Journal of Inflammation Research
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2026
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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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高影响因子
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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高影响因子
Scientific Reports
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2025
·Vol. 15
·期 1
·1-13
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IF 3.9
Fan Xinyu,Zhang Ying,Li Xinyu,Ding Junhui,Huang Jiaolong,Lian Kai,Duan Peng,Hu Chunhui,Xu Junchang
In this study, the effects of Ginsenoside Rg1 (Rg1), the primary bioactive constituent of Panax ginseng roots, on glucocorticoid-induced osteoporosis (GIOP) were examined using a zebrafish model, with a focus on elucidating its underlying mechanisms. Our findings demonstrated that Rg1 treatment inhibited osteoporosis induced by methylprednisolone (PN), as evidenced by increased mineralisation area and integrated optical density in the spine and skull of zebrafish larvae. Rg1 reduced the expression of bglap (an osteogenic marker gene) and increased the expression of traf (an osteoclast marker gene) compared with the PN group. Behavioural analysis revealed that Rg1 alleviated PN-induced hypoactivity, resulting in enhanced motion speed. Furthermore, transcriptome analysis identified 383 genes reversed by Rg1 treatment, with significant enrichment in skeletal system development. KEGG analysis indicated that Rg1 influenced several signalling pathways primarily involved in retinol, fat, protein and lipid metabolism. Several genes related to skeletal system development and retinol metabolism were validated by qRT-PCR. In summary, this study provides scientific evidence for the potential mechanisms of Rg1 in the therapeutic intervention of GIOP, highlighting its promise as a potential pharmacological agent for the prevention and treatment of osteoporosis.
研究领域:
药理学
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分子生物学
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生物信息学
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内分泌学
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发育生物学
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代谢学
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PubMed
高影响因子
JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
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2026
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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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高影响因子
Oncotarget
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2017
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IF 5.168
Chen Zhu,Yi Wang,Hua Liu,Haiman Mu,Yue Lu,Jiayi Zhang,Jianhua Huang
Although Ginsenoside Rg1 has been reported to have protective cardiac effects, its effects on cardiac toxicity induced by doxorubicin needs to be studied. The present study investigated the effects of oral administration of Rg1 on the heart in mice treated with doxorubicin and found improved fractional shortening and ejection fraction of the heart and decreased cardiac apoptosis in mice treated with doxorubicin. The underlying mechanisms include increased phosphorylation of Akt and Erk by Rg1, increased ratio of Bcl-2 and Bax, and decreased release of cytochrome c from mitochondria, thereby protecting the heart from doxorubicin-induced apoptosis. This phenotype suggested that the oral administration of Rg1 may be a potential method preventing the cardiac toxicity caused by doxorubicin in clinical practice.
研究领域:
药理学
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心脏病学
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肿瘤学
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PubMed
高影响因子
MACROMOLECULAR BIOSCIENCE
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2025
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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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高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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2018
·Vol. 19
·期 11
·3658
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IF 3.687
Zhi-Meng Xu,Cheng-Bin Li,Qing-Ling Liu,Ping Li,Hua Yang
Ginsenoside Rg1, a saponin that is a primary component of ginseng, has been demonstrated to protect hearts from diverse cardiovascular diseases with regulating multiple cellular signal pathways. In the present study, we investigated the protective role of ginsenoside Rg1 on doxorubicin-induced cardiotoxicity and its effects on endoplasmic reticulum stress and autophagy. After pre-treatment with ginsenoside Rg1 (50 mg/kg i.g.) for 7 days, male C57BL/6J mice were intraperitoneally injected with a single dose of doxorubicin (6 mg/kg) every 3 days for four injections. Echocardiographic and pathological findings showed that ginsenoside Rg1 could significantly reduce the cardiotoxicity induced by doxorubicin. Ginsenoside Rg1 significantly inhibited doxorubicin-induced formation of autophagosome. At the same time, ginsenoside Rg1 decreased the doxorubicin-induced cardiac microtubule-associated protein-light chain 3 and autophagy related 5 expression. Ginsenoside Rg1 can reduce endoplasmic reticulum dilation caused by doxorubicin. Compared with the doxorubicin group, the expression of cleaved activating transcription factor 6 and inositol-requiring enzyme 1 decreased in group ginsenoside Rg1. Treatment with ginsenoside Rg1 reduces the expression of TIF1 and increases the expression of glucose-regulated protein 78. In the ginsenoside Rg1 group, the expression of p-P70S6K, c-Jun N-terminal kinases 1 and Beclin1 declined. These results indicate that ginsenoside Rg1 may improve doxorubicin-induced cardiac dysfunction by inhibiting endoplasmic reticulum stress and autophagy.Keywords:ginsenoside Rg1;doxorubicin;cardiotoxicity;autophagy;endoplasmic reticulum stress
研究领域:
药理学
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心脏病学
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分子生物学
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高影响因子
INTERNATIONAL JOURNAL OF PHARMACEUTICS
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2023
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IF 5.8
Shangmin Yu,Xinying Wang,Linlin Lv,Tongyan Liu,Qingxiang Guan
Depression is a chronic mental disorder which threatens human health and lives. However, the treatment of depression remains challenging largely due to blood brain barrier (BBB), which restricts drugs from entering the brain, resulting in a poor distribution of antidepressants in the brain. In this work, a novel brain-targeted drug delivery system was developed based on borneol-modified PEGylated graphene oxide (GO-PEG-BO). GO-PEG-BO was characterized and proved to possess excellent biocompatibility . By incorporating borneol , GO-PEG-BO could penetrate BBB efficiently by opening tight junctions and inhibiting the efflux system of BBB. The targeted distribution of GO-PEG-BO in the brain was observed by an in vivo biodistribution study. Moreover, GO-PEG-BO exhibited a neuroprotective effect, which is beneficial to the treatment of depression. Ginsenoside Rg1 (GRg1), which can relieve depressive symptoms but difficult to cross BBB, was loaded to GO-PEG-BO for the therapy of depression. In depressive rats, GRg1/GO-PEG-BO improved stress-induced anhedonia, despair and anxiety, and comprehensively relieved the depressive symptoms. In conclusion, GO-PEG-BO could serve as a promising nanocarrier for brain-targeted drug delivery, and provide a new strategy for the therapy of depression.
研究领域:
药学
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纳米技术
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神经科学
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药物递送系统
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2024
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IF 4.8
Liangliang Kong,Yan Liu,Jingwei Li,Yanyan Wang,Pengmin Ji,Qifeng Shi,Min Han,Hanyang Xu,Weiping Li,Weizu Li
Ethnopharmacological relevance Ginseng is a valuable herb in traditional Chinese medicine. Modern research has shown that it has various benefits, including tonifying vital energy, nourishing and strengthening the body, calming the mind, improving cognitive function, regulating fluids, and returning blood pressure, etc. Rg1 is a primary active component of ginseng. It protects hippocampal neurons, improves synaptic plasticity, enhances cognitive function, and boosts immunity. Furthermore, it exhibits anti-aging and anti-fatigue properties and holds great potential for preventing and managing neurodegenerative diseases (NDDs). Aim of the study The objective of this study was to examine the role of Rg1 in treating chronic inflammatory NDDs and its molecular mechanisms. Materials and methods In vivo , we investigated the protective effects of Rg1 against chronic neuroinflammation and cognitive deficits in mice induced by 200 μg/kg lipopolysaccharide (LPS) for 21 days using behavioral tests, pathological sections, Western blot, qPCR and immunostaining. In vitro experiments involved the stimulation of HT22 cells with 10 μg/ml of LPS, verification of the therapeutic effect of Rg1, and elucidation of its potential mechanism of action using H2DCFDA staining, BODIPY™ 581/591 C11, JC-1 staining, Western blot, and immunostaining. Results Firstly, it was found that Rg1 significantly improved chronic LPS-induced behavioral and cognitive dysfunction in mice. Further studies showed that Rg1 significantly attenuated LPS-induced neuronal damage by reducing levels of IL-6, IL-1β and ROS, and inhibiting AIM2 inflammasome. Furthermore, chronic LPS exposure induced the onset of neuronal ferroptosis by increasing the lipid peroxidation product MDA and regulating the ferroptosis-associated proteins Gpx4, xCT, FSP1, DMT1 and TfR, which were reversed by Rg1 treatment. Additionally, Rg1 was found to activate Nrf2 and its downstream antioxidant enzymes, such as HO1 and NQO1, both in vivo and in vitro . In vitro studies also showed that the Nrf2 inhibitor ML385 could inhibit the anti-inflammatory, antioxidant, and anti-ferroptosis effects of Rg1. Conclusions This study demonstrated that Rg1 administration ameliorated chronic LPS-induced cognitive deficits and neuronal ferroptosis in mice by inhibiting neuroinflammation and oxidative stress. The underlying mechanisms may be related to the inhibition of AIM2 inflammasome and activation of Nrf2 signaling. These findings provide valuable insights into the treatment of chronic neuroinflammation and associated NDDs.
研究领域:
神经药理学
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药理学
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神经科学
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免疫学
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分子生物学
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PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2018
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IF 3.118
Yuzhu Ye,Yuanlu Shan,Caiying Bao,Yi Hu,Liangrong Wang
Background/aims Ginsenoside Rg1 is regarded as the primary bioactive ingredient in Panax notoginseng that has been well recognized for its protective effects against ischemia/reperfusion (IR) injury. However, the mechanisms still remain elusive. Our study aims to investigate the effects of Rg1 against lung injury induced by hind-limb IR in rats. Methods Twenty-four Sprague Dawley rats were randomly submitted to sham operation (SM group), hind-limb IR (IR group), hind-limb IR + Rg1 (Rg1 group), and hind-limb IR + Pro-DTC group (PD group). All the rats except those in SM group were subjected to 3 h of ischemia followed by 6 h of reperfusion , and extra intravenous Rg1 and pyrrolidine dithiocarbamate (Pro-DTC), a selective inhibitor of nuclear factor kappa B (NF-κB), was administered intravenously before ischemia in the Rg1 and PD group, respectively. The activities of myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT), as well as protein expressions of NF-κB p65 and cyclooxygenases-2 (COX-2) in lung tissue, and thromboxane B2 (TXB2) and 6-keto-ProstaglandinF 1α (6-keto-PGF 1α ) levels in bronchoalveolar lavage (BAL) fluid were detected. Morphological changes, index of quantitative assessment of histologic lung injury (IQA), apoptosis index (AI) and lung Wet/Dry ratio were also evaluated. Results The levels of Wet/Dry ratio, IQA, AI, activities of MPO and 6-keto-PGF 1α /TXB 2 ratio were increased, and NF-κB p65 and COX-2 protein expression were upregulated, while SOD and CAT levels were decreased in lung tissue in IR group as compared with SM group ( p < 0.05), all the alterations could be significantly reversed by Rg1 or Pro-DTC pretreatment ( p < 0.05). And Rg1 and Pro-DTC also significantly attenuated the pulmonary histological abnormalities induced by IR. Conclusion Ginsenoside Rg1 potentially attenuated lung injury induced by hind-limb IR by regulating NF-κB/COX-2 signaling pathway .
研究领域:
药理学
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免疫学
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病理学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2023
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IF 5.4
Qianyan Gao,Guodong Li,Yue Zu,Yanjiao Xu,Congyi Wang,Dong Xiang,Wenxi He,Tianze Shang,Xinwei Cheng,Dong Liu,Chengliang Zhang
Ethnopharmacological relevance Ginseng ( Panax ginseng C. A. Mey) is a common traditional Chinese medicine used for anti-inflammation, treating colitis, type 2 diabetes, diarrhea, and recovering hepatobiliary function. Ginsenosides, the main active components isolated from ginseng, possess liver and gallbladder diseases therapeutic potential. Aims of the study Cholestatic liver injury (CLI) is a liver disease induced by intrahepatic accumulation of toxic bile acids and currently lacks clinically effective drugs. Our previous study found that ginsenosides alleviated CLI by activating sirtuin 1 (SIRT1), but the effective ingredients and the underlying mechanism have not been clarified. This study aimed to identify an effective ingredient with the most significant activation effect on SIRT1 from the five major monomer saponins of ginsenosides: Rb1, Rd, Rg1, 20s-Rg3, and Rc further explore its protective effects on CLI, and elaborate its underlying mechanism. Materials and methods Discovery Studio 3.0 was used to conduct molecular docking between monomer saponins and SIRT1, and further detect the influence of monomer saponins on SIRT1 activity in vitro. Finally, it was determined that Rg1 had the most significant stimulative effect on SIRT1, and the hepatoprotective activity of Rg1 in CLI was explored in vivo. Wild-type mice were intragastrically α-naphthylisothiocyanate (ANIT) to establish an experimental model of intrahepatic cholestasis and Rg1 intervention, and then liver injury and cholestasis related indexes were detected. In addition, Liver-specific SIRT1 gene knockout (SIRT1 -/- ) mice were administered with ANIT and/or Rg1 to further investigate the mechanism of action of Rg1. Results The results of molecular docking and in vitro experiments showed that all the five ginsenoside monomers could bind to the active site of SIRT1 and promote SIRT1 activity in HepG2 cells. Among them, Rg1 exhibited the most significant stimulation of SIRT1 activity in cholestasis. Besides, it could ameliorate ANIT-induced inflammation and oxidative stress in HepG2 cells. Therefore, we investigated the hepatoprotective effect and mechanism of Rg1 on CLI. Results showed that Rg1 reversed the ANIT-induced increase in biochemical parameters, improved liver pathological injury, and decreased liver lipid accumulation, reactive oxygen species and pro-inflammatory factor levels. Mechanistically, Rg1 induced SIRT1 expression, followed by promoted the activity of Nrf2 and suppressed the activation of NF-κB. Interestingly, the hepatoprotective effect of Rg1 was blocked in SIRT1 -/- mice. Conclusion Rg1 mitigated ANIT-induced CLI via upregulating SIRT1 expression, and our results suggested that Rg1 is a candidate compound for treating CLI.
研究领域:
药理学
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肝病学
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分子生物学
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高影响因子
Oxidative Medicine and Cellular Longevity
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2015
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IF 3.516
Dan Lu,Anding Xu,Hongcheng Mai,Jiayi Zhao,Chanjuan Zhang,Renbin Qi,Huadong Wang,Daxiang Lu,Lihong Zhu
Neural stem cells (NSCs) transplanted is one of the hottest research to treat Alzheimer’s disease (AD), but cholinergic neurons from stem cells were also susceptible to cell death which Heat shock protein 70 (HSP70) was affirmed to reverse. Related to cognitive impairment, cholinergic nervous cells should be investigated and ginsenoside Rg1 (G-Rg1) was considered to increase them. We chose tert-butyl hydroperoxide (t-BHP) damage model to study in vitro. Functional properties of our recombination plasmid pEGFP-C2-HSP70 were affirmed by SH-SY5Y cells. To opposite the transitory appearance of HSP70, NSCs used as the vectors of HSP70 gene overexpressed HSP70 for at least 7 days in vitro. After transfection for 3 days, G-Rg1 pretreatment for 4 hours, and coculture for 3 days, the expression of acetylcholinesterase (ChAT), synaptophysin, and the ratio of NeuN and GFAP were assessed by western blot; Morphological properties were detected by 3D reconstruction and immunofluorescence. ChAT was markedly improved in the groups contained G-Rg1. In coculture system, the ratio of neurons/astrocytes and the filaments of neurons were increased; apoptosis cells were decreased, compared to monotherapy (). In conclusion, we demonstrated that, as a safe cotreatment affirmed in vitro, overexpression of HSP70 in NSCs plus G-Rg1 promoted nervous cells regeneration from chronic oxidative damage.
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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分子生物学
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干细胞研究
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PubMed
高影响因子
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