Effect of Ginsenoside-Rb_1 on Cardiomyocyte Apoptosis after Ischemia and Reper fusion in Rats

The effect of ginsenoside Rb 1 on cardiomyocyte apotosis after ischemia (30 min ) and reperfusion (6 h) in rats was observed. The ischemia/ reperfusion heart mo del was established by ligating left anterior descending branch of coronary arte ry in Wistar rats. The apoptotic cardiomyocytes were examined under transmission electron microscopy and counted by in situ nick end labeling (TUNEL) method and light microscopy. Results showed that (1) The apoptotic cardiomyocytes were found in ischemic regions in the ischemia/reperfusion group, but not in the sh am oper ating group under transmission electron microscopy; (2) The number of apoptotic cells were 134.45±45.61/field in the ischemia/reperfusion group, 0/field in the sham operating group and 51.65±13.71/field in the ginsenoside Rb 1 treated group. The differences were significant among the three groups ( P <0.01). It was concluded that myocardial ischemia reperfusion could induce cardiomyocyte a poptosis, and ginsenoside Rb 1 could significantly inhibit cardiomyocyte apopto sis induced by ischemia reperfusion in rats, indicating that ginsenoside Rb 1 could inhibit cardiomyocyte apoptosis induced by ischemia reperfusion, thus alleviating ischemia reperfusion injury.

Effects of Ginsenoside Rb_1 on proliferation of Schwann cells in culture

To investigate the effects of Ginse noside Rb 1 on the proliferation of Schwann cells in culture.Methods: Applying MTT assay and Thymidine incorporation assay, the effects of Ginsenoside Rb 1 on the proliferation of Schwann cells isolated from the sciatic nerve of adult rat were studied.Results: Ginsenoside Rb 1 (10 μg/ml) significantly induced Sc hwann cell proliferation, the effect was similar to NGF (50 μg/ml). At high con centrations of Ginsenoside Rb 1 (1 mg/ml), the proliferation of Schwann cells w as significantly inhibited. Conclusions: Ginsenoside Rb 1 at the optimal concentrations is found to be effective in inducing the proliferation of Schwann cells, but at hi gher concentrations the drug is cytotoxic for Schwann cells.

Ginsenoside Rb1 induces hepatic stellate cell ferroptosis to alleviate liver fibrosis via the BECN1/SLC7A11 axis

Liver fibrosis is primarily driven by the activation of hepatic stellate cells(HSCs),a process associated with ferroptosis.Ginsenoside Rb1(GRb1),a major active component extracted from Panax ginseng,inhibits HSC activation.However,the potential role of GRb1 in mediating HSC ferroptosis remains unclear.This study examined the effect of GRb1 on liver fibrosis both in vivo and in vitro,using CCl4-induced liver fibrosis mouse model and primary HSCs,LX-2 cells.The findings revealed that GRb1 effectively inactivated HSCs in vitro,reducing alpha-smooth muscle actin(a-SMA)and type I collagen(Col1A1)levels.Moreover,GRb1 significantly alleviated CCl4-induced liver fibrosis in vivo.From a mechanistic standpoint,the ferroptosis pathway appeared to be central to the antifibrotic effects of GRb1.Specifically,GRb1 promoted HSC ferroptosis both in vivo and in vitro,characterized by increased glutathione depletion,malondialdehyde production,iron overload,and accumulation of reactive oxygen species(ROS).Intriguingly,GRb1 increased Beclin 1(BECN1)levels and decreased the System Xc-key subunit SLC7A11.Further experiments showed that BECN1 silencing inhibited GRb1-induced effects on HSC ferroptosis and mitigated the reduction of SLC7A11 caused by GRb1.Moreover,BECN1 could directly interact with SLC7A11,initiating HSC ferroptosis.In conclusion,the suppression of BECN1 counteracted the effects of GRb1 on HSC inactivation both in vivo and in vitro.Overall,this study highlights the novel role of GRb1 in inducing HSC ferroptosis and promoting HSC inactivation,at least partly through its modulation of BECN1 and SLC7A11.

Crosstalk among Oxidative Stress,Autophagy,and Apoptosis in the Protective Effects of Ginsenoside Rb1 on Brain Microvascular Endothelial Cells:A Mixed Computational and Experimental Study

Objective Brain microvascular endothelial cells (BMECs) were found to shift from their usually inactive state to an active state in ischemic stroke (IS) and cause neuronal damage. Ginsenoside Rb1 (GRb1),a component derived from medicinal plants,is known for its pharmacological benefits in IS,but its protective effects on BMECs have yet to be explored. This study aimed to investigate the potential protective effects of GRb1 on BMECs. Methods An in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model was established to mimic ischemia-reperfusion (I/R) injury. Bulk RNA-sequencing data were analyzed by using the Human Autophagy Database and various bioinformatic tools,including gene set enrichment analysis (GSEA),Gene Ontology (GO) classification and enrichment analysis,Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis,protein-protein interaction network analysis,and molecular docking. Experimental validation was also performed to ensure the reliability of our findings. Results Rb1 had a protective effect on BMECs subjected to OGD/R injury. Specifically,GRb1 was found to modulate the interplay between oxidative stress,apoptosis,and autophagy in BMECs. Key targets such as sequestosome 1 (SQSTM1/p62),autophagy related 5 (ATG5),and hypoxia-inducible factor 1-alpha (HIF-1α) were identified,highlighting their potential roles in mediating the protective effects of GRb1 against IS-induced damage. Conclusion GRbl protects BMECs against OGD/R injury by influencing oxidative stress,apoptosis,and autophagy. The identification of SQSTM1/p62,ATG5,and HIF-1α as promising targets further supports the potential of GRb1 as a therapeutic agent for IS,providing a foundation for future research into its mechanisms and applications in IS treatment.

Effect of ginsenoside Rg1 on hematopoietic stem cells in treating aplastic anemia in mice via MAPK pathway

BACKGROUND Aplastic anemia(AA)presents a significant clinical challenge as a life-threatening condition due to failure to produce essential blood cells,with the current the-rapeutic options being notably limited.AIM To assess the therapeutic potential of ginsenoside Rg1 on AA,specifically its protective effects,while elucidating the mechanism at play.METHODS We employed a model of myelosuppression induced by cyclophosphamide(CTX)in C57 mice,followed by administration of ginsenoside Rg1 over 13 d.The invest-igation included examining the bone marrow,thymus and spleen for pathological changes via hematoxylin-eosin staining.Moreover,orbital blood of mice was collected for blood routine examinations.Flow cytometry was employed to identify the impact of ginsenoside Rg1 on cell apoptosis and cycle in the bone marrow of AA mice.Additionally,the study further evaluated cytokine levels with enzyme-linked immunosorbent assay and analyzed the expression of key proteins in the MAPK signaling pathway via western blot.RESULTS Administration of CTX led to significant damage to the bone marrow’s structural integrity and a reduction in hematopoietic cells,establishing a model of AA.Ginsenoside Rg1 successfully reversed hematopoietic dysfunction in AA mice.In comparison to the AA group,ginsenoside Rg1 provided relief by reducing the induction of cell apoptosis and inflammation factors caused by CTX.Furthermore,it helped alleviate the blockade in the cell cycle.Treatment with ginsenoside Rg1 significantly alleviated myelosuppression in mice by inhibiting the MAPK signaling pathway.CONCLUSION This study suggested that ginsenoside Rg1 addresses AA by alleviating myelosuppression,primarily through modulating the MAPK signaling pathway,which paves the way for a novel therapeutic strategy in treating AA,highlighting the potential of ginsenoside Rg1 as a beneficial intervention.

GPCR-Gs mediates the protective effects of ginsenoside Rb1 against oxygen-glucose deprivation/re-oxygenation-induced astrocyte injury

Objectives:To investigate whether the protective actions of ginsenoside Rb1(Rb1)on astrocytes are mediated through the G_(s)-type G-protein-coupled receptor(GPCR-G_(s)).Methods:Primary astrocyte cultures derived from neonatal mouse brain were used.Astrocyte injury was induced via oxygen-glucose deprivation/re-oxygenation(OGD/R).Cell morphology,viability,lactate dehydrogenase(LDH)leakage,apoptosis,glutamate uptake,and brain-derived neurotrophic factor(BDNF)secretion were assessed to gauge cell survival and functionality.Western blot was used to investigate the cyclic adenosine monophosphate(cAMP)and protein kinase B(Akt)signaling pathways.GPCR-G_(s)-specific inhibitors and molecular docking were used to identify target receptors.Results:Rb1 at concentrations ranging from 0.8 to 5μM did not significantly affect the viability,glutamate uptake,or BDNF secretion in normal astrocytes.OGD/R reduced astrocyte viability,increasing their LDH leakage and apoptosis rate.It also decreased glutamate uptake and BDNF secretion by these cells.Rb1 had protective effects of astrocytes challenged by OGD/R,by improving viability,reducing apoptosis,and enhancing glutamate uptake and BDNF secretion.Additionally,Rb1 activated the cAMP and Akt pathways in these cells.When the GPCR-G_(s) inhibitor NF449 was introduced,the protective effects of Rb1 completely disappeared,and its activation of cAMP and Akt signaling pathways was significantly inhibited.Conclusion:Rb1 protects against astrocytes from OGD/R-induced injury through GPCR-G_(s) mediation.

A novel cabazitaxel liposomes modified with ginsenoside Rk1 for cancer targeted therapy

Objective:In this study,we aim to enhance the anti-prostate cancer efficacy of cabazitaxel(CTX)and reduce its immunosuppression and systemic toxicity by developing CTX-loaded liposomes modified with ginsenoside Rk1(Rk1/CTX-Lip).Methods:Physical and chemical properties of Rk1/CTX-Lip were investigated.We evaluated the biological functions of Rk1/CTXLip,both in vitro and in vivo.A subcutaneous prostate cancer(RM-1)-bearing mouse model was established to study the efficacy of Rk1/CTX-Lip inhibition in tumors.Simultaneously,a Candida albicans infection model was established in tumor-bearing mice to study the infection-relieving efficacy of Rk1/CTX-Lip.Finally,biocompatibility and in vivo safety of Rk1/CTX-Lip were evaluated.Results:We successfully prepared Rk1/CTX-Lip,achieving high CTX encapsulation efficiency(97.24±0.75)%and physical stability.Rk1/CTX-Lip demonstrated evasion of macrophage phagocytosis,effective tumor tissue targeting,and a significant reduction(>50%)in average tumor volume compared with Chol/CTX-Lip.Moreover,it relieved the concurrent infection burden and effectively regulated immune organs and cells,demonstrating superior biocompatibility.Conclusion:Rk1/CTX-Lip presents a promising new therapy for prostate cancer and holds potential for relieving concurrent fungal infections in cancer patients with low immunity.

Potential of ginsenoside Rg1 to treat aplastic anemia via mitogen activated protein kinase pathway in cyclophosphamide-induced myelosuppression mouse model

Aplastic anemia(AA)is a rare but serious condition in which the bone marrow fails to produce sufficient new blood cells,leading to fatigue,increased susceptibility to infection,and uncontrolled bleeding.In this editorial,we review and comment on an article by Wang et al published in 2024.This study aimed to evaluate the potential therapeutic benefits of ginsenoside Rg1 in AA,focusing on its protective effects and uncovering the underlying mechanisms.Cyclophosphamide(CTX)administration caused substantial damage to the structural integrity of the bone marrow and decreased the number of hematopoietic stem cells,thereby establishing an AA model.Compared with the AA group,ginsenoside Rg1 alleviated the effects of CTX by reducing apoptosis and inflammatory factors.Mechanistically,treatment with ginsenoside Rg1 significantly mitigated myelosuppression in mice by inhibiting the mitogen activated protein kinase signaling pathway.Thus,this study indicates that ginsenoside Rg1 could be effective in treating AA by reducing myelosuppression,primarily through its influence on the mitogen activated protein kinase signaling pathway.We expect that our review and comments will provide valuable insights for the scientific community related to this research and enhance the overall clarity of this article.

Microbiological Transformation of Ginsenoside Rg_1

Forty-nine microbial strains were used to screen their ability for the microbiological transforma-tion of ginsenoside Rg1. Aspergillus niger (3.1858) and Absidia coerulea (3.3538) were found to convert ginsenoside Rg1 efficiently to less polar metabolites. Preparative scale transformation with both fungi Absidia coerulea (3.3538) and Aspergillus niger (3.1858) have resulted in the production of one same metabolite (MT1). Its structure was char-acterized as 6-O-b-D-glucopyranosyl-20(S)-protopanaxatriol (Ginsenoside Rh1) on the basis of its TOF-MS and 1H, 13C NMR spectral data. The biotransformation kinetic curves for Ginsenoside Rg1 and MT1 were reported for the first time, and the biotransformation pathway was proposed.

高效液相色谱法同时测定三七总皂苷中人参皂苷Rg_1、Re、Rb_1与三七皂苷R_1含量

目的建立高效液相色谱法同时测定三七总皂苷中人参皂苷Rg1、Re、Rb1与三七皂苷R1的方法。方法采用高效液相色谱法 ,固定相为氨基键合相 ,流动相为乙腈 水 ( 81∶1 9,V∶V) ,检测波长2 0 3nm。结果三七总皂苷中人参皂苷Rg1、Re、Rb1和三七皂苷R1与其他成分分离良好 ,保留时间分别约为 5 7min、8 9min、2 5 1min和 9 9min。人参皂苷Rg1在 80～ 2 80mg/L(r =0 9992 )、Re在 2 0～ 1 80mg/L(r=0 9993 )、Rb1在 95～ 2 85mg/L(r=0 9991 )、三七皂苷R1在1 8～ 1 4 6mg/L(r=0 9991 )内线性关系良好 ,人参皂苷Rg1、Re、Rb1和三七皂苷R1的回收率分别为 99 1 %、98 4 %、98 6%和 97 1 % ,RSD分别为 2 1 %、2 0 %、2 2 %、2 8%。

人参皂苷Rb_1和Rd对不同类型记忆障碍模型小鼠学习记忆功能的影响

分别以东莨菪碱 ,环己米特和乙醇致小鼠获得性 ,巩固性和再现性记忆障碍 ,用跳台实验观察人参皂苷Rb1和Rd对学习记忆功能的影响 .结果表明 ,人参皂苷Rb1(10 0 ,5 0mg·kg- 1,ig)和人参皂苷Rd(2 0 ,10mg·kg- 1,ip)每天上午 9:0 0给药 1次 ,连续给药 7d ,对东莨菪碱和环己米特所致的小鼠获得性及巩固性记忆障碍均具有明显的改善作用 ,而对乙醇所致的小鼠记忆再现障碍则无明显影响 .结果表明 ,人参皂苷Rb1(ig)和Rd(ip)对小鼠学习记忆功能有增强作用 .

人参皂甙Rb_1与Re对大鼠缺血再灌注心肌细胞凋亡的影响

目的 观察人参皂甙Rb1与Re对缺血再灌注心肌细胞凋亡的影响 ,并比较两者的效应差异。方法 结扎Wistar大鼠左冠状动脉前降支 ,建立大鼠缺血再灌注动物模型 ;采用透射电镜、缺口末端标记法检测心肌凋亡细胞 ,利用光学显微镜进行细胞计数。结果 (1)透射电镜发现缺血再灌注组缺血区出现心肌凋亡细胞 ,假手术组未发现心肌凋亡细胞 ;(2 )缺血再灌注组心肌细胞凋亡数为 134 45± 45 6 1个 /视野 ,人参皂甙Rb1治疗组 5 1 6 5± 13 71个 /视野 ,人参皂甙Re治疗组 90 6 6± 19 2 2个 /视野 ,三组间有非常显著性差异 (P <0 0 1)。结论 心肌缺血再灌注诱导心肌细胞凋亡 ,人参皂甙Rb1和Re均可显著减少缺血再灌注心肌细胞的凋亡。证实人参皂甙Rb1与Re均有抑制缺血再灌注心肌细胞凋亡 ,减轻心肌缺血再灌注损伤的作用 ;人参皂甙Rb1的抗心肌细胞凋亡作用较Re的效果为佳。

HPLC法同时测定三七总皂苷中人参皂苷Rg_1与Rb_1的含量

目的 建立 HPL C同时测定三七总皂苷中人参皂苷 Rg1 与 Rb1 的方法。方法 采用 HPL C法 ,以茶碱为内标 ,氨基键合相为固定相 ,流动相为乙腈 -水 (80∶ 2 0 ) ,检测波长 2 0 3nm。结果 三七总皂苷中人参皂苷 Rg1 和 Rb1与其他成分分离良好 ,保留时间分别约为 5 .7和 2 1.5 min。人参皂苷 Rg1 在 80～ 2 80μg/ m L (r=0 .9995 ) ,Rb1 在80～ 2 4 0 μg/ m L(r=0 .9993)线性关系良好 ,Rg1 和 Rb1 加样回收率分别为 97.1%和 98.4 %,RSD分别为 2 .4 4 %和 2 .35 %(n=9)。结论 本法操作简便 ,准确 ,重现性好 ,可用于人参及三七的质量控制。

真菌对人参皂苷Rb_1及人参二醇系皂苷的代谢作用

目的 研究真菌对人参皂苷Rb1 (G Rb1 )及人参二醇系皂苷 (PDS)的代谢作用。方法 在恒温振荡条件下 ,10种真菌对其底物G Rb1 及PDS分别进行代谢 ,不同时间采集代谢物 ,正丁醇萃取 ,用薄层色谱 (TLC)、高效液相色谱 (HPLC)和电喷雾质谱 (ESI MS)检测代谢成分。结果 代谢产物中存在化合物G Rb1 ,G Rd ,G F2 ,CK和Ppd。结论 发现 6种真菌对底物有不同程度的代谢作用 ,其代谢过程可能为G Rb1 (或PDS)→G Rd→G F2 →CK→Ppd ,并通过控制这一过程可获得目的代谢产物CK。

人参皂甙Rb_1促进大鼠雪旺细胞增殖的实验研究

目的 观察人参皂甙 Rb1 对体外培养的大鼠坐骨神经雪旺细胞增殖能力的影响 ,探讨其促进神经再生的作用机制。 方法 取 SD雄性大鼠坐骨神经体外培养第 2代第 5天 ,加入不同浓度的人参皂甙 Rb1 ,利用 MTT比色分析法、3H-胸腺嘧啶核甙测定法检测不同浓度人参皂甙 Rb1 在不同培养时间对体外培养大鼠雪旺细胞增殖的影响。 结果 人参皂甙 Rb1 在 10μg/ ml的浓度对雪旺细胞增殖有明显促进作用 ,高浓度的人参皂甙 Rb1 1mg/ ml则显示抑制作用。而 2 0 0μg/ ml人参皂甙 Rb1 对细胞增殖的促进作用与对照组相近。 结论 人参皂甙 Rb1 在适当浓度范围内可以促进雪旺细胞的增殖 ,从而为促进活体神经损伤的修复途径提供了一些研究基础。

超高速液相测定西洋参中人参皂苷Rg_1、Re、Rb_1的含量研究

目的:建立测定西洋参中人参皂苷Rg_1、Re、Rb_1含量的超高速液相色谱法。方法:采用Waters Acquity UPLC BEHC_(18)(100 mm×2.1 mm,1.7μm)柱分离,以甲醇-水为流动相进行梯度洗脱,流速为0.2ml·min^(-1),柱温为35℃,在203 nm处检测。结果:人参皂苷Rg_1、Re、Rb_1在测定范围内有良好的线性关系,其平均回收率为97.36%～99.23%,RSD为1.16%～1.39%(n=6)。结论:本法操作简便,准确度高,重复性好,可作为西洋参质量控制方法之一。

人参皂苷Rb_1在心肌缺血大鼠体内的药动学研究

目的研究人参皂苷Rb_1在正常大鼠和急性心肌缺血模型大鼠体内的药动学。方法以垂体后叶素(PIT)制备急性心肌缺血大鼠模型,实验分3个正常对照组和3个模型组,分别给予高、中、低剂量的人参皂苷Rb_1(400,200,100 mg·kg^(-1)),单次灌胃给药后于不同时点采血,以三七皂苷R_1为内标,采用LC-MS/MS测定各时点血药浓度,并运用PK Solution 2.0软件计算药动学参数;Western Blot法测定大鼠肝脏中药物代谢酶CYP3a2、CYP2c9、CYP2c19、CYP1a1和CYP1a2蛋白表达。结果人参皂苷Rb_1的线性范围为5~10000 ng·mL^(-1),方法的专属性、提取回收率、日间及日内精密度、稳定性符合生物样品处理要求。与正常组比较,模型组大鼠AUC_(0-t)和C_(max)增加,t_(1/2)和T_(max)延长,CL降低(P<0.05或P<0.01)。与正常组比较,模型组大鼠CYP3a2、CYP2c9、CYP2c19、CYP1a1和CYP1a2代谢酶蛋白表达明显下降(P<0.05或P<0.01);人参皂苷Rb_1给药后12 h可诱导CYP1a1和CYP1a2表达。结论该方法专属性强、灵敏度高、准确性好,可用于人参皂苷Rb_1的含量测定及药动学研究。

RP-HPLC梯度法测定血塞通滴丸中三七皂苷R_1、人参皂苷Rb_1及人参皂苷Rg_1的含量

目的 :用高效液相色谱梯度洗脱法同时检测血塞通滴丸中三七皂苷R1、人参皂苷Rb1、人参皂苷Rg13种皂苷含量的方法 ,为制定质量标准中含量测定方法及含量限度提供了依据。方法 :用大连SpherisorbC18分析柱 ,乙腈 水线性梯度洗脱 ,0～ 15min(2 0∶80 - 4 0∶6 0 ) ,流速 1.0mL·min-1,检测波长 2 0 3nm。结果 :R1,Rf1和Rb1线性范围分别为 1.0 2～ 9.18μg ,4 .8～ 4 3.4 μg和 4 .6～ 4 1.6 μg。该方法回收率R1为 10 1.0 % (RSD =3.18% ) ,Rb1为 10 0 .0 % (RSD =1.19% ) ,Rg1为 99.5 % (RSD =3.0 2 % )。结论 :HPLC梯度洗脱法能将多种皂苷很好地分离检测 ,提高了时效 ,减少了误差 ,结果表明该方法准确可靠 ,重现性好 。

HPLC-ELSD测定三七胶囊中人参皂苷Rg_1和Rb_1

目的 :研究三七胶囊的质量标准。方法 :应用HPLC ELSD对三七胶囊中的活性成分人参皂苷Rg1和Rb1的含量进行测定。结果 :人参皂苷Rg1在 1.3 μg～ 6.5μg范围内呈现良好的线性关系 (r =0 .9994) ,平均回收率为 98.3 0 % ,RSD为 1.2 0 % (n =5)。人参皂苷Rb1在 1.0 μg～ 5.0 μg范围内呈现良好的线性关系 (r =0 .9996) ,平均回收率为 97.12 % ,RSD为 1.17% (n =5)。结论 :该方法简便 ,快速 ,重现性好 。

人参皂甙Rb_1、Rg_1、Re和Rh_1对HeLa细胞的影响

本研究应用细胞化学及ＭＴＴ法，测定人宫颈癌细胞（ＨｅＬａ）在人参皂甙Ｒｂ１、Ｒｇ１、Ｒｅ、Ｒｈ１作用３～５ｄ后，细胞增殖和细胞化学含量的变化。结果表明，四种人参单体皂甙与人参根总皂甙作用相似，可以抑制ＨｅＬａ细胞的增殖，降低ＨｅＬａ细胞内多糖（ＰＡＳ）、葡萄糖６磷酸脱氢酶（Ｇ６ＰＤＨ）、葡萄糖６磷酸酶（Ｇ６Ｐａｓｅ）、乳酸脱氢酶（ＬＤＨ）和琥珀酸脱氢酶（ＳＤＨ）的含量。本文提示，不同的人参单体皂甙均可以降低癌细胞的增殖和代谢活性，但Ｒｅ、Ｒｈ１的作用更显著。