MOLECULES
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2026
·Vol. 31
·期 15
·2559
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IF 5.1
Yiyao Gong,Jie Zhang,Tingting Wang,Xiang Li,Hao Wang,Li Ren
Chronic exposure to lead (Pb) represents a persistent environmental hazard that can impair hippocampal integrity and cognitive function, while effective protective strategies remain limited. Ginsenoside Rg1 is an important bioactive constituent derived fromPanax ginsengand has been reported to possess antioxidant and neuroprotective activities; however, its involvement in Pb-triggered ferroptosis-associated neuronal damage remains unclear. In the present study, a male C57BL/6J mouse model of subchronic lead acetate exposure and a lead-exposed HT22 cell model were established. Behavioral and histopathological changes were assessed, followed by analysis of inflammatory responses, oxidative stress, ferroptosis-related alterations, and Nrf2-associated signaling. Rg1 improved cognitive performance and attenuated hippocampal neuronal loss, neuroinflammatory activation, oxidative injury, and ferroptosis-related alterations, including ferrous ion accumulation and mitochondrial damage. Consistently, Rg1 restored SLC7A11/xCT and GPX4 expression and enhanced Nrf2-associated antioxidant signaling, whereas the Nrf2 inhibitor ML385 weakened the Rg1-induced increases in nuclear Nrf2, NQO1, and GPX4. Collectively, these findings indicate that Rg1 alleviates lead-induced neurotoxicity and support the involvement of Nrf2 signaling in the regulation of oxidative stress and ferroptosis-related injury. These findings provide experimental evidence supporting further preclinical investigation of Rg1 and its Nrf2-associated neuroprotective mechanisms in Pb-induced neuronal injury.
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Journal of Inflammation Research
·
2026
·
IF 4.6
Yuandi Huang,Dexi Su,Jinshan You,Yu Zhang,Zeyu Li,Hao Liu,Qiang Fang,Yi Zhi,Weibing Li
Objective: This study aimed to investigate the protective effects and underlying mechanisms of ginsenoside Rg1 in renal ischemia-reperfusion injury, with a focus on oxidative stress, macrophage polarization, and prevention of early profibrotic responses.Methods: An in vivo mouse renal IRI model and an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model using RAW264.7 macrophages were employed to evaluate renal function, oxidative stress, macrophage polarization, pro-inflammatory cytokine expression, and activation of the STING-NF-κB signaling pathway.Results: Rg1 alleviated renal tubular injury, preserved renal function, and reduced oxidative stress and tubular apoptosis in IRI mice. It also inhibited systemic leukocyte activation and local inflammatory cell infiltration. In vitro, Rg1 suppressed OGD/R-induced M1 polarization, pro-inflammatory cytokine expression, and ROS accumulation, and inhibited activation of the STING-NF-κB signaling pathway. Additionally, Rg1 attenuated early renal fibrosis post-IRI.Conclusion: Rg1 exerts dual protective effects against renal IRI by reducing oxidative stress and restraining macrophage-mediated inflammation. These findings highlight Rg1 as a promising therapeutic candidate for ischemic kidney injury.
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JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
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2026
·
IF 1.6
Yan Wu,Juan Du,Xiao-Lei Zhang
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor dysfunction and neuroinflammation. This study investigated the neuroprotective effects of ginsenoside Rg1 in an MPTP-induced PD mouse model. Behavioral tests showed that Rg1 significantly improved motor coordination and emotional behavior. Rg1 also stabilized monoamine neurotransmitter levels in the cortex, striatum, and substantia nigra, and reduced the expression of inflammatory cytokines. Histological and molecular analyses further demonstrated that Rg1 alleviated nigrostriatal injury. Mechanistically, Rg1 increased PPARγ expression and inhibited MAPK signaling activation. These findings suggest that Rg1 ameliorates PD-like pathology through modulation of neuroinflammation and neurotransmitter homeostasis.
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MACROMOLECULAR BIOSCIENCE
·
2025
·
IF 4.1
Zhongke Wang,Long Chen,Yunan Zhang,Yang Zhou,Xiaorong Lan,Ling Guo
The healing of skin wounds is a complex process, the outcome of which is determined by a combination of factors. Adverse factors, such as infection, chronic inflammatory infiltration, and poor vascularity, can impede the healing process, significantly reducing the quality of life. The primary method of promoting wound healing is pharmacotherapy; however, pharmacotherapy alone has several disadvantages, including poor release control, a short half-life, and low bioavailability. Therefore, designing materials with well-controlled release properties and increased bioavailability is important. In this study, ginsenoside Rg1 was incorporated into a photo-crosslinking (LAP/UV) and chemical cross-linking (EDC-mediated amide bond formation) hydrogel synthesized from hyaluronic acid methacrylamide and silk fibroin to enhance drug activity. The resulting composite hydrogel has good hydrophilicity, mechanical properties, and stability, enabling the slow release of Rg1 for up to 14 days. In addition, in vitro experiments revealed that the composite hydrogel exhibits good biocompatibility (Cell viability > 90%) and promotes angiogenesis and maturation. In subsequent in vivo experiments, the composite hydrogel showed a good ability to promote vascular regeneration ( p < 0.0001) and collagen deposition. Finally, Western blotting and qPCR analysis of rat tissues showed that the drug-loaded composite hydrogel group possessed anti-inflammatory and tissue healing abilities. This suggests that the composite hydrogel developed shows great promise in promoting wound healing.
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JOURNAL OF MOLECULAR HISTOLOGY
·
2025
·Vol. 57
·期 1
·11
·
IF 2.2
Wang Huan,Han Jian,Li Lin,Li Yan,Yang Jun,Qiu Wangzhong,Yao Liuhua,Zhou Jianjun
Background Shen-Ling-Bai-Zhu-San (SLBZS), a classic formula, shows excellent therapeutic effects on ulcerative colitis (UC). However, its pharmacological mechanism remains unclear. This study aims to explore the SLBZS’s mechanism on mitophagy and inflammation in UC. Method The UC rat model was constructed using 4.5% DSS. The in vivo effects of SLBZS on mitophagy and inflammation were investigated by combining the autophagy inhibitor 3-MA. Caco-2 cells were co-treated with DSS and LPS to mimic UC-like inflammatory. The main active components of SLBZS were analyzed by HPLC. Combined with 3-MA or knockdown of Nrf2, the mechanism by which the main active component of SLBZS Ginsenoside Rg1 affected oxidative stress and inflammation was investigated. Results SLBZS administration alleviated colonic injury in UC rats, reduced disease activity index, increased colonic length, promoted ZO-1, occludin, LGR5, and MUC-2 expressions, decreased ROS production, MDA level, and TNF-α, IL-1β, IL-6, IL-17, and p62 expressions, increased SOD and GSH-PX levels, mitochondrial membrane potential, and PINK1, TOM20, Nrf2, LC3, PINK1, and Parkin levels. 3-MA prevented this phenomenon, indicating that SLBZS inhibited UC inflammation by enhancing mitophagy. The molecular docking results showed that Ginsenoside Rg1 bound to Nrf2. The interaction between Nrf2 and PINK1 was confirmed. Mechanistically, Ginsenoside Rg1 relieved oxidative stress and inflammation in UC-like Caco-2 cell model by Nrf2/PINK1/Parkin pathway-mediated mitophagy. Conclusion Our results indicated that the Ginsenoside Rg1 promoted Nrf2/PINK1/Parkin pathway-mediated mitophagy, thereby alleviating UC, suggesting that Ginsenoside Rg1 could serve as a promising therapeutic agent for clinical UC, with the Nrf2/ PINK1/Parkin axis representing a potential strategy.
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JOURNAL OF SEPARATION SCIENCE
·
2016
·Vol. 40
·期 3
·744-752
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IF 2.741
Qing-Shan Liu,Jie He,Wen-Bin Zhou,Yu-Long Gu,Huoqiang Huang,Ke-Qin Li,Xiao-Ying Yin
Ginsenoside Rg1 is a valuable bioactive molecule but its high polarity and low concentration in complex mixtures makes it a challenge to separate Ginsenoside Rg1 from other saponins with similar structures, resulting in low extraction efficiency. The successful development of effective Rg1 molecularly imprinted polymers that exhibit high selectivity and adsorption may offer an improved method for the enrichment of active compounds. In this work, molecularly imprinted polymers were prepared with two different methods, precipitation polymerization or surface imprinted polymerization. Comparison of the adsorption abilities showed higher adsorption of the surface molecularly imprinted polymers prepared by surface imprinted polymerization, 46.80 mg/g, compared to the 27.74 mg/g observed for the molecularly imprinted polymers prepared by precipitation polymerization. Therefore, for higher adsorption of the highly polar Rg1, surface imprinted polymerization is a superior technique to make Rg1 molecularly imprinted polymers. The prepared surface molecularly imprinted polymers were tested as a solid-phase extraction column to directionally enrich Rg1 and its analogues from ginseng tea and total ginseng extracts. The column with surface molecularly imprinted polymers showed higher enrichment efficiency and better selectivity than a C 18 solid-phase extraction column. Overall, a new, innovative method was developed to efficiently enrich high-polarity bioactive molecules present at low concentrations in complex matrices.
研究领域:
药理学
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分离科学
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材料科学
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International Journal of Nanomedicine
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2022
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IF 7.033
Wei Shang,Xin Zhao,Fan Yang,Dongyi Wang,Le Lu,Zihan Xu,Zhiming Zhao,Hui Cai,Junyi Shen
Background: Compared with traditional drugs, nanomaterial drugs have the benefits of improving the solubility, bioavailability, and absorption rate of insoluble drugs. Nanoporous complexes can increase the efficiency with which drugs can penetrate the blood-brain barrier and reach target organs. Ginsenoside Rg1 is an effective drug that promotes angiogenesis. Ginsenoside Rg1 composite nanoparticles were employed to induce the expression of several key epigenetic enzymes and then activate the VEGF and Notch pathways after the onset of ischemic brain lesions. Methods: We constructed nanoparticles to fully encapsulate the therapeutic drug (ginsenoside Rg1), which can be transferred into brain tissue via the receptor-mediated transfer of drug-encapsulated nanoparticles. Evaluation of the therapeutic effect of ginsenoside Rg1 complex nanovesicles (CNV) was performed by in vitro and in vivo experiments. Real-time polymerase chain reaction (RT- PCR), Western blot, immunohistochemistry staining (IHC), and Co-immunoprecipitation (co-IP) were employed to screen for epigenetic enzymes with an up-regulated expression post ginsenoside Rg1-CNV intervention. RNA sequencing, shRNA knockdown, and chromatin Immunoprecipitation (ChIP) sequencing were performed to detect the target genes of ginsenoside Rg1-CNV that regulate angiogenesis. Then, bioinformatic analysis was performed to investigate the mechanism of action of epigenetic modifying enzymes in regulating target genes. Results: The average of the synthesized ginsenoside Rg1-CNV was 203.78±6.83 nm, the polydispersion index was 0.135±0.007, and the Zeta potential was 23.13±1.65 mV. Through in vivo and in vitro experiments, we found that it promotes the proliferation, migration, and tubular formation of brain microvascular endothelial cells (BMECs). Meanwhile, the intervention of ginsenoside Rg1-CNV promoted the demethylation of H3K27me3 within the promoter region of VEGF-A and Jagged1 genes and reduced the H3K27me3 modification within this region. Conclusion: The ginsenoside Rg1 nanoparticles may be an available blood-brain barrier penetrating agent for ischemic stroke.
研究领域:
药理学
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神经科学
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分子生物学
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表观遗传学
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Experimental and Therapeutic Medicine
·
2023
·Vol. 27
·期 1
·1-13
·
IF 2.7
Qiankun Quan,Xinxin Ma,Ming Li,Xi Li,Haifeng Yuan
β‑Amyloid peptide (Aβ) deposition in the brain is an important pathological change in Alzheimer's disease (AD). Insulin‑degrading enzyme (IDE), which is regulated transcriptionally by peroxisome proliferator‑activated receptor γ (PPARγ), is able to proteolyze Aβ. One of the members of the MAPK family, ERK, is able to mediate the phosphorylation of PPARγ at Ser112, thereby inhibiting its transcriptional activity. Ginsenoside Rg1 is one of the active ingredients in the natural medicine ginseng and has inhibitory effects on Aβ production. The present study was designed to investigate whether ginsenoside Rg1 is able to affect the regulation of PPARγ based on the expression of its target gene, IDE, and whether it is able to promote Aβ degradation via inhibition of the ERK/PPARγ phosphorylation pathway. In the present study, primary cultured rat hippocampal neurons were treated with Aβ1‑42, ginsenoside Rg1 and the ERK inhibitor PD98059, and subsequently TUNEL staining was used to detect the level of neuronal apoptosis. ELISA was subsequently employed to detect the intra‑ and extracellular Aβ1‑42 levels, immunofluorescence staining and western blotting were used to detect the translocation of ERK from the cytoplasm to the nucleus, immunofluorescence double staining was used to detect the co‑expression of ERK and PPARγ, and finally, western blotting was used to detect the phosphorylation of PPARγ at Ser112 and IDE expression. The results demonstrated that ginsenoside Rg1 or PD98059 were able to inhibit primary cultured hippocampal neuron apoptosis induced by Aβ1‑42 treatment, reduce the levels of intra‑ and extraneuronal Aβ1‑42 and inhibit the translocation of ERK from the cytoplasm to the nucleus. Furthermore, administration of ginsenoside Rg1 or PD98059 resulted in attenuated co‑expression of ERK and PPARγ, inhibition of phosphorylation of PPARγ at Ser112 mediated by ERK and an increase in IDE expression. In addition, the effects when PD98059 to inhibit ERK followed by treatment with ginsenoside Rg1 were found to be more pronounced than those when using PD98059 alone. In conclusion, ginsenoside Rg1 was demonstrated to exert neuroprotective effects on AD via inhibition of the ERK/PPARγ phosphorylation pathway, which led to an increase in IDE expression, the promotion of Aβ degradation and the decrease of neuronal apoptosis. These results could provide a theoretical basis for the clinical application of ginsenoside Rg1 in AD.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2026
·
IF 8
Rucui Yu,Yan Zhang,Ruiying Wu,Jingwei Xu
Objective Mitochondrial dysfunction and dysregulated cell death are key drivers of diabetic kidney disease (DKD) progression. This study aimed to construct CD44-targeted chitosan (Cs) nanoparticles encapsulating ginsenoside Rg1 (CD44-Cs@Rg1) for targeted delivery, and to evaluate their ability to regulate autophagy, pyroptosis, and mitochondrial function in DKD. Methods CD44-Cs@Rg1 nanoparticles were synthesized using a covalent modification strategy. Their targeting uptake, effects on GSDMD-mediated pyroptosis, autophagic flux, and energy metabolism were systematically evaluated in renal tubular epithelial cells under high-glucose (HG) conditions and in DKD mouse models. Mitochondrial function was assessed by Western blotting, immunostaining, MitoSOX, JC-1, and ATP assays. Transcriptomic profiling and pharmacological interventions were applied to elucidate the involvement of the AMPK/mTOR signaling axis. Results CD44-Cs@Rg1 nanoparticles were efficiently internalized by renal tubular epithelial cells, significantly reducing pyroptosis while restoring autophagic flux through AMPK activation and mTOR inhibition. These effects improved mitochondrial membrane potential, reduced reactive oxygen species accumulation, and enhanced ATP production. In vivo , CD44-Cs@Rg1 treatment markedly ameliorated renal dysfunction and histopathological injury in DKD mice. Transcriptomic and protein-level analyses consistently revealed enrichment of pathways related to AMPK signaling, autophagy, and energy metabolism. Conclusion CD44-targeted Cs nanoparticles enable precise delivery of ginsenoside Rg1 to renal tubular cells in DKD, restoring mitochondrial homeostasis and regulating autophagy–pyroptosis balance via the AMPK/mTOR axis. This nanotherapeutic platform demonstrates strong translational potential for DKD treatment.
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PHYTOTHERAPY RESEARCH
·
2024
·
IF 6.1
Taiping Li,Yougang Zhang,Rong Dong,Wenjie Bi,Songsong Wang,Kewu Zeng,Liwen Han
American ginseng (AG) has been reported to have anti-inflammatory effects in many diseases, but the key molecules and mechanisms are unclear. This study aims to evaluate the anti-inflammatory mechanism of AG and identify the key molecules by in vivo and in vitro models. Zebrafish was employed to assess the anti-inflammatory properties of AG and the compounds. Metabolomics was utilized to identify potential anti-inflammatory molecules in AG, while molecular dynamics simulations were conducted to forecast the interaction capabilities of these compounds with inflammatory targets. Additionally, macrophage cell was employed to investigate the anti-inflammatory mechanisms of the key molecules in AG by enzyme-linked immunosorbent assay and western blotting. Seven potential anti-inflammatory molecules were discovered in AG, with ginsenoside Rg1, ginsenoside Rs3 (G-Rs3), and oleanolic acid exhibiting the strongest affinity for signal transducer and activator of transcription 3. These compounds demonstrated inhibitory effects on macrophage migration in zebrafish models and the ability to regulate ROS levels in both zebrafish and macrophages. The cell experiments found that ginsenoside Rg1, ginsenoside Rs3, and oleanolic acid could promote macrophage M2/M1 polarization ratio and inhibit phosphorylation overexpression of signal transducer and activator of transcription 3. This study revealed the key anti-inflammatory molecules and mechanisms of AG, and provided new evidence of anti-inflammatory for the scientific use of AG.
研究领域:
药理学
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免疫学
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分子生物学
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生物化学
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ACS Applied Materials & Interfaces
·
2023
·
IF 9.5
Tianqi Shi,Penghui Wang,Yanhan Ren,Wenjie Zhang,Juping Ma,Shuang Li,Xiaoyan Tan,Bo Chi
Remodeling the conductive zone to assist normal myocardial contraction and relaxation during myocardial fibrosis has become the primary concern of myocardial infarction (MI) regeneration. Herein, we report an unbreakable and self-recoverable hyaluronic acid conductive cardiac patch for MI treatment, which can maintain structural integrity under mechanical load and integrate mechanical and electrical conduction and biological cues to restore cardiac electrical conduction and diastolic contraction function. Using the free carboxyl groups and aldehyde groups in the hydrogel system, excellent adhesion properties are achieved in the interface between the myocardial patch and the tissue, which can be closely integrated with the rabbit myocardial tissue, reducing the need for suture. Interestingly, the hydrogel patch exhibits sensitive conductivity (ΔR/R0 ≈ 2.5) for 100 cycles and mechanical stability for 500 continuous loading cycles without collapse, which allows the patch to withstand mechanical damage caused by sustained contraction and relaxation of the myocardial tissue. Moreover, considering the oxidative stress state caused by excessive ROS in the MI area, we incorporated Rg1 into the hydrogel to improve the abnormal myocardial microenvironment, which achieved more than 80% free radicalscavenging efficiency in the local infarcted region and promoted myocardial reconstruction. Overall, these Rg1-loaded conductive hydrogels with highly elastic fatigue resistance have great potential in restoring the abnormal electrical conduction pathway and promoting the myocardial microenvironment, thereby repairing the heart and improving the cardiac function.
研究领域:
生物医学工程
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组织工程
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心脏病学
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材料科学
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JOURNAL OF SEPARATION SCIENCE
·
2021
·Vol. 44
·期 7
·1552-1563
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IF 3.645
Rui-Jia Fu,Wen-Xiao Wang,Hui-Juan Tao,Mei Wang,Yan-Yan Chen,Huan Gao,Shi-Jun Yue,Yu-Ping Tang
Danqi tablet composed of the dried roots of Salvia miltiorrhiza and Panax notoginseng is a well-known Chinese patent medicine commonly used for the treatment of cardio-cerebrovascular diseases such as coronary heart disease and myocardial ischemia. Numerous chemical constituents belonging to S. miltiorrhiza and P. notoginseng were detectable in Danqi tablet. Here, we established and validated a rapid and sensitive ultra-performance liquid chromatography coupled with triple quadrupole mass spectrometry method for simultaneous quantification of 23 components in Danqi tablet and then successfully applied to assay 12 batches of samples from ten manufacturers. Our results demonstrated that the contents of 23 components in 12 batches of Danqi tablets varied significantly and their quality indeed existed differently based on the principal component analysis. According to the quantitative data and the loading plot of principal component analysis, five abundant compounds in Danqi tablet were selected as characteristic chemical markers possibly responsible for the quality assessment. Among them, salvianolic acid B and ginsenoside Rg 1 were further chosen to be combined at 2:5 ratio to evaluate the anti-thrombotic activity on phenylhydrazine-induced zebrafish heart thrombosis model. Expectedly, this component combination increased the heart red blood cells intensity compared with the model group and the median effective concentration was 123.4 µg/mL, suggestive of its well anti‑thrombotic effect. This study contributed to the quantitative evaluation of Danqi tablet and indicated the combination of salvianolic acid B and ginsenoside Rg 1 may be capable of reflecting the effect of Danqi tablet, thereby providing a reference for further investigations on the improvement of quality control and clinical application of Danqi tablet.
研究领域:
药理学
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分析化学
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中药学
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生物化学
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危险品化学品经营许可证（带存储）