CHEMICAL ENGINEERING JOURNAL
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2024
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IF 13.3
Xuezhi Wang,Yuan Sun,Ming Liu,Guyu You,Ting Fan,Hongmiao Wu,Liwei Xu,Xiaoli Zhao,Dongjie Ma
Polylactic acid (PLA) plastic is increasingly recognized as a sustainable alternative to petroleum-based plastics. However, its biodegradability remains a challenge, requiring substantial improvements to its biodegradation efficiency. This study explored the use of combined hydrothermal treatment (HTT) (160°C–240°C) and anaerobic digestion (AD) to improve methane yield from PLA. HTT enhanced significant structural changes in PLA, yielding 2-hydroxypropanoic acid, 1-decanol, 1-tetradecanol, pentan-2-one, and butyl 2-hydroxypropanoate, which facilitated PLA degradation. The methane yield from AD of hydrothermal-treated PLA (HTT-PLA) products at 180°C was 493 NmL/g-volatile solid, a 21.4-fold increased compared to untreated PLA. Genomic and proteomic analyses identified key genes and proteins involved in HTT-PLA products biodegradation, elucidating pathway for HTT-PLA products transformation in biodegradation process. The residues from AD of HTT-PLA products at 180°C exhibited rapeseeds germination index of approximately 90% and maintain stability locomotion and vitality in Caenorhabditis elegans , indicating their suitability for land application. Enhanced methane production offers a renewable energy source, and reduces PLA’s environmental footprint, providing significant practical implications for bioplastic waste management and sustainability.
研究领域:
环境科学
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生物技术
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可再生能源
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微生物学
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毒理学
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DOI
高影响因子
Materials Today Chemistry
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2022
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IF 7.613
Q. Wang,X. Yu,Y. Zhao,Y. Wang,K. Chen,Y. Liu,B. Wang,H. Zhang,Y. Sun
Owing to the overuse of rough articular cartilage, it increases the friction of joint and further leads to inflammation in joint cavities. However, the pathological changes also bring a new opportunity to achieve the treatment of osteoarthritis (OA). The increasing friction from damaged articular cartilage can convert more mechanical energy to heat. The higher localized temperature can reduce supramolecular interactions in general. Therefore, friction becomes another new activation to operate nanovalve systems for the targeting treatment of OA. Here, we designed and prepared a friction-induced nanovalve system constructed with β-cyclodextrins (β-CD)-modified mesoporous silica nanoparticles (MSN). Besides, a copolymer containing two components – guest molecules (adamantane, AD) and poly(2-methacryloyloxyethyl phosphorylcholine) (PMPC) – has been self-assembled on the surface of β-CD-modified MSN (MSN-CD) by supramolecular host–guest interactions. In this design, the charged PMPC on the MSN surface can form a dense hydration layer by ion–dipole interactions, switch the friction from surfaces to water molecules to achieve hydration lubrication , and sharply reduce the coefficient of friction (COF). Besides, the higher localized temperature from the mechanical conversion can weaken the supramolecular host–guest interactions and turn on the nanovalves to accomplish the targeted release near rough articular cartilage of OA. Even when PMPC is peeled off, the hydrophilic surface of β-CD on MSN surface can still perform the acceptable lubricating properties. The following testings of cytotoxicity by CCK-8 and live/dead staining indicated the excellent biocompatibility. Further analysis of protein expression levels has also shown the potential application in OA.
研究领域:
纳米技术
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生物材料
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药物递送系统
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生物医学工程
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骨科
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产品关联
DOI
高影响因子
CHEMICAL ENGINEERING JOURNAL
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2024
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IF 13.3
Yutong Chen,Ji-an Wei,Liqiang Wang,Qianyu Cai,Fang Yang,Li Zhang,Jie Liu,Yanan Liu
Mitochondrial damage induced by reactive oxygen species and mitochondrial autophagy dysfunction are closely related to the pathogenesis of Alzheimer's disease (AD). Therefore, the recovery of mitochondrial autophagy disorder is crucial in maintaining mitochondrial homeostasis, protecting neurons, and improving AD. Herein, Ruthenium dioxide nanoparticles (RuO 2 ) have multi-enzyme activities, such as superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD). And the multi-enzyme activity depends on the size, oxygen vacancy, morphology and specific surface area of the nanoparticles. The ultrasmall Ruthenium dioxide showed excellent antioxidant activity in the enzyme activity experiment. The results of in vitro experiments show that RuO 2 can restore damaged neurons by clearing Aβ and H 2 O 2 -induced reactive oxygen species (ROS). It maintains mitochondrial function, restores mitochondrial autophagy and normalizes mitochondrial dysfunction, thereby restoring injured neuronal cells. At the same time, it also showed the ability to regulate microglia polarization, inhibit microglia overactivation, and relieve neuroinflammation. After screening the results of enzyme activity experiment and in vitro experiment, sRuO 2 with small particle size and good enzyme activity was selected for in vivo experiment. sRuO 2 can inhibit oxidative stress in vivo , reduce the burden of Aβ, regulate the neuroprotective function of microglia and improve neuroinflammation. It ultimately improve memory decline and cognitive impairment in Aβ mice. These results suggest that sRuO 2 nanoenzymes with antioxidant activity have great potential in the treatment of AD. The multi-target strategy also offers a promising treatment option for AD.
研究领域:
神经科学
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纳米技术
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药理学
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分子生物学
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产品关联
DOI
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
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2024
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IF 6.9
Yuanfang Sun,Qi Xia,Lijing Du,Yu Gan,Xiaopeng Ren,Gang Liu,Yongkuan Wang,Shikai Yan,Shasha Li,Xiuyun Zhang,Xue Xiao,Huizi Jin
Alzheimer's disease (AD) presents a significant challenge due to its prevalence and lack of cure, driving the quest for effective treatments. Anshen Bunao Syrup , a traditional Chinese medicine known for its neuroprotective properties, shows promise in addressing this need. However, understanding its precise mechanisms in AD remains elusive. This study aimed to investigate Anshen Bunao Syrup's therapeutic potential in AD treatment using a scopolamine-induced AD rat model. Assessments included novel-object recognition and Morris water maze tasks to evaluate spatial learning and memory, alongside Nissl staining and ELISA analyses for neuronal damage and biomarker levels. Results demonstrated that Anshen Bunao Syrup effectively mitigated cognitive dysfunction by inhibiting amyloid-β and phosphorylation Tau aggregation, thereby reducing neuronal damage. Metabolomics profiling of rats cortex revealed alterations in key metabolites implicated in tryptophan and fatty acid metabolism pathways, suggesting a role in the therapeutic effects of Anshen Bunao Syrup . Additionally, ELISA and correlation analyses indicated attenuation of oxidative stress and immune response through metabolic remodeling. In conclusion, this study provides compelling evidence for the neuroprotective effects of Anshen Bunao Syrup in AD models, shedding light on its potential as a therapeutic agent for AD prevention and treatment.
研究领域:
神经科学
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药理学
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中医药
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神经退行性疾病
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产品关联
DOI
PubMed
高影响因子
Asian Journal of Pharmaceutical Sciences
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2024
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IF 10.7
Kang Qian,Peng Yang,Yixian Li,Ran Meng,Yunlong Cheng,Lingling Zhou,Jing Wu,Shuting Xu,Xiaoyan Bao,Qian Guo,Pengzhen Wang,Minjun Xu,Dongyu Sheng,Qizhi Zhang
Alzheimer's disease is a neurodegenerative disease induced by multiple interconnected mechanisms. Peptide drug candidates with multi-modal efficacy generated from fusion strategy are suitable for addressing multi-facet pathology. However, clinical translation of peptide drugs is greatly hampered by their low permeability into brain. Herein, a hybrid peptide HNSS is generated by merging two therapeutic peptides (SS31 and S-14G Humanin (HNG)), using a different approach from the classical shuttle-therapeutic peptide conjugate design. HNSS demonstrated increased bio-permeability, with a 2-fold improvement in brain distribution over HNG, thanks to its structure mimicking the design of signal peptide-derived cell-penetrating peptides. HNSS efficiently alleviated mitochondrial dysfunction through the combined effects of mitochondrial targeting, ROS scavenging and p-STAT3 activation. Meanwhile, HNSS with increased Aβ affinity greatly inhibited Aβ oligomerization/fibrillation, and interrupted Aβ interaction with neuron/microglia by reducing neuronal mitochondrial Aβ deposition and promoting microglial phagocytosis of Aβ. In 3 × Tg-AD transgenic mice, HNSS treatment efficiently inhibited brain neuron loss and improved the cognitive performance. This work validates the rational fusion design-based strategy for bio-permeability improvement and efficacy amplification, providing a paradigm for developing therapeutic peptide candidates against neurodegenerative disease.
研究领域:
神经科学
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药理学
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生物技术
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
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2022
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IF 6.656
Chang-Long He,Yong Tang,Xue Chen,Tao Long,Yan-Ni He,Jing Wei,Jian-Ming Wu,Cai Lan,Lu Yu,Fei-Hong Huang,Cong-Wei Gu,Jian Liu,Chong-Lin Yu,Vincent Kam-Wai Wong,Betty Yuen-Kwan Law,Da-Lian Qin,An-Guo Wu,Xiao-Gang Zhou
Background Protein aggregates are considered key pathological features in neurodegenerative diseases (NDs). The induction of autophagy can effectively promote the clearance of ND-related misfolded proteins. Objective In this study, we aimed to screen natural autophagy enhancers from traditional Chinese medicines (TCMs) presenting potent neuroprotective potential in multiple ND models. Methods The autophagy enhancers were broadly screened in our established herbal extract library using the transgenic Caenorhabditis elegans ( C. elegans ) DA2123 strain. The neuroprotective effects of the identified autophagy enhancers were evaluated in multiple C. elegans ND models by measuring Aβ-, Tau-, α-synuclein-, and polyQ40-induced pathologies. In addition, PC-12 cells and 3 × Tg-AD mice were employed to further validate the neuroprotective ability of the identified autophagy enhancers, both in vitro and in vivo . Furthermore, RNAi bacteria and autophagy inhibitors were used to evaluate whether the observed effects of the identified autophagy enhancers were mediated by the autophagy-activated pathway. Results The ethanol extract of Folium Hibisci Mutabilis (FHME) was found to significantly increase GFP::LGG-1-positive puncta in the DA2123 worms. FHME treatment markedly inhibited Aβ , α-synuclein, and polyQ40, as well as prolonging the lifespan and improving the behaviors of C. elegans , while siRNA targeting four key autophagy genes partly abrogated the protective roles of FHME in C. elegans . Additionally, FHME decreased the expression of AD-related proteins and restored cell viability in PC-12 cells, which were canceled by cotreatment with 3-methyladenine (3-MA) or bafilomycin A1 (Baf). Moreover, FHME ameliorated AD-like cognitive impairment and pathology, as well as activating autophagy in 3 × Tg-AD mice. Conclusion FHME was successfully screened from our natural product library as a potent autophagy enhancer that exhibits a neuroprotective effect in multiple ND models across species through the induction of autophagy. These findings offer a new and reliable strategy for screening autophagy inducers, as well as providing evidence that FHME may serve as a possible therapeutic agent for NDs.
研究领域:
神经科学
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药理学
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中药
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自噬研究
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神经退行性疾病
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
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2024
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IF 4.5
Hongming Tang,Tao Hou,Han Zhou,Han Liao,Fangfang Xu,Xiaomin Xie,Wenjie Yuan,Zhixin Guo,Yanfang Liu,Jixia Wang,Weijia Zhou,Xinmiao Liang
Histamine 4 receptor (H4R), the most recently identified subtype of histamine receptor, primarily induces inflammatory reactions upon activation. Several H4R antagonists have been developed for the treatment of inflammatory bowel disease (IBD) and atopic dermatitis (AD), but their use has been limited by adverse side effects, such as a short half-life and toxicity. Natural products, as an important source of anti-inflammatory agents, offer minimal side effects and reduced toxicity. This work aimed to identify novel H4R antagonists from natural products. An H4R target-pathway model deconvoluted downstream G i and MAPK signaling pathways was established utilizing cellular label-free integrative pharmacology (CLIP), on which 148 natural products were screened. Cryptotanshinone was identified as selective H4R antagonist, with an IC 50 value of 11.68 ± 1.30 μM, which was verified with Fluorescence Imaging Plate Reader (FLIPR) and Cellular Thermal Shift (CTS) assays. The kinetic binding profile revealed the noncompetitive antagonistic property of cryptotanshinone. Two allosteric binding sites of H4R were predicted using SiteMap, Fpocket and CavityPlus. Subsequent molecular docking and dynamics simulation indicated that cryptotanshinone interacts with H4R at a pocket formed by the outward interfaces between TM3/4/5, potentially representing a new allosteric binding site for H4R. Overall, this study introduced cryptotanshinone as a novel H4R antagonist, offering promise as a new hit for drug design of H4R antagonist. Additionally, this study provided a novel screening model for the discovery of H4R antagonists.
研究领域:
药理学
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药物发现
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炎症
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天然产物化学
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分子生物学
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细胞信号传导
✓ 已验证
产品关联
DOI
PubMed
高影响因子
SENSORS AND ACTUATORS B-CHEMICAL
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2021
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IF 7.46
Kai-Xin Song,Dong Chen,Zi-Yang Liao,Xuan Yu,Fei-Fei Guo,Ri-Lei Yu,Meng-Zhen Xu,Ya-Mu Xia,Wei-Wei Gao
In this work, an efficient electrochemical biosensor for the detection of DNA damage induced by the interaction of a novel antitumor agent AD-NU was investigated by CV , DPV and SWV methods. The GCE was modified with calf thymus DNA, G-quadruplexes, poly dA and poly dG, respectively. Among all the candidates, compound AD-NU was the optimum ligand because of the minimum energy when binding to DNA or TOP II by molecular docking. The electrochemical analysis revealed the redox mechanism of AD-NU on the GCE surface, which included two consecutive reversible processes of 9,10-diquinone and irreversible redox of nitroso group . The DNA damage caused by AD-NU was investigated by comparing the intensity changes of dGuo and dAdo oxidation peaks in DNA strands, and monitoring the appearance of peak for oxidative product 8-oxoGua. Further confirmation for the interaction between AD-NU and DNA was performed by UV–vis absorption and fluorescence titration, which implied the intercalation of AD-NU into DNA base pairs with a high affinity constant ( K b = 13.7 ×10 5 M −1 ). The electrophoresis also revealed the potency of AD-NU to cleave and unwind DNA strands. Finally, AD-NU was proved to have good antiproliferative activity toward tumor cells, with IC 50 values of 3.0 μmol ∙ L −1 for A549 cell lines and 3.3 μmol ∙ L −1 for Hela cell lines, superior to MTZ reference.
研究领域:
电化学
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生物传感器
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分子生物学
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癌症研究
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分析化学
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药理学
✓ 已验证
DOI
高影响因子
危险品化学品经营许可证（带存储）