem cell-derived small extracellular vesicles potentiate the therapeutic efficacy of retinal progenitor cells in retinal degeneration by promoting their survival and differentiation.
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高影响因子
Neural Regeneration Research
·
2024
·
IF 5.9
Fu Lanya,Hu Xiaofang,Xu Jiawei,Li Zhenlin,Cai Jiale,Ma Xinrui,Zou Ying,He Ye,Xu Shuyi,Xu Yizhou,Zhang Jiaqi,Li Yunlun,Liu Jingmin,Fong Tsz Hei,Wang Xianghai,Zhu Lixin,Chen Dongfeng,Liu Aijun,Ma Xiaodong,Guo Jiasong
Our recent study demonstrated that knockout of microRNA-301a attenuates migration and phagocytosis in macrophages. Considering that macrophages and Schwann cells synergistically clear the debris of degraded axons and myelin during Wallerian degeneration, which is a prerequisite for nerve regeneration, we hypothesized that microRNA-301a regulates Wallerian degeneration and nerve regeneration via impacts on Schwann cell migration and phagocytosis. Herein, we found low expression of microRNA-301a in intact sciatic nerves, with no impact of the microRNA-301a knockout on nerve structure and function. By contrast, we found significant upregulation of microRNA- 301a in injured sciatic nerves. We established a sciatic nerve crush model in microRNA-301a knockout mice, which exhibited attenuated morphological and functional regeneration following sciatic nerve crush injury. The microRNA-301a knockout also led to significantly inhibited Wallerian degeneration in an in vivo sciatic nerve-transection model and in an in vitro nerve explant block model. Schwann cells with the microRNA-301a knockout showed inhibition of phagocytosis and migration, which was reversible under transfection with microRNA-301a mimics. Rescue experiments involving transfection of microRNA-301a-knockout Schwann cells with microRNA-301a mimics or treatment with the C–X–C motif receptor 4 inhibitor WZ811 indicated the mechanistic involvement of the Yin Yang 1/C–X–C motif receptor 4 pathway in the role of microRNA-301a. Combined with our previous findings in macrophages, we conclude that microRNA-301a plays a key role in peripheral nerve injury and repair by regulating the migratory and phagocytic capabilities of Schwann cells and macrophages via the Yin Yang 1/C–X–C motif receptor 4 pathway.
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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.
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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.
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高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2023
·
IF 15.1
Jinxiang Zuo,Donglei Fu,Pengwei Yan,Shuyu Wang,Yabin Li,Linlu Shen,Yizhen Cheng,Jimin Shen,Jing Kang,Zhonglin Chen
In this study, Al-doped NiFe 2 O 4 (NiAl x Fe 2-x O 4 ) was synthesized by the isomorphic substitution strategy, which was further employed for peroxymonosulfate (PMS) activation to remove 2,4-dichlorophenoxyacetic acid (2,4-D) in water. Doping of Al could construct oxygen vacancies (OVs) in the structure of NiAl x Fe 2-x O 4 , which further facilitates the exposure of metal sites for PMS activation. The removal rate of 2,4-D increased greatly compared to the NiFe 2 O 4 -activated process. By the density functional theory (DFT) process, it was verified that Al was more likely to replace Fe rather than Ni. OVs sites have the lowest adsorption energy of H 2 O ( E ads = -0.95 eV), and easily formed surface hydroxyl groups (–OH), which were further replaced by PMS (HSO 5 - ). The formed surface complex Me-O-O-SO 3 - was readily activated via electron transfer between O-O bond, thus promoting the cleavage of it and inducing SO 4 · - generation. This process induced the high performance of the NiAl x Fe 2-x O 4 /PMS system for effective 2,4-D degradation. Furthermore, the purified water showed relatively low toxicity. The present study proposed new insights into the interface mechanism of PMS triggering.
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高影响因子
BIOTECHNOLOGY LETTERS
·
2023
·Vol. 45
·期 10
·1355-1364
·
IF 2.7
Gao Yahui,Li Fen,Wang Yulu,Chen Zhou,Li Zijie
Purpose In our previous study, we constructed a one-pot multi-enzyme system for rare ketoses synthesis based on L-rhamnulose-1-phosphate aldolase (RhaD) from accessible glycerol in vitro. To eliminate tedious purification of enzymes, a facile Escherichia coli whole-cell cascade platform was established in this study. Methods To enhance the conversion rate, the reaction conditions, substrate concentrations and expressions of related enzymes were extensively optimized. Results The biosynthetic route for the cascade synthesis of rare ketoses in whole cells was successfully constructed and three rare ketoses including D-allulose, D-sorbose and L-fructose were produced using glycerol and D/L-glyceraldehyde (GA). Under optimized conditions, the conversion rates of rare ketoses were 85.0% and 93.0% using D-GA and L-GA as the receptor, respectively. Furthermore, alditol oxidase (AldO) was introduced to the whole-cell system to generate D-GA from glycerol, and the total production yield of D-sorbose and D-allulose was 8.2 g l −1 only from the sole carbon source glycerol. Conclusion This study demonstrates a feasible and cost-efficient method for rare sugars synthesis and can also be applied to the green synthesis of other value-added chemicals from glycerol.
研究领域:
生物化学
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合成生物学
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代谢工程
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高影响因子
Journal of Physical Chemistry C
·
2024
·
IF 3.3
Zhi-Qiang Wang,Wanjun Guo,Shengchao Jia,Yaxuan Jing,Shiting Li,Yong Guo,Xiaohui Liu,Xue-Qing Gong,Yanqin Wang
The selective production of primary amines through reductive amination has received increasing attention due to their extensive applications, while efficient reductive amination is still challenging. Herein, a novel strategy was developed to realize the efficient reductive amination of carbonyl compounds with NH3 via d–d orbital coupling strategies in RuCo alloys. The designed series of RuCo alloy catalysts not only exhibited excellent performance in conversion of various substrates but also demonstrated universal applicability across different supports. The key role of RuCo alloy is its unique ability to effectively catalyze the ammonolysis of a Schiff base, the rate-determining step in reductive amination. Theoretical studies reveal that the d–d orbital coupling strategies break the five d orbital equivalent contributions of metal (Co or Ru) atoms, and the d orbitals primarily contribute through the dz2 and dx2-y2 orbitals of Ru and the dz2 orbital of Co on the RuCo(001) surface, which significantly driving the homolytic NH3 dissociation during the ammonolysis of the Schiff base. Furthermore, stable Co–H covalent bond species and RuCo-NH2 half-ionic and half-covalent bond species on the RuCo(001) surface were generated with lower energy levels. This work not only achieves efficient reductive amination but also provides an atomic orbital-level understanding of the d–d orbital coupling strategies for heterogeneous catalysis.
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APPLIED CATALYSIS B-ENVIRONMENTAL
·
2024
·
IF 20.2
Ruichen Geng,Ranran Wei,Xuewen Wei,Xiaoying Zhang,Yaxuan Li,Zekai Shen,Yinglong Wang,Liang Wang,Shuli Yin
Designing highly active and selective electrocatalytic catalysts to accelerate 5-hydroxymethylfurfural (HMF) oxidation is significant but challenging in biomass upgrading. Herein, the high-entropy alloy AuCuAgPdNi nanowires catalyst with a self-complementary effect via a simple one-pot wet chemical method is reported. Notably, AuCuAgPdNi NWs show excellent activity and selectivity during HMF oxidation with a 2,5-furandicarboxylic acid (FDCA) yield of 95.5 % and a selectivity of 98.4 % at the potential of 1.60 V vs. RHE. Moreover, a flow electrolytic cell is designed to couple the high-performance HMF oxidation reaction (HMFOR) at the anode and the faradaic efficiency of the hydrogen evolution reaction approaching 100 % at the cathode. In-situ Fourier transform infrared (in-situ FTIR) results reveal the relationship between the HMFOR pathway and potential. Theoretical calculation shows that AuCuAgPdNi NWs promote the exchangeability of surface electrons through the self-complementary effect generated by d - d orbital coupling, thus achieving efficient HMFOR. This work provides insights into the innovative synthesis and mechanisms inherent catalytic of high-entropy alloy systems and offers ideas for the value-added conversion of biomass.
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IRANIAN POLYMER JOURNAL
·
2016
·Vol. 25
·期 5
·443-454
·
IF 1.684
Kong Lingqian,Ju Xiuping,Zhang Yan,Zhao Jinsheng,Xu Jianzhong
Abstract Two new donor–acceptor–donor (D–A–D) type monomers, 2-dodecyl-4,7-bis(4-methoxythiophen-2-yl)-2 H -benzo[ d ] [ 1 – 3 ] triazole (MOTBT) and 2-dodecyl-4,7-bis(4-methylthiophen-2-yl)-2 H -benzo[ d ] [ 1 – 3 ] triazole (MTBT) were synthesized by Stille coupling and the corresponding polymers, PMOTBT and PMTBT were obtained by electropolymerization method. The properties of the monomers and the polymers were studied by cyclic voltammetry (CV), ultraviolet–visible–near-infrared (UV–Vis–NIR) and spectroelectrochemistry. The CV results demonstrated ambipolar processes (n- and p-doping) for both polymers. According to the spectroelectrochemistry tests, the polymer PMOTBT revealed a saturated blue color in the reduced state and a transparent light blue color in the oxidized state, and the PMTBT polymer could switch between neutral orange color and oxidized light bluish-green color in the redox process. Furthermore, in the visible region, the optical contrasts were 51 % (at 645 nm) and 34 % (at 430 nm) for PMOTBT and PMTBT, respectively, with the switching times of 0.29 and 1.2 s from reduced state to oxidized state. In the NIR region, higher optical contrast ratios of 76 % (at 1600 nm for PMOTBT) and 67 % (at 1500 nm for PMTBT) as well as faster response times (0.90 and 0.35 s) were obtained. We also found that both polymers had the relative high coloration efficiency as much as 372 and 312 cm 2 /C and a satisfactory stability. Therefore, both polymers are promising candidates in displays and opto-electronic devices as electrochromic materials. Graphical abstract
研究领域:
材料科学
·
电化学
·
光学
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高影响因子
危险品化学品经营许可证（带存储）