查找使用阿拉丁产品的科研文献

Green carbon dots derived from Zingiberis Rhizoma Carbonisatum alleviate ovalbumin-induced allergic rhinitis

Long Zhou,Yingxin Yang,Tingjie Li,Yafang Zhao,Jinye Yuan,Chenxin He,Yan Huang,Jinyu Ma,Yue Zhang,Fang Lu,Jiaze Wu,Zijian Li,Hui Kong,Yan Zhao,Huihua Qu

Background: Allergic rhinitis (AR) affects up to 40% of the population, leading to significant healthcare expenditures. Current mainstream treatments, while effective, can lead to side effects and do not address the underlying immunological imbalances. Zingiberis Rhizoma Carbonisatum (ZRC), the partially charred product of Zingiberis Rhizoma (ZR), has been widely used clinically in China since ancient times to treat respiratory disorders.Methods: Inspired by the similarity between high-temperature pyrolysis and carbonization processing of herbal medicine, ZRC derived CDs (ZRC-CDs) were extracted and purified through several procedures. Then, the physicochemical characteristics of CDs were delineated through a suite of characterization methods. Moreover, our investigation zeroed in on elucidating the ameliorative impacts of CDs on ovalbumin-induced rat models alongside their underlying mechanisms.Results: ZRC-CDs with particle sizes ranging from 1.0 to 3.5 nm and rich surface functional groups. Additionally, we observed that ZRC-CDs significantly attenuated nasal symptoms and pathological damage in ovalbumin-induced AR rats, and modulated lipid metabolism and type 2 inflammatory responses. They also inhibit PI3K/AKT and JAK/STAT pathways, which are associated with metabolism and inflammation. Importantly, ZRC-CDs demonstrated high biocompatibility, underscoring their potential as a novel therapeutic agent.Conclusion: ZRC-CDs offer a promising alternative for AR treatment and could help facilitate broader clinical use of the ZRC. In addition, the exploration of the inherent bioactivity of CDs can help to broaden their biological applications.

Ginsenoside Ro attenuates aging-related cognitive impairment and associated neuroinflammatory changes via multi-target modulation of the PI3K-Akt axis: a convergent network pharmacology and experimental validation study

Hou Jingyi,Yang Kailan,Zhang Dandan,Ba Yi,Wang Yubo,Zhao Changqi,Zhu Naiqiang,Gu Miao

The increasing global burden of aging-related cognitive impairment (ACI) highlights an urgent need for disease-modifying therapeutics, as current pharmacological options provide only temporary symptomatic relief without affecting underlying pathological trajectories. Ginsenoside Ro, an oleanane-type saponin derived from Panax ginseng, displays anti-inflammatory and cytoprotective properties; however, the target network and signaling mechanisms through which it may alleviate ACI remain inadequately defined. This study aims to thoroughly define the therapeutic efficacy and underlying molecular mechanisms of Ginsenoside Ro against ACI utilizing a convergent analytical approach that integrates network pharmacology, in silico molecular simulation, and empirical validation in aging-model mice and senescent PC12 cells. Putative targets of Ginsenoside Ro were sourced from PubChem, SwissTargetPrediction, STITCH, ChEMBL, and SEA databases. ACI-relevant and aging-associated targets were curated from HAGR, OMIM, and GeneCards databases. A protein–protein interaction (PPI) network was constructed using STRING, and hub targets were identified with the cytoHubba algorithm. Functional enrichment analysis, including GO and KEGG analyses, was performed via DAVID. Binding interactions were evaluated using molecular docking and 100 ns molecular dynamics (MD) simulations. In vivo characterization involved the development of a senescence mouse model via intraperitoneal D-galactose (D-Gal) administration (125 mg/kg/d for 10 weeks), followed by oral treatment with Ginsenoside Ro (5 and 10 mg/kg) or melatonin (100 mg/kg) for 6 weeks. Cognitive performance was assessed using the Morris water maze (MWM) and open field test (OFT). Systemic oxidative status was monitored by measuring serum MDA, SOD, and MAO, while neural tissue integrity was examined through H&E and Nissl staining. In vitro, D-Gal-induced senescent PC12 cells were treated with Ginsenoside Ro (3.125–12.5 µM), followed by evaluations of cell viability, SA- β -galactosidase activity, ROS accumulation, SOD function, and expression levels of TNF-α, IL-6, EGFR, and components of the PI3K-Akt cascade using CCK-8, flow cytometry, RT-qPCR, and Western blot. Target intersection analysis identified 30 overlapping nodes between Ginsenoside Ro and ACI, with TNF-α, IL-6, AKT1, and EGFR recognized as core targets. KEGG enrichment analysis highlighted PI3K-Akt signaling as a key mechanistic pathway. Molecular docking yielded binding energies ranging from − 8.8 to − 4.8 kcal/mol, while MD trajectories demonstrated RMSD/RMSF profiles, hydrogen-bond interactions, and distinct deep free-energy minima consistent with sustained complex formation over the simulation period. In the D-Gal mouse model, Ginsenoside Ro reduced escape latency, increased platform crossings and exploratory behavior, decreased serum MDA, restored SOD and MAO levels, and ameliorated neuronal loss and nuclear pyknosis in the hippocampus and cortex. In PC12 cells, Ginsenoside Ro improved viability, diminished SA- β -gal positivity and ROS accumulation, enhanced SOD activity, restored EGFR expression, suppressed IL-6/TNF-α induction, and normalized the elevated p-PI3K/PI3K and p-AKT/AKT ratios. These findings suggest that Ginsenoside Ro is associated with the modulation of TNF-α, IL-6, AKT1, and EGFR, and that the PI3K-Akt pathway may serve as a central axis correlated with its observed neuroprotective effects. Ginsenoside Ro emerges as a promising candidate for ameliorating aging-associated cognitive dysfunction and related pathological changes, providing a preclinical basis for future translational development.

Antioxidative Lignin Materials Attenuate Type 2 Diabetes Mellitus (T2DM) Progression by Preserving Glutathione via Insulin Receptor Substrate 1/Phosphoinositide 3-Kinase/Protein Kinase B (IRS1/PI3K/AKT) Axis

Shuang Qi,Hui Yang,Tian Fang,Tingwei Zhang,Bo Jiang,Sehrish Manan,Chaofeng Zhang,Peng Wang,Caoxing Huang,Wenjuan Wu,Yongcan Jin

Lignin, a natural and renewable aromatic biopolymer, has gained attention in various biomedical applications due to its diverse structure, excellent biocompatibility, and antioxidant activity. However, the effects of lignin with tailored molecular weight on treating type 2 diabetes mellitus (T2DM) remain largely unexplored. In this study, a series of heterogeneous natural phenolic kraft lignin (KL) with tailored molecular weights, derived through an anti-sugar strategy, were prepared by continuous fractionation. The lignin fractions were categorized as F1, F2, and F3, corresponding to high, medium, and low molecular weights, respectively. Their therapeutic effects on T2DM were evaluated using a fractionated lignin culture cell model and intravenous injection into the tail vein of diabetic rats. The results demonstrated that lignin's protective effects in attenuating T2DM progression were molecular weight-dependent. Specifically, F3 reduced fasting blood glucose, reversed insulin resistance, and improved insulin sensitivity by mitigating oxidative stress and inflammatory responses. Mechanistic investigations revealed that F3 positively regulated glucose and lipid metabolism, inhibited hepatic gluconeogenesis, and enhanced hepatic glycogen synthesis by activating the insulin receptor substrate 1/phosphoinositide 3-kinase/protein kinase B (IRS1/PI3K/AKT) signaling pathway. Results revealed that lignin exerts its therapeutic effects on T2DM in a molecular weight-dependent manner, with IRS1/PI3K/AKT signaling as a potential underlying mechanism. This highlights lignin with a defined molecular weight as a promising candidate for T2DM treatment.

Elucidation of the mechanism of the fruit of Rubus chingii Hu against CCl4-induced liver injury in mice based on met/Tlr2/Tlr4 -mediated PI3K-Akt signaling pathway

Ping Jiang,Yanfei He,Guangpei Xu,Chuanbo Sun

This study aims to evaluate the mechanism of RCH against CCl 4 -induced liver injury in mice. RCH treatment effectively inhibited CCl 4 -induced liver injury and apoptosis in mice, and reduced liver enzyme activities, blood inflammatory cell and serum inflammatory factor levels. Network pharmacology and machine learning predicted that PI3K-Akt pathway and Met proteins play important roles in RCH anti-CCl 4 -induced liver injury. The results of qRT-PCR and Western blot showed that RCH could down-regulate the expression of the receptor proteins Met, Tlr2, and Tlr4, and inhibit the phosphorylation of Pik3ca and Akt1, and prevent the phosphorylation of NF-κB P65, and decrease cleaved Caspase3 expression. These findings suggest that RCH effectively alleviated liver injury in CCl 4 -induced mice by inhibiting the Met/Tlr2/Tlr4-mediated PI3K-Akt signaling pathway.

A Glutathione Peroxidase-Mimicking Nanozyme Precisely Alleviates Reactive Oxygen Species and Promotes Periodontal Bone Regeneration

Bijun Zhu,Jiangjiexing Wu,Tong Li,Songtao Liu,Junheng Guo,Yijun Yu,Xinyi Qiu,Yue Zhao,Haoran Peng,Jinli Zhang,Leiying Miao,Hui Wei

The use of oxidoreductase nanozymes to regulate reactive oxygen species (ROS) has gradually emerged in periodontology treatments. However, current nanozymes for treating periodontitis eliminate ROS extensively and non-specifically, ignoring the physiological functions of ROS under normal conditions, which may result in uncontrolled side effects. Herein, using the MIL-47(V)-F (MVF) nanozyme, which mimics the function of glutathione peroxidase (GPx), we propose that ROS can be properly regulated by specifically eliminating H 2 O 2 , the most prominent ROS. Through H 2 O 2 elimination, MVF contributes to limiting inflammation, regulating immune microenvironment, and promoting periodontal regeneration. Moreover, MVF stimulates osteogenic differentiation of periodontal stem cells directly, further promoting regeneration due to the vanadium in MVF. Mechanistically, MVF regulates ROS by activating the Nrf2/HO-1 pathway and promotes osteogenic differentiation directly through the PI3K/Akt pathway. We present a promising periodontitis therapy strategy using GPx-mimicking nanozymes through their triple effects of antioxidation, immunomodulation, and bone remodeling regulation, making nanozymes an excellent tool for developing precision medicine. This article is protected by copyright. All rights reserved

Paeonia delavayi seed oil rich in oleic acid and linolenic acid alleviates UVB-induced inflammation and oxidative stress in keratinocytes through inhibition of PI3K/Akt and NF-κB pathways

Rencong Wang,Peng Xu,Yindi Zhang,Xiaoli Jin,Ziyan Zhao,Liping Qu,Feifei Wang

Excessive exposure to UVB can induce inflammatory responses and oxidative stress, leading to skin damage. Peony seed oil is rich in unsaturated fatty acids and has been reported to possess anti-inflammatory and antioxidant properties. This study investigated the protective effects and underlying mechanisms of Paeonia delavayi seed oil (PDSO) against UVB-induced damage in human keratinocytes. PDSO at 30–120 μg/mL attenuated UVB-induced inflammation by reducing the mRNA expression of TNF , IL6 , CXCL8 , and PTGS2 and suppressing the secretion of IL-6 and IL-8. PDSO also inhibited UVB-induced activation of NF-κB signaling. Regarding oxidative stress, 120 μg/mL PDSO reduced intracellular ROS production, decreased MDA levels by approximately 29.4%, and increased SOD activity by approximately 122.0% compared with the UVB group. PDSO also increased the mRNA expression of antioxidant-related genes, including NFE2L2, HMOX1, SOD1, CAT, GCLC, and GCLM . In addition, PDSO alleviated the UVB-induced reduction in keratinocyte viability and attenuated photoaging-related changes. Transcriptomic analysis identified PI3K/Akt signaling as a candidate pathway associated with PDSO treatment, and western blotting further showed that PDSO inhibited UVB-induced PI3K/Akt signaling. Pharmacological intervention with the PI3K activator 740Y P partially reversed the anti-inflammatory effects of PDSO, whereas LY294002 exerted anti-inflammatory effects and further enhanced those of PDSO. Moreover, oleic acid and linolenic acid alleviated UVB-induced inflammation and oxidative stress. Collectively, PDSO protects keratinocytes against UVB-induced damage, with PI3K/Akt and NF-κB signaling contributing to its protective effects. Download: Download high-res image (117KB) Download: Download full-size image

Muscle-Targeted Nanocomposite Therapy Alleviates Age-Related Sarcopenia via Antioxidant and Metabolic Reprogramming

Zhang Liu,Zile Shen,Hengli Lu,Bingqiang Lu,Peng Zhang,Wenhao Chen,Guowei Huang,Xinyu Qu,Zhen Yu,Feng Chen,Wangfu Zang

Sarcopenia, a progressive skeletal muscle disorder marked by loss of mass and function, presents growing societal challenges due to limited therapeutic options. Here, we identify mitochondrial dysfunction and oxidative stress as central drivers of sarcopenia through integrated bioinformatics and clinical validation. To address this pathophysiology, we engineer a muscle-targeted nanocomposite (BP-PEG-MOTS-c, BM) combining mitochondrial-derived peptide MOTS-c with antioxidant black phosphorus nanosheets (BP). BM exhibits dual functionality: MOTS-c restores mitochondrial function, while BP synergistically amplifies ROS scavenging capacity. In cellular and murine models with age-related sarcopenia, BM treatment alleviates muscle dysfunction and muscle loss, concurrently normalizing mitochondrial function and reducing lipid peroxidation. Mechanistic profiling via RNA-seq reveals BM’s activation of PI3K/AKT/Nrf2 and suppression of ROS/p38 MAPK signaling pathway, mediating antioxidant responses and maintenance of mitochondrial homeostasis. The nanocomposite demonstrats superior biocompatibility in toxicity assays, outperforming conventional delivery systems. Our findings establish that BM has been established as a promising mitochondrial redox modulator with translational potential for sarcopenia and related age-associated pathologies.

Lactoferrin improves hepatic insulin resistance and pancreatic dysfunction in high-fat diet and streptozotocin-induced diabetic mice

Yafang Du,Deming Li,Jingsi Chen,Yun-Hong Li,Zixiang Zhang,Khemayanto Hidayat,Zhongxiao Wan,Jia-Ying Xu,Li-Qiang Qin

Lactoferrin (Lf) is an iron-binding glycoprotein with potentially beneficial biological functions. However, the interaction between Lf and type 2 diabetes mellitus (T2DM) remains unclear. We hypothesized that Lf would improve hepatic insulin resistance and pancreatic dysfunction in diabetic mice. Male C57BL/6J mice were fed a high-fat diet for 15 weeks and injected with streptozotocin (STZ) for 5 consecutive days to establish a T2DM model. One week after STZ injection, mice with ≥11.1 mmol/L fasting blood glucose concentration were considered T2DM mice. These mice received 0.5% or 2% Lf solution for another 12 weeks. Biochemical parameters were measured, and histopathological examination of the pancreas and liver was performed. Hepatic protein expression related to the insulin signalling pathway was also assessed. Diabetic mice showed insulin resistance and abnormal glucolipid metabolism. Lf decreased serum concentrations of glycated serum protein , fasting insulin, cholesterol, and triglyceride and increased liver insulin sensitivity . Hematoxylin-eosin staining showed that Lf reversed the abnormal pancreatic islets of diabetic mice. Lf improved pancreatic dysfunction by reducing oxidative stress and inflammation responses. Furthermore, Lf upregulated the protein expression of insulin receptor , insulin receptor substrate-1, glucose transporter 4 , phosphor phosphatidylinositol 3-kinase/phosphatidylinositol 3-kinase (PI3K), and phosphor protein kinase B/protein kinase B (AKT) in the liver. This study indicated that Lf supplementation improved hepatic insulin resistance and pancreatic dysfunction, possibly by regulating the PI3K/AKT signaling pathway in T2DM mice.

Synthesis and biological activity study of tanshinone I-pyridinium salt derivatives

Zhao Huimin,Wang Yuyang,Liu Zining,Lin Lin,Xiang Jiasi,Zhu Zihao,Yang Xiongli,Fang Yongsheng,Kong Lingmei,Li Yan

Natural product tanshinone I exhibits weak potency and poor drug-like properties, which have restricted its clinical development as an anticancer agent. Herein, twenty novel tanshinone I-pyridinium salt derivatives and a pyridinium salt precursor were designed and synthesized, and their antitumor activities were evaluated. Among these tanshinone I-pyridinium salts, compound a4 , bearing a 4-bromobenzoylmethyl substituent at the N -1 position of the pyridine ring, showed the most potent cytotoxicity against breast cancer (MDA-MB-231), hepatocellular carcinoma (HepG2), and prostate cancer (22RV1) cell lines, with IC 50 values of 1.40–1.63 μM. Preliminary mechanistic studies suggest that a4 targets PI3Kα with the IC 50 of 9.24 ± 0.20 μM and exerts effective inhibition of the phosphorylation of key PI3K/Akt/mTOR signaling proteins. Besides, a4 significantly downregulates the expression of the immune checkpoint protein PD-L1, indicating its potential to activate tumor immunity. These findings demonstrate that tanshinone I-pyridinium salt derivative a4 is a novel PI3Kα inhibitor, providing a solid foundation for further development of antitumor agents. Graphical

Montmorillonite-loaded magnesium alloy with photothermal and drug-enhanced anti-tumor and regulation of immune microenvironment for SVCS interventional therapy

Zhu Yi-Bing,Zang Yu-Fan,Yu Jia-Nan,Li Cheng-Yu,Jia Shao-Sheng,Liang Yu-Han,Bai Ling-Chuang,Li Bin,Li Jing-An,Chen Lan

Superior vena cava syndrome (SVCS) caused by lung cancer accounts for 75% of patients with SVCS, which is one of the common complications of tumors. Interventional therapy is currently the most effective approach to relieve obstruction, but existing stents cannot inhibit or eliminate tumors, requiring postoperative radiotherapy and chemotherapy that may lead to secondary obstruction. Based on the characteristics of the tumor microenvironment and the interlayer ion replaceable properties of the layered material-montmorillonite (MMT), the composite coating (MMT/Em/PDA) of emodin (Em)-loaded MMT and dopamine was constructed on the magnesium alloy by liquid phase ion exchange technology and hydrothermal technology. The in vitro and in vivo results showed that the modified samples showed excellent corrosion resistance, the drug loading through adsorption and complexation with Zn 2+ between MMT layers, and the drug-loaded samples possessed good pH and near-infrared response-controlled release drug performances. The MMT/Em/PDA sample exhibited an excellent photothermal conversion performance. Photothermal (PTT) synergistic drug therapy of samples could significantly promote the production of ROS in lung cancer cells damage mitochondria, and further inhibit cell adhesion, proliferation, and invasion by down-regulating PI3K-AKT and EMT signaling pathways, thereby causing tumor cell death. Furthermore, the multimodal therapies of samples promoted the repolarization of tumor-associated macrophages into the M1 phenotype to re-activate tumor immunity through activating the AKT-NF-κB signaling pathway. In normal tissues, they can significantly promote the M2 phenotype polarization to promote vascular tissue repair by inhibiting the AKT-NF-κB signaling pathway. This work helps to provide a new insight into designing the modified magnesium alloy. Graphical abstract

MicroRNA miR-106a-5p targets forkhead box transcription factor FOXC1 to suppress the cell proliferation, migration, and invasion of ectopic endometrial stromal cells via the PI3K/Akt/mTOR signaling pathway

Xinyue Zhou,Zhenyu Chen,Lipeng Pei,Jingli Sun

Emerging evidence has exhibited an obvious decreased expression of miR-106a-5p in the ectopic endometrial tissue of endometriosis (EMS) patients. Thus far, the pathophysiological function of miR-106a-5p in EMS is unknown. A previous study showed an increased FOXC1 expression in the ectopic endometrial tissue of patients with EMS. Moreover, we found that there was a binding site of miR-106a-5p on the 3ʹUTR of FOXC1 through bioinformatics predictions. Hence, we speculated that miR-106a-5p might affect the development of EMS via targeting FOXC1. We first showed a decreased level of miR-106a-5p and an increased level of FOXC1 mRNA in ectopic endometrial tissues compared with normal tissues. Functionally, we transfected ectopic endometrial stromal cells (ESCs) with miR-106a-5p mimics or NC mimics and indicated an inhibitory role of miR-106a-5p on ESC proliferation, invasion, and migration. Mechanistically, FOXC1 was found to be a target gene of miR-106a-5p. To confirm whether miR-106a-5p exerted an inhibitory activity in ESCs via targeting FOXC1, miR-106a-5p mimic was co-transfected into ESCs with the FOXC1-plasmid or vector. We found that FOXC1 overexpression evidently reversed the results caused by a miR-106a-5p mimic in ESCs. Additionally, our results demonstrated that miR-106a-5p mimic inhibited the expression of p-Akt and p-PI3K. Collectively, these results revealed that miR-106a-5p inhibited the proliferative, migratory, and invasive ability of ESCs via directly binding to FOXC1, likely through the suppression of the PI3K and its downstream signaling pathway, which offered a potential and novel therapeutic strategy for EMS treatment.

The ameliorating effects of Guizhi Fuling Wan combined with rosiglitazone in a rat ovarian model of polycystic ovary syndrome by the PI3K/AKT/NF-κB and Nrf2/HO-1 pathways

Yongju Ye,Weimei Zhou,Yuefang Ren,Jiali Lu,Aixue Chen,Ruiying Jin,Feilan Xuan