What Is the Use of Ginseng Extract Ginsenoside?

Ginsenosides are the main pharmacologically active ingredients extracted from the roots, stems and leaves of the Panax ginseng plant in the Araliaceae family. They have the effects of boosting the body's immune system, promoting material metabolism, fighting tumours, combating fatigue and anti-ageing. In recent years, research into the individual active ingredients of ginsenosides has made good progress in treating diseases. The following is a review of the research progress over the past two years.

1. Enhancing the immune system

Zhang Caixun et al. found that after ginseng saponin Rhl [20, 40, 80 mg/(kg·d)] was administered to mice with low immune function, the spleen and thymus indices, MФ phagocytic function, and T lymphocyte proliferation of mice in each dose group were significantly improved.

Pan Weihua et al. used the MTT method and neutral red test to determine the effects of each ginseng saponin component on the proliferation of splenic lymphocytes and the phagocytic function of macrophages. The results showed that ginseng saponin components eluted with different concentrations of ethanol had varying degrees of promotion of the proliferation of mouse splenic lymphocytes and the phagocytic function of macrophages within the test range. Among them, the ginsenoside fraction eluted with 70% ethanol had the strongest promoting effect, suggesting that the ginsenoside fraction obtained by eluting ginsenosides with 70% ethanol has a good immune enhancer effect.

Zhou Yingwu et al. used biochip technology to detect the effect of ginsenoside Rgl on the expression of genes related to the functional regulation of mouse dendritic cells (Dc), and found that ginsenoside Rg3 affects Dc by regulating the expression of multiple genes, which control and affect the function, differentiation and maturation of Dc, providing clues for further identification of drug targets.

The above suggests that ginsenoside components can be developed and utilized as effective immune enhancers.

2 Antitumor effects

Fang et al. studied the effect of Rg3 on the microvascular density (MVD) of a nude mouse hepatoma transplant model. The results showed that the Rg3 group of nude mice did not experience obvious drug toxicity, and the quality of life was the best. The average tumor weight in the Rg3 group was lower than in the control group, and the difference was significant (P<0. 05). The MVD in the Rg3 group was significantly lower than in the control group (P<0. 001). The study also found that Rg3 combined with arsenic trioxide had the strongest effect on transplanted human liver cancer tumors in mice, significantly inhibiting the proliferation of transplanted liver cancer cells. Suggestion: Rg3 can reduce the expression of MVD in tumor tissue and inhibit the neovascularization of liver cancer. The combined application also has a better synergistic effect.

Liao Danqiong et al. used the MTT method and BrdU immunofluorescence method to detect the effect of ginsenoside Rg3 on the proliferation of C6 glioma tumor stem cells. The study found that ginsenoside Rg3 has a significant inhibitory effect on the proliferation of glioma tumor stem cells.

Liao Yilin et al. used MTT, soft agar clonogenic formation rate, morphology and glial fibrillary acidic protein (GFAP) immunofluorescence to identify the degree of induction of differentiation of ginseng saponins on rat C6 glioma cells. The results showed that 10ug/mL ginseng saponins can significantly induce the differentiation of rat C6 glioma cell lines, which is manifested as suppression of proliferation, loss of clonogenic ability, growth of cell protrusions, and increased expression of glial fibrillary acidic protein (GFAP). This indicates that ginsenosides at a certain dose can induce the differentiation of rat glioma cells to achieve an anti-tumor effect.

Zhao Ying et al. found that ginsenosides combined with clematis saponins showed a very significant inhibitory effect on transplanted tumors of mouse sarcoma 180 (S180), hepatoma ascites (HepA) and leukemia ascites (P388) transplanted tumors all showed a very significant inhibitory effect, with inhibition rates of 52.41%, 53.57% and 54.15% respectively, and a significant effect on prolonging the life of mice. This suggests that the combined use of individual Chinese herbal medicines can also have a better anti-tumor effect.

A study by Cong Zhongyi showed that ginsenoside Rg3 can inhibit the proliferation of human colon cancer cells SW480 in vitro, suggesting that ginsenosides can be used as adjuvant drugs in the clinical treatment of colon cancer to reduce the side effects of chemotherapeutic drugs.

Using a mouse transplant tumor model, Xiaojie Gong and others found that ginsenoside M1 stearate SMl can significantly inhibit the growth of liver cancer cells and gastric cancer cells in mice after a period of action, and has significant anti-tumor effects with no toxic side effects.

Jiang Xin et al. used melanoma cells B16 to establish a spontaneous lung metastasis and solid tumor model in mice by subcutaneous inoculation, and observed the number of lung tumor metastases after intraperitoneal injection of different doses of Rg3 (the control group was given 0.9% sodium chloride solution), and detected the expression of matrix metalloproteinase-9 (MMP-9) protein in the solid tumors. The Boyden chamber invasion assay and immunohistochemical staining were used to detect the effect of Rg3 on the invasion ability of tumor cells and MMP-9 expression. The results showed that after treatment with different doses of Rg3 (0. 3, 1. 0 and 3. 0 mg/kg), the number of lung metastases in mice was lower, and the expression level of MMP-9 in tumor tissue was reduced, which was statistically significant (P<0. 05) compared with the control group. In vitro, the number of B16 cells that invaded through the artificial basement membrane in the 2.5 and 5.0 μg/mL Rg3 treatment groups was significantly lower than that in the control group (P<0.01), and 5.0 μg/mL Rg3 could inhibit the expression of MMP-9 in tumor cells. This indicates that Rg3 can inhibit the lung metastasis of mouse melanoma cells, and its anti-tumor metastasis effect may be achieved by reducing the expression level of MMP-9 in tumor cells and the invasion ability of cells.

The study also found that ginsenoside Rg3 at certain concentrations can enhance the gene expression of human breast cancer cells MCF-7 Cx26 and restore the intercellular 0-gap junctional communication (GJIC) function of MCF-7 cells. This may be one of the mechanisms by which ginsenoside Rg3 inhibits MCF-7 cell proliferation and exerts an antitumor effect.

Wang Yan et al. found that in patients with stage III B non-small cell lung cancer that is inoperable, after two courses of chemotherapy and oral administration of ginsenoside Rg3, the serum vascular endothelial growth factor (VEGF) and CEA levels decreased significantly on average, the quality of life KPS score improved significantly, and the incidence of toxic side effects was significantly reduced.

Huang Jingzi et al. found that ginsenoside Rg3 inhibited the growth of non-small cell lung cancer, induced apoptosis of tumor cells, and significantly increased the sensitivity to radiotherapy through experimental studies on the radiosensitizing effect of ginsenoside Rg3 in non-small cell lung cancer.

In summary: ginsenoside Rg3 can inhibit tumor angiogenesis, induce tumor cell differentiation, and reduce tumor cell invasion, providing a reliable basis for the development of anti-tumor drugs.

3 Anti-aging effect

Zhou Liping et al. studied the anti-aging effect of ginsenoside Rg1. Ginsenoside Rg1 was given by intraperitoneal injection to a mouse model of Alzheimer's disease (AD) caused by beta-amyloid protein 25-35 (Aβ25-35), and the Morris water maze test was used to test the narrow-interval learning and memory ability of the mice, and RT-PCR technology was used to detect the expression of the bcl-2 gene in the hippocampus. The results showed that Rg1 can reduce the latency and total distance of AD mice (q=5.478, 6.097, P<0.05), increase the number of times they cross the platform (g=6.023, P<0.05), reversing the decrease in bcl-2 gene expression caused by Aβ25-35 (q=9.661, P<0.05). This indicates that Rg1 can reduce the damage caused by Aβ25-35 to hippocampal neurons in mice, and the mechanism may be related to the activation of the estrogen receptor pathway.

Ginsenoside Rg1 can inhibit the aging process by downregulating the expression of P16 INK4a and P21 Cip/WaflmRNA and protein in D-galactose-induced aging rats, thus preventing cells in the brain tissue from entering the aging process. Zhou Yue et al. found that ginsenoside Rgl can delay the aging of hematopoietic stem cells (HSCs) and its related mechanisms through research: Rgl has the effect of delaying and treating the aging of Sca-1+HSCs, and the p16INK4a_Rb and p19Arf_Mdm2-p53-p2-P21 cip1/wmfl signaling pathways may play an important role.

Li Xi et al. studied the effect of ginsenoside Rg1 on the phosphorylation of tau protein in rat brain slices caused by okadaic acid (OA), and found that ginsenoside Rg1 can upregulate the expression of protein phosphatase 2A (PP2A) in a rat brain slice model of AD-like tau protein phosphorylation, thereby promoting the dephosphorylation of phosphorylated tau protein (P-tau) in the hippocampus, and thus inhibiting the phosphorylation of tau protein. This suggests that Rg1 has a certain preventive and therapeutic effect on AD. 4 Anti-inflammatory and antioxidant effects PP2A) expression, thereby promoting the dephosphorylation of phosphorylated tau protein (P-tau) in the hippocampus, and in this way inhibiting tau protein phosphorylation. It is suggested that Rgl has a certain preventive and therapeutic effect on AD.

4 Anti-inflammatory and antioxidant effects

Zhao Baosheng et al. found that ginsenoside Rgl in the high, medium and low dose groups all significantly inhibited the degree of ear swelling in mice caused by xylene (P<0. 05 or P<0. 01). It was also found that high-dose ginsenoside Rgl showed a certain inhibitory effect on the proliferation of subacute inflammatory granulation tissue (P<0. 01).

Lü Zhenchao et al. aseptically removed full-thickness cartilage pieces from the knee joints of New Zealand white rabbits and cultured the cartilage cells externally. After successfully culturing the cartilage cells, they set up a group with ginsenosides Rg1 and Rb1 and a control group. IL-1 was used to induce apoptosis in the cartilage cells, and a flow cytometer was used to detect the number and proportion of apoptotic cells. Transmission electron microscopy was used to observe the morphological and submicroscopic structure of the apoptotic cells. The results showed that ginsenosides Rg1 and Rb1 can significantly inhibit excessive apoptosis of chondrocytes, inhibit the occurrence and development of knee osteoarthritis, and there is no significant difference between the two in the process of proliferation and apoptosis. The mechanism is mainly to remove free radicals produced during cell metabolism and reduce the production of cell lipid peroxides, creating a favorable environment for preventing cell aging and repairing cells, and providing a theoretical basis for further in vivo experiments.

Zhang Dailei et al. used in vitro cultured mouse spermatogonial cells, and added ginsenoside GS (0.1-10 mg/L) and hypoxanthine/xanthine oxidase (HX/XO) alone or in combination. The active oxygen produced by the (HX/XO) system can cause a decrease in germ cell activity, an increase in the amount of MDA produced, and a decrease in SOD activity and GSH levels. The addition of ginsenoside (0. 1-10mg/L) can restore the reproductive cell activity, SOD activity and GSH levels caused by (HX/XO), as well as the increase in the production of MDA. This indicates that ginsenoside GS can protect germ cells from oxidative damage caused by reactive oxygen species by inhibiting lipid peroxidation and scavenging free radicals in germ cells through its antioxidant effect, thereby maintaining a normal antioxidant system.

Li Zhenbin et al. established a rat model of adjuvant arthritis by intradermal injection of complete Freund's adjuvant, and studied the effects of tigogenin TG from thunder god vine in combination with ginsenoside GS on TNF-α, IL-1β and MIF in rats with adjuvant arthritis. The results showed that both TG and GS significantly inhibited the arthritis index AI in rats with adjuvant arthritis, reduced the levels of serum inflammatory cytokines TNF-α, IL-1β and MIF levels, and may have a beneficial effect on joint pathology. TG and GS in combination showed a certain synergistic effect, and the mechanism of action may be related to their inhibition of the expression of the inflammatory cytokines TNF-α, IL-1β and MIF. It is speculated that the combination of effective Chinese medicine ingredients may be an important way to further improve the clinical efficacy of rheumatoid arthritis (AR), and is worthy of in-depth research.

The above shows that ginsenosides can exert anti-inflammatory and antioxidant effects by scavenging free radicals in the body and inhibiting oxidative damage.

5 Inhibition of vascular endothelial cell apoptosis

He Guoyang et al. Cultivated human umbilical vein endothelial cells (HU VECs) in vitro and observed the effect of ginsenoside Rg 1 on angiotensin II (Ang Ⅱ)-induced HUVECs apoptosis. apoptosis was detected using agarose gel electrophoresis and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) staining. It was found that 40 μg/mL ginsenoside Rg1 can to some extent reverse Ang Ⅱ-induced HUVECs apoptosis, suggesting that ginsenoside Rg1 has a certain protective and therapeutic effect on vascular endothelial damage. The molecular mechanism of ginsenoside Rg1 in reversing Ang II-induced vascular endothelial cell apoptosis requires further investigation. Ginsenoside Rg1 has also been found to inhibit homocysteine (Hcy)-induced apoptosis of human umbilical vein endothelial cells, and this effect may be related to upregulation of eNOS levels in vascular endothelial cells.

6 Antiviral effect

Chu Xiuling et al. used a model of chickens artificially infected with Marek's disease virus (MDV) and administered ginsenoside Rg3 orally. The protective effect of the drug on the body was evaluated using indicators such as incidence, protection rate, and mean survival age. The results showed that ginsenoside Rg3 can significantly reduce the incidence and tumor detection rate of experimental chickens, protect the immune organs of infected chickens, enhance the immunity of infected chickens, and has antiviral effects. The study also found that ginsenoside and modified derivative 7 can reduce the degree of damage to (MD V) infected chick embryo fibroblasts (CEF). The above suggests that ginsenosides can be used as a good antiviral traditional Chinese medicine, providing a basis for the development of new antiviral drugs.

7 Protective effect on cardiomyocytes

Ma Yongjie et al. used primary cultured cardiomyocytes to cause cell damage using an hypoxia-reoxygenation model. The protective effect was evaluated by measuring cell viability and lactate dehydrogenase (LDH) leakage, and the intracellular antioxidant status was evaluated by measuring superoxide dismutase (SOD) activity. The results showed that ginsenoside Rg1 (120 μmol/L) and tanshinone II A (4 μmol/L) monomers, as well as the combination of ginsenoside Rg1 and tanshinone II A, can significantly increase the viability of hypoxic-reoxygenated injured cardiomyocytes. The combined effect is better than monotherapy. The combination of ginsenoside Rg1 (160 μmol/L) and tanshinone IIA (2 μmol/L) has the best effect. The combination of the two monomers can also reduce LDH leakage and increase SOD activity in hypoxia-reoxygenation-induced myocardial injury. This shows that the combination of the two monomers, ginsenoside Rg1 and tanshinone IIA, has a significant protective effect on myocardial cells damaged by hypoxia and reoxygenation. The mechanism of their anti-oxidative damage may be partially achieved by increasing SOD enzyme activity. Zhao Yingjun et al. also found that Gs-Rb1 can inhibit the hypoxia-induced apoptosis of myocardial cells by increasing the expression of survivin.

Wen Fei et al. observed the protective effect of ginsenoside Rb1 on hydrogen peroxide-induced cardiomyocyte apoptosis and found that ginsenoside Rb1 can significantly reduce the damage to cardiomyocytes caused by hydrogen peroxide, improving cell viability (P<0. 01); reducing LDH leakage (P<0. 01); inhibiting a decrease in mitochondrial membrane potential (P<0. 01); and significantly reducing the level of apoptosis (P<0. 01). It can be seen that ginsenoside Rb1 can reduce cell damage caused by hydrogen peroxide to a certain extent, stabilize the structure and function of cell mitochondria, and inhibit hydrogen peroxide-induced myocardial cell apoptosis.

Li Xuefeng et al. studied the effect of ginsenoside Re on myocardial cell hypoxia in rats and found that ginsenoside Re pretreatment can reduce the release of lactate dehydrogenase (LD H) from hypoxic rat myocardial cells, significantly improve intercellular communication, and has a significant protective effect on hypoxic myocardial cells. The dosage is especially suitable for 20g/L.

The above suggests that ginsenoside Rg1 has a good preventive and therapeutic effect on coronary heart disease, angina pectoris, heart failure, etc.

8 Cosmetic effects

Zhao Ziran et al. created a rabbit ear hypertrophic scar model, with the experimental group injected with ginsenoside GS-Rg3 (concentration 6mg/mL) and the control group injected with an equal volume of 0.9% saline. After 2, 4, and 6 weeks of administration, scar tissue was removed and compared with the control group using the in situ terminal labeling operation process (TUNE L), histological observation, and other methods. Compared with the control group, the skin in the treatment group became thinner after 6 weeks of administration, the collagen arrangement was more orderly, the number of fibroblasts and blood vessels decreased; and the number of fibroblasts undergoing apoptosis increased significantly with prolonged administration. Gross observation showed that about 60 days after the application of the drug, the scar gradually began to soften, shrink in size, and tend to flatten. The control group, however, continued to proliferate. This indicates that ginsenoside Rg3 can induce apoptosis of fibroblasts, thereby inhibiting the formation of pathological scars, providing an important theoretical basis for future clinical applications.

Song Wengang et al. studied the effect of ginsenoside Rb1 on mushroom tyrosinase in vitro by detecting the activity of mushroom tyrosinase, and studied the effect of ginsenoside Rb1 on the proliferation of B16 melanoma cells by measuring the cell proliferation rate. The results showed that the effect of ginsenoside Rb1 on B16 melanoma cell proliferation changes with the concentration. When the mass concentration of Rb1 is <125 μg/mL, it promotes the proliferation of B16 melanoma cells; when it is >125 μg/mL, it inhibits the proliferation of B16 melanoma cells. It is suggested that ginsenoside Rb1 has a certain whitening effect.

In summary, ginsenosides can be widely used for the protection and treatment of the cardiovascular, nervous, immune and endocrine systems. Currently, ginsenosides are used in the following four main ways: first, the individual components of ginsenosides are used separately, with clear goals and immediate results; second, the combined use of individual components of ginsenosides treating multiple targets simultaneously; third, the combined use of different effective monomeric ingredients of traditional Chinese medicine based on the idea of syndrome differentiation and treatment in traditional Chinese medicine. I believe this is the development trend of compound prescriptions; fourth, the combined use of ginseng saponins and chemical drugs can enhance the efficacy while effectively reducing the toxic side effects of chemical drugs. This is also the development trend of combining traditional Chinese medicine with Western medicine.

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