JOURNAL OF MOLECULAR HISTOLOGY
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2025
·Vol. 57
·期 1
·11
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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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高影响因子
CELL BIOCHEMISTRY AND BIOPHYSICS
·
2025
·
IF 2.5
Li Xia,Weng Shi-Qi,Li Qing-Hui,Ji Min,Zhou Yan,Xiao Qin,Luo Tao,Liu Zhao-Xia
Oxidative stress results in the apoptosis of ovarian granulosa cells (GCs) and premature ovarian failure (POF). Ginsenoside Rg1 possesses natural antioxidant and anti-apoptotic properties. However, the underlying mechanisms by which it regulates mitochondrial function in ovarian GCs remain unclear. To investigate the potential mechanism of ginsenoside Rg1 (Rg1) in mitigating oxidative stress, autophagy and apoptosis in POF. This study employed network pharmacology and in vitro experiments to identify the key targets and pathways associated with the therapeutic effects of Rg1 in the treatment of POF. An oxidative stress model was established using H₂O₂-treated KGN cells to validate the network pharmacology predictions in vitro. In the Rg1-treated group, cell viability was significantly improved, while the rate of apoptosis was reduced. Furthermore, Rg1 suppressed the production of reactive oxygen species and malondialdehyde, and increased the levels of glutathione and adenosine triphosphate. Additionally, Rg1 downregulated pro-apoptotic and mitophagy-related markers (Bax, Caspase-3, Parkin, PINK1) and upregulated Bcl-2, p-PI3K, p-AKT, and p-mTOR, suggesting involvement of the PI3K/AKT/mTOR signaling pathway. These findings suggest that Rg1 protects against H 2 O 2 -induced apoptosis in ovarian GCs by preserving mitochondrial function and inhibiting mitophagy. Graphical
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Nanomedicine
·
2021
·
IF 5.307
Chaoqi Li,Xiangbo Gou,Hui Gao
Aim: The authors aimed to develop Dox@Rg1 nanoparticles with decreased cardiotoxicity to expand their application in cancer. Materials & methods: Dox@Rg1 nanoparticles were developed by encapsulating doxorubicin (Dox) in a self-assembled Rg1. The antitumor effect of the nanoparticles was estimated using 4T1 tumor-bearing mice and the protective effect on the heart was investigated in vitro and in vivo. Results: Different from Dox, the Dox@Rg1 nanoparticles induced increased cytotoxicity to tumor cells, which was decreased in cardiomyocytes by the inhibition of apoptosis. The study in vivo revealed that the Dox@Rg1 nanoparticles presented a perfect tumor-targeting ability and improved antitumor effects. Conclusion: Dox@Rg1 nanoparticles could enhance the antitumor effects and decrease the cardiotoxicity of Dox.Lay abstractDoxorubicin (Dox) is a drug used to treat cancer; however, it can be toxic to the heart. In this study, researchers made nanoparticles containing Dox and a component of ginseng, a root similar to ginger. They tested the nanoparticles in mice with tumors. The nanoparticles appeared to gather at the tumor site in greater amounts than free Dox. In healthy mice, the nanoparticles gathered less in the heart than free Dox. This means that putting Dox into nanoparticles such as these could improve their anticancer effect and decrease harm to the heart.Graphical abstract
研究领域:
药学
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纳米技术
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肿瘤学
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心脏病学
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BIOCATALYSIS AND BIOTRANSFORMATION
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2025
·
IF 1.9
Yanho Hu,Yakun Shan,Yue Yang,Yudi Song,Yiming Li,Xi Wang,Ruining Zhang,Jun Zhao
Rare ginsenoside F1, a bioactive component of ginseng, possesses notable anti-tumour, anti-aging, and antioxidant properties; however, its low natural abundance and the difficulty of large-scale preparation limit its practical application. In this study, ginsenoside Rg1 was converted into rare ginsenoside F1 using a recombinant β-glucosidase (BgpA), BaBgl1A, and the products were analysed by thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC). The results demonstrated that BaBgl1A selectively hydrolysed the glucose moiety at the C-6 position of Rg1. The biotransformation conditions were optimised to pH 5.0, 45 °C, a substrate concentration of 2 mg/mL, and an enzyme loading of 2.0 U/mg. Under these conditions, the biotransformation was completed within 12 h with a biotransformation conversion of 98%, and the product structure was confirmed by matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOF-MS). Molecular docking analysis revealed that hydrogen bonding was the dominant interaction between Rg1 and BaBgl1A, with an optimal binding energy of −7.9 kcal/mol. Rg1 bound to the active site of BaBgl1A through three key amino acid residues (ALA-178, SER-43, and SER-354), which facilitated the hydrolysis of the outer Glc residue at the C-6 position. These findings provide a novel strategy for the efficient large-scale preparation of rare ginsenoside F1.
研究领域:
生物化学
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生物技术
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酶学
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天然产物化学
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制药生物技术
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高影响因子
REPRODUCTION
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2026
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IF 3.4
Li Yan,Chang Zixin,Zhuang Chenyu,Zhu Shenfan,Hou Jiong,Huang Tiantian,Yang Niuniu,Wang Haibo,Liu Yanqing
Cyclophosphamide (CP) is a widely prescribed chemotherapeutic and immunosuppressive agent known to cause significant reproductive toxicity. Ginseng effectively counteracts CP-induced reproductive toxicity, exhibiting pharmacological effects that resemble enhanced orexin signaling. In this study, molecular docking identified ginsenoside Rg1 as the candidate with the highest binding affinity for orexin receptor 1 (OX1R). In CP-treated male mice, Rg1 dose-dependently ameliorated reproductive toxicity, as evidenced by improved sexual behavior, sperm motility and DNA integrity, serum testosterone levels, and testicular histology. These protective effects were significantly attenuated by co-administration of the OX1R antagonist SB-334867. Notably, serum orexin-A levels did not differ significantly across all experimental groups, indicating that Rg1 acts directly on testicular OX1R rather than by elevating circulating orexin-A. Mechanistically, Rg1 restored testicular PI3K/AKT phosphorylation in an OX1R-dependent manner and preserved GLUT3 and GLUT8 immunoreactivity in germ cells. These findings demonstrate that Rg1 protects against CP-induced reproductive toxicity through OX1R-dependent activation of the PI3K/AKT pathway and maintenance of glucose transporter-mediated metabolism. Thus, OX1R represents a crucial mechanistic node, and Rg1 is a promising adjunct therapy to mitigate chemotherapy-related male infertility.
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高影响因子
NEUROPEPTIDES
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2025
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IF 2.7
Qiankun Quan,Xinxin Ma,JianJun Feng,Wanni Li,Xi Li
Alzheimer's disease (AD) is a neurodegeneration driven by beta-amyloid (Aβ) deposits in the brain involving autophagy dysfunction. Ginsenoside Rg1, a pharmacologically active compound found in ginseng, has possible therapeutic effects for AD. This study discovered that FGR proto-oncogene (FGR) was a therapeutic target of Rg1 in AD and it was possibly involved in autophagy. C57BL/6 J mice were injected with 5 μL (1 μg/mL) Aβ 1–42 in the right lateral ventricle to establish an AD model. AD mouse hippocampus had high FGR expression. Intragastrically administered Rg1 (40 mg/kg) decreased FGR protein levels in AD mice's hippocampus and improved memory function in AD mice. Both sides of the mice hippocampal fissure were administered with 2 μL lentiviral particles (1 × 10 7 TU) containing FGR overexpression plasmids. FGR overexpression rendered Rg1 ineffectual in restoring memory function and reducing hippocampal neuron damage. We injected 2 μL lentiviral particles (1 × 10 7 TU/mL) containing short hairpin RNA plasmids targeting FGR to the mice hippocampal fissures. FGR knockdown improved spatial memory function of AD mice, reduced hippocampal neuron apoptosis, and prevented Aβ accumulation. HT22 cells were transfected with small interfering RNA targeting FGR. FGR knockdown increased the viability of Aβ 1–42 treated HT22 cells. BACE1 and LC3II/I protein levels were decreased and p62 and SIRT1 were increased in AD mice and cells with FGR knockdown. LC3 was down-regulated after inhibiting FGR expression in Aβ 1–42 treated hippocampal neurons. In conclusion, Rg1 exerts anti-AD functions by targeting FGR and downregulating its expression.
研究领域:
神经生物学
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药理学
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PubMed
高影响因子
Frontiers in Bioengineering and Biotechnology
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2020
·
IF 3.644
Luo Peng,Yu Lan,Lin Qiang,Wang Changde,Yang Dazhi,Tang Shuo
The aim of this study was to prepare a promising biomaterial for bone tissue repair and regeneration. The Strontium – calcium sulfate hemihydrate (Sr-α-CaS) scaffold incorporating gelatin microspheres (GMs) encapsulated with Ginsenoside Rg1 (Rg1) was designed. The scaffolds of Rg1/GMs/Sr-α-CaS showed sustained release of Rg1, good biocompatibility and ability of promoting osteogenic differentiation and angiogenesis in vitro. The scaffolds were implanted into animal model of cranial bone defect to characterize bone tissue repair and regeneration in vivo. From the images of Micro-CT, it was obvious that the most bone tissue was formed in Rg1/GMs/Sr-α-CaS group in 12 weeks. New bone structure, collagen and mineralization were analyzed with staining of HE, Masson and Safranin O-Fast green and showed good distribution. The expression of osteocalcin of Rg1/GMs/Sr-α-CaS indicated new bone formation in defect site. The results revealed that synergy of Rg1 and Sr showed the best effect of bone repair and regeneration, which provided a new candidate for bone defect repair in clinic.
研究领域:
生物材料学
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组织工程学
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骨科医学
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JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
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2015
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IF 0.913
Dan Lu,Li-Hong Zhu,Xiao-Ming Shu,Chan-Juan Zhang,Jia-Yi Zhao,Ren-Bin Qi,Hua-Dong Wang,Da-Xiang Lu
Microglial activation plays an important role in neurodegenerative diseases associated with oxidative stress. tert-Butyl hydroperoxide (t-BHP), an analog of hydroperoxide, mimics the oxidative damage to microglial cells. It has been reported that ginsenoside Rg1 (G-Rg1), an active ingredient of Panax ginseng, has anti-stress and anti-inflammatory properties. The present study aims to investigate the ability of G-Rg1 to decrease the t-BHP-mediated cell damage of BV2 microglial cells. We performed flow cytometry assays to facilitate the detection of reactive oxygen species as well as Western blotting analyses and immunofluorescence assays using specific antibodies, such as antibodies against phospho-mitogen-activated protein kinases (p-MAPKs), phospho-nuclear factor-κB (p-NF-κB), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X (Bax), Caspase-3, autophagy marker light chain 3 (LC3), and Becline-1. We found that treatment with 50 μM G-Rg1 protected microglial cells against oxidative damage induced by 10 μM t-BHP.
研究领域:
神经科学
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药理学
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细胞生物学
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Frontiers in Immunology
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2022
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IF 8.786
Hao Cheng,Juan Liu,Dandan Zhang,Jing Wang,Yuzhu Tan,Wuwen Feng,Cheng Peng
Ulcerative colitis (UC) is a chronic and recurrent inflammatory disorder in the gastrointestinal tract. Here, we examined the pharmacological effects of ginsenoside Rg1, a natural compound with low bioavailability, on the acute experimental colitis mice induced by dextran sulfate sodium (DSS) and explored underlying mechanisms. Acute UC was induced in C57BL/6 mice by 2.5% DSS for 7 days, meanwhile, 2 mg/10 g b.w. ginsenoside Rg1 was administrated to treat the mice. Body weight, colon length, colon tissue pathology, and colon tissue inflammatory cytokines were assessed. The composition structure of gut microbiota was profiled using 16s rRNA sequencing. Global metabolomic profiling of the feces was performed, and tryptophan and its metabolites in the serum were detected. The results showed that Rg1 significantly ameliorated DSS-induced colonic injury and colonic inflammation. In addition, Rg1 also partly reversed the imbalance of gut microbiota composition caused by DSS. Rg1 intervention can regulate various metabolic pathways of gut microbiota such as valine, leucine, and isoleucine biosynthesis and vitamin B6 metabolism and the most prominent metabolic alteration was tryptophan metabolism. DSS decreased the levels of tryptophan metabolites in the serum, including indole-3-carboxaldehyde, indole-3-lactic acid, 3-indolepropionic acid, and niacinamide and Rg1 can increase the levels of these metabolites. In conclusion, the study discovered that Rg1 can protect the intestinal barrier and alleviate colon inflammation in UC mice, and the underlying mechanism is closely related to the regulation of gut microbiota composition and microbial tryptophan metabolism.Keywords: ginsenoside Rg1, gut microbiota, tryptophan, metabolomics, ulcerative colitis
研究领域:
药理学
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免疫学
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微生物学
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代谢学
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高影响因子
Journal of Ginseng Research
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2022
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IF 5.735
Ye-ying Jiang,Rong-yun Wei,Kai Tang,Zhen Wang,Ning-hua Tan
Background Mechanisms of synaptic plasticity in retinal ganglion cells (RGCs) are complex and the current knowledge cannot explain. Growth and regeneration of dendrites together with synaptic formation are the most important parameters for evaluating the cellular protective effects of various molecules. The effect of ginsenoside Rg1 (Rg1) on the growth of retinal ganglion cell processes has been poorly understood. Therefore, we investigated the effect of ginsenoside Rg1 on the neurite growth of RGCs. Methods Expression of proteins and mRNA were detected by Western blot and qPCR. cAMP levels were determined by ELISA. In vivo effects of Rg1 on RGCs were evaluated by hematoxylin and eosin, and immunohistochemistry staining. Results This study found that Rg1 promoted the growth and synaptic plasticity of RGCs neurite by activating the cAMP/PKA/CREB pathways. Meanwhile, Rg1 upregulated the expression of GAP43, Rac1 and PAX6, which are closely related to the growth of neurons. Meantime, H89, an antagonist of PKA, could block this effect of Rg1. In addition, we preliminarily explored the effect of Rg1 on enhancing the glycolysis of RGCs, which could be one of the mechanisms for its neuroprotective effects. Conclusion Rg1 promoted neurite growth of RGCs through cAMP/PKA/CREB pathways. This study may lay a foundation for its clinical use of optic nerve diseases in the future.
研究领域:
神经科学
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药理学
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分子生物学
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细胞生物学
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高影响因子
MICROSCOPY RESEARCH AND TECHNIQUE
·
2023
·Vol. 86
·期 8
·1037-1046
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IF 2.5
Shengli Zhang,Zhankun Weng,Zuobin Wang,Bowei Wang,Yi Zeng,Jiani Li,Cuihua Hu
Alcoholic liver disease is an important cause of death worldwide. Hepatocyte apoptosis is commonly observed in alcoholic liver disease. In this study, we investigated the effect of ginsenoside Rg1 (G-Rg1), an organic component of ginseng, on the alcohol-induced morphological and biophysical properties of hepatocytes. Human hepatocytes (HL-7702) were treated in vitro with alcohol and G-Rg1. The cell morphology was observed using scanning electron microscopy. Cell height, roughness, adhesion, and elastic modulus were detected using atomic force microscopy. We found that alcohol significantly induced hepatocyte apoptosis, whereas G-Rg1 attenuated the alcohol-induced hepatocyte damage. Scanning electron microscopy revealed that alcohol-induced significant morphological changes in hepatocytes, including decreased cell contraction, roundness, and pseudopods, whereas G-Rg1 inhibited these negative changes. Atomic force microscopy revealed that alcohol increased the cell height and decreased the adhesion and elastic modulus of hepatocytes. Following treatment with G-Rg1, the cell height, adhesion, and elastic modulus of alcohol-injured hepatocytes were all similar to those of normal cells. Thus, G-Rg1 can attenuate the alcohol-induced damage to hepatocytes by modulating the morphology and biomechanics of the cells. Research Highlights In this study, the morphological characteristics of hepatocytes were observed using SEM. The changes in hepatocyte three-dimensional images and biomechanical action caused by alcohol and G-Rg1 were examined at the nanoscale using AFM under near-physiological conditions. Alcohol-induced hepatocytes showed abnormal morphology and biophysical properties. G-Rg1 attenuated the alcohol-induced damage to hepatocytes by modulating the morphology and biomechanics of the cells.
研究领域:
药理学
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细胞生物学
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DOI
PubMed
高影响因子
MICRON
·
2023
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IF 2.4
Shengli Zhang,Yi Zeng,Bowei Wang,Jiani Li,Cuihua Hu,Zhankun Weng,Zuobin Wang
The quantification of mitochondrial morphology and mechanical properties is useful for the diagnosis and treatment of mitochondrial and alcoholic liver disease. In this study, the effects of ginsenoside Rg1 (G-Rg1) on the morphology and mechanical properties of mitochondria that had suffered alcohol-induced damage were investigated under near-physiological conditions. Additionally, the morphological and mechanical properties of mitochondria were quantified through atomic force microscopy . Atomic force microscopy revealed that alcohol-induced significant morphological changes in mitochondria. Compared with that of the mitochondria of normal hepatocytes, the average surface area of the damaged mitochondria was found to have increased significantly under the influence of alcohol. Furthermore, the mitochondrial area tended to be normal under the action of G-Rg1, whilst other parameters (length, width and perimeter) were significantly different from those of the mitochondria with the alcohol-induced damage. Simultaneously, alcohol significantly reduced the adhesion and elastic modulus of mitochondria, whilst the adhesion and elastic modulus of mitochondria in the G-Rg1 treatment group were closer to the values of normal mitochondria. This study overall showed that G-Rg1 could effectively alleviate the swelling and anomalous mechanical properties of mitochondria induced by alcohol.
研究领域:
医学
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细胞生物学
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药理学
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高影响因子
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