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Ginsenoside M1

Ginsenoside M1 is a naturally occurring compound derived from the root of the ginseng plant.
It has been the subject of increasing research interest due to its potential therapeutic properties, including anti-inflammatory, anti-oxidant, and neuroprotective effects.
PubCompare.ai's AI-driven protocols can help optimize your research on Ginsenoside M1 by locating relevant protocols from the literature, pre-prints, and patents, and using advanced AI comparisons to identify the best protocols and products.
This can simplify your research and accelerate your discoveries around this important comound.

Most cited protocols related to «Ginsenoside M1»

1
Establishing ASLN Mouse Model with LPS
Cited 2 times
All animal experiments were performed with the ethical approval of the Institutional Animal Care and Use Committee of The National Defense Medical Center, Taiwan, in compliance with the NIH Guide for the Care and Use of Laboratory Animals. The ASLN mouse model was established in 8-week-old female NZB/WF1 mice (prior to autoantibody production) (purchased from Jackson Laboratory, ME, USA), with twice weekly intraperitoneal injections of lipopolysaccharide (LPS) (0.8 mg/kg body weight, Sigma, MO, USA) as described previously (8 (link), 10 (link)). Seven days after the first injection of LPS, the mice were divided into 2 groups of 8 mice each and were given either M1 (50 mg/kg body weight) or vehicle (corn oil) daily via oral gavage. Age-matched female NZB/WF1 mice injected with normal saline served as normal controls. The mice were sacrificed at week 3 and week 5, respectively, after the induction of disease.
Lin T.J., Wu C.Y., Tsai P.Y., Hsu W.H., Hua K.F., Chu C.L., Lee Y.C., Chen A., Lee S.L., Lin Y.J., Hsieh C.Y., Yang S.R., Liu F.C, & Ka S.M. (2019). Accelerated and Severe Lupus Nephritis Benefits From M1, an Active Metabolite of Ginsenoside, by Regulating NLRP3 Inflammasome and T Cell Functions in Mice. Frontiers in Immunology, 10, 1951.
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Publication 2019
Animals, Laboratory Autoantibodies Body Weight Corn oil Females Injections, Intraperitoneal Institutional Animal Care and Use Committees Lipopolysaccharides Mice, House Mice, Inbred NZB Normal Saline Tube Feeding
2
Apoptosis Induction by Ginsenoside M1
Not available on PMC !

Example 3

To gain further insight into the mode of action of ginsenoside M1, three assays targeting hallmarks of apoptosis, namely (1) the apoptotic DNA breaks assayed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, (2) the cell cycle assayed by flow cytometry after propidium iodide (PI)-staining nuclei, (3) the PI/Annexin V double staining assay, and (4) caspase activation were performed. Plate 1×106 human oral cancer cells OECM-1 per 6-cm dish in 2 ml of culture medium and were grown overnight at 37° C. in a 5% CO2 incubator. The cells were incubated for 24 h with ginsenoside M1 (10˜20 μg/ml), 50 μM cistaplatin (CDDP) or vehicle. Each group contains a final DMSO concentration of 0.1%. Thereafter, three assays were performed. We found that 20 μg/ml ginsenoside M1 and 50 μM CDDP, but not 10 μg/ml ginsenoside M1 significantly induced apoptotic DNA breaks in OECM-1 cells (FIG. 3A). In addition, the effect of ginsenoside M1 on the cell cycle distribution in OECM-1 cells was determined and we found that the cells in G1 phase increased in a concentration-dependent manner after treatment with ginsenoside M1 and CDDP, while concomitantly decreasing the percentage of cells in S and G2/M phase as compared with the control cells, indicating that ginsenoside M1 and CDDP induced cell cycle arrest at G1 phase (FIG. 3B). The cells in sub-G1 phase increased after treatment with ginsenoside M1 and CDDP. (FIG. 3B). Moreover, we found that 20 μg/ml ginsenoside M1 and 50 μM CDDP, but not 10 μg/ml ginsenoside M1 significantly increased the percentage of OECM-1 cells with PI/Annexin V double positive staining (FIG. 3C). These results indicated that ginsenoside M1 induced human oral cancer cells OECM-1 apoptosis significantly at concentration of 20 μg/ml. The apoptosis induction activity of ginsenoside M1 in human oral cancer SAS cells was confirmed as ginsenoside M1 induced a decrease of the precursors of caspase-3 and caspase-9 in a dose-dependent manner, indicating that caspase 3 and caspase-9 were activated by ginsenoside M1 (FIG. 3D). The data were expressed as mean±SD; n=3. ** and *** indicate a significant difference at the level of p<0.01 and p<0.001, respectively, compared to vehicle-control cells. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
3
Ginsenoside M1 Inhibits Oral Cancer Xenografts
Not available on PMC !

Example 6

To evaluate the anti-cancer activity of ginsenoside M1 in vivo, human oral cancer xenografts were used. Six-week-old male congenital athymic BALB/c nude (nu/nu) mice were purchased from BioLASCO Taiwan Co., Ltd (Ilan, Taiwan), and housed in a room under controlled temperature (23±3° C.) and relative humidity (50±5%). Animal experiments were performed with the approval of the Institutional Animal Care and Use Committee of the National Ilan University (approval number: No. 106-13) according to the NIH Guide for the Care and Use of Laboratory Animals. Xenografts mice were established by subcutaneous (SC) injection of 2×106 human oral cancer cells SAS (in 75 μl PBS+75 μl Matrigel) on the backs of the nude mice. After the tumor has reached about 40˜60 mm3 in size, the mice were randomized into six groups (six mice each): (1) oral vehicle control; (2) oral 30 mg/kg ginsenoside M1; (3) oral 60 mg/kg ginsenoside M1; (4) oral 90 mg/kg ginsenoside M1; (5) SC vehicle control; (6) SC 20 mg/kg ginsenoside M1. The mice were given a daily oral administration or SC injection of either vehicle or ginsenoside M1 for 5 successive days. The mice were scarified at 24 h after received the last dose of ginsenoside M1 or vehicle. The tumor volume (TV) was determined by measurement of the length (L) and width (W) of the tumor. The TV on day n (TVn) was calculated as TV (mm3)=(L×W2)/2. The relative tumor volume on day n (RTVn) versus day 0 was expressed according to the following formula: RTVn=TVn/TV0. We found that oral administration of ginsenoside M1 at 90 mg/kg significantly reduced the tumor size compared to vehicle control group; however, oral administration of ginsenoside M1 at 30 and 60 mg/kg did not significant reduce the tumor size (FIG. 6A) and tumor weight (FIG. 6B). Oral administration of ginsenoside M1 did not significantly affect the body weight of mice (FIG. 6C). The data were expressed as mean±SD; n=6. ** and *** indicate a significant difference at the level of p<0.01 and p<0.001, respectively, compared to vehicle-control mice. (One-way ANOVA with Dunnett's multiple comparisons test).

In addition, SC injection of 20 mg/kg ginsenoside M1 also significantly reduced the tumor size (FIG. 7A) and tumor weight (FIG. 7B) compared to vehicle control group. SC injection of ginsenoside M1 did not significantly affect the body weight of mice (FIG. 7C). The data were expressed as mean±SD; n=6. ** indicates a significant difference at the level of p<0.01, compared to vehicle-control mice. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
4
Comparative Cytotoxicity of Ginsenosides
Not available on PMC !

Example 2

Plate 5×105 normal human gingival epithelioid cell line SG per 6-cm dish in 2 ml of culture medium and were grown overnight at 37° C. in a 5% CO2 incubator. The cells were incubated for 24 h with ginsenoside M1 (5˜20 μg/ml), ginsenoside Rh2 (5˜20 μg/ml) or vehicle. Each group contains a final DMSO concentration of 0.1%. Thereafter, the cell numbers were counted by Trypan blue exclusion method. We found that ginsenoside M1 showed less toxic to SG cells than ginsenoside Rh2 (FIG. 2). Ginsenoside Rh2 at 20 μg/ml completely killed the SG cells; however, ginsenoside M1 at 20 μg/ml only reduced 50% cell number compared to control cells (namely at least 50% normal cells were preserved) (FIG. 2). The data were expressed as mean±SD; n=3. ** and *** indicate a significant difference at the level of p<0.01 and p<0.001, respectively, compared to vehicle-control cells. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
Cell Lines Cells Culture Media Epithelioid Cells Gingiva Ginsenoside ginsenoside Rh2 Homo sapiens Hyperostosis, Diffuse Idiopathic Skeletal neuro-oncological ventral antigen 2, human Sulfoxide, Dimethyl Trypan Blue
5
Ginsenoside Inhibition of Oral Cancer Cells
Not available on PMC !

Example 1

Plate 5×105 human oral cancer cells SAS per 6-cm dish in 2 ml of culture medium and were grown overnight at 37° C. in a 5% CO2 incubator. The cells were incubated for 24 h with ginsenoside M1 (5˜20 μg/ml), ginsenoside Rh2 (5˜20 μg/ml) or vehicle. Each group contains a final DMSO concentration of 0.1%. Thereafter, the cell numbers were counted by Trypan blue exclusion method. We found that ginsenoside M1 and ginsenoside Rh2 dose-dependently inhibited the cell numbers of human oral cancer SAS cells (FIG. 1A) and human oral cancer OECM-1 cells (FIG. 1B). These results indicated that both ginsenoside M1 and ginsenoside Rh2 inhibited the viability of human oral cancer cells; however, there was no significant difference between ginsenoside M1 and ginsenoside Rh2. The data were expressed as mean±SD; n=3. *, ** and *** indicate a significant difference at the level of p<0.05, p<0.01 and p<0.001, respectively, compared to vehicle-control cells. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
Cancer of Mouth Cells Cell Survival Culture Media Ginsenoside ginsenoside Rh2 Homo sapiens Hyperostosis, Diffuse Idiopathic Skeletal neuro-oncological ventral antigen 2, human Sulfoxide, Dimethyl Trypan Blue

Most recents protocols related to «Ginsenoside M1»

1
Quantification of Ginsenoside Content in Ginseng
The gross ginsenosides content was determined by using the reference method of the State Standard of the People's Republic of China (GB/T 19506-2009): GF powder (passed through a 60-mesh sieve) was accurately weighed (about 1.0 g) then packaged in a neutral filter paper. The powder was extracted with ether using a Soxhlet extractor for 1 h. The sample package was then dried to evaporate the ether solvent. Methanol was added to the extractor to soak overnight. The next day, the appropriate amount of methanol was added to repeat the extraction for 6 times. The methanol extracts were combined and recovered, steaming a small amount of methanol extracts in the water bath and then dissolving them in water. 30 mL water extract was extracted for 4 times with 30 mL of water-saturated n-butanol. The upper liquid was steamed, then dissolved in methanol and made up to 10 mL. Finally, the end product was used as the ginsenosides sample solutions for further analysis.
The total ginsenoside content was determined using the reference method of the product of geographical indication-Jilin Changbaishan ginseng (GB/T 19506-2009), Ginsenoside Re (National Institutes for Food and Drug Control, Beijing, China)was used as the standard to calculate the content of the gross ginsenoside. In order to prepare the ginsenoside Re standard solution, 10 mg ginsenoside Re was put into a 10 mL volumetric flask, dilute to scale with methanol as solvent and mixed. 10 μL, 20 μL, 30 μL, 40 μL, 60 μL, 80 μL, and 100 μL of the standard solution and 30 μL sample solution were transferred to 10 mL tubes and dried (60°C water bath). Then, 0.5 ml 8% vanillin-ethanol and 5 ml 72% concentrated sulfuric acid were added to the prepared tubes. After fully shaking and mixing, the solution was heated in a 60°C water bath for 10 min and then cooled down in an ice-water bath for 10 min immediately. The mixed reagent without ginsenoside was used as a reference. Finally, both were determined at 544 nm using an enzyme calibration (Infinite M200 PRO, Tecan, Switzerland). To reduce the error in determining the gross ginsenosides content, three parallel extracts were obtained from the same origin of GF raw materials. The changes in gross ginsenosides content in GFs of various ages were then compared. The following equation was used to calculate the gross ginsenoside content:
Equation (1) of Cui et al. [22 (link)] was used to calculate the gross ginsenosides content: X%=m1∗A2/A1m2∗ 100%, where X is the gross ginsenosides content; m1 represents the weight of ginsenoside Re, m2 is the weight of GF powder, and A1 and A2 are the absorbances of the ginsenoside Re standard solution and sample solution, respectively.
Du L.Y., Zhang H.E., Zhang Y., Han Y.Y., Ye P., Meng X.R., Shen Y.L., Chen C.B., Fan M.L, & Wang E.P. (2023). Comparative Study on Chemical Constituents of Ginseng Flowers with Four Consecutive Cultivation Age. International Journal of Analytical Chemistry, 2023, 1771563.
Full text: Click here
Publication 2023
Bath Butyl Alcohol Enzymes Ethanol Ethyl Ether Food Genetic Materials Ginseng Ginsenoside ginsenoside Re Ginsenosides Ice M-200 Methanol Powder Solvents Sulfuric Acids Technique, Dilution vanillin
2
Comparative Evaluation of DDA Strategies for Ginsenoside Profiling
The performance of three DDA approaches (M1 to M3) in acquiring the collision-induced dissociation (CID)-MS2 data of PJM was compared. The general settings in Auto MS/MS (M1) were common for all three methods, and their only difference was the absence or inclusion of different PILs. In M1, no PIL was input, and intensity ranking-based selection of top 3 most intense precursors was achievable. M2 and M3 could be regarded as the PIL-including improved DDA strategies. For M2, the target masses (including 305 different m/z values, in total) corresponding to the known 579 ginsenosides, by considering the different adduct forms (e.g. both [M−H]− and [M−H + HCOOH]− for the neutral ginsenosides; [M−H]− for the acidic saponins such as the OA-type and malonylated), were input. For M3, the target masses (103 different m/z values; Additional file 1: Table S2) resulting from the screening of the high-accuracy MS1 data of PJM with MDF were input.
Development of the “Ginsenoside Sieve” was generally consistent with our previous report [44 (link)], which was based on the fixed variation range MDF and the in-house ginsenoside library. In detail, these 579 ginsenosides collected in the in-house database were in accordance with 185 different masses after removing the repeated values. The integer mass and decimal mass were distinguished by using the mod and trunc functions of Excel. The variation range, {Decimal mass − 10 mDa, Decimal mass + 10 mDa}, combined with the integer mass, could generate a sieve for ginsenosides. The established “Ginsenoside Sieve” was utilized to screen target m/z values from the MS1 raw data of PJM processed by the MassHunter Workstation software.
Jiang M., Li X., Zhao Y., Zou Y., Bai M., Yang Z., Wang W., Xu X., Wang H., Yang W., Chen Q, & Guo D. (2023). Characterization of ginsenosides from Panax japonicus var. major (Zhu-Zi-Shen) based on ultra-high performance liquid chromatography/quadrupole time-of-flight mass spectrometry and desorption electrospray ionization-mass spectrometry imaging. Chinese Medicine, 18, 115.
Full text: Click here
Publication 2023
1-naphthol-8-amino-3,6-disulfonic acid cDNA Library Ginsenoside Ginsenosides Saponins Tandem Mass Spectrometry Torso
3
Apoptosis Induction by Ginsenoside M1
Not available on PMC !

Example 3

To gain further insight into the mode of action of ginsenoside M1, three assays targeting hallmarks of apoptosis, namely (1) the apoptotic DNA breaks assayed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, (2) the cell cycle assayed by flow cytometry after propidium iodide (PI)-staining nuclei, (3) the PI/Annexin V double staining assay, and (4) caspase activation were performed. Plate 1×106 human oral cancer cells OECM-1 per 6-cm dish in 2 ml of culture medium and were grown overnight at 37° C. in a 5% CO2 incubator. The cells were incubated for 24 h with ginsenoside M1 (10˜20 μg/ml), 50 μM cistaplatin (CDDP) or vehicle. Each group contains a final DMSO concentration of 0.1%. Thereafter, three assays were performed. We found that 20 μg/ml ginsenoside M1 and 50 μM CDDP, but not 10 μg/ml ginsenoside M1 significantly induced apoptotic DNA breaks in OECM-1 cells (FIG. 3A). In addition, the effect of ginsenoside M1 on the cell cycle distribution in OECM-1 cells was determined and we found that the cells in G1 phase increased in a concentration-dependent manner after treatment with ginsenoside M1 and CDDP, while concomitantly decreasing the percentage of cells in S and G2/M phase as compared with the control cells, indicating that ginsenoside M1 and CDDP induced cell cycle arrest at G1 phase (FIG. 3B). The cells in sub-G1 phase increased after treatment with ginsenoside M1 and CDDP. (FIG. 3B). Moreover, we found that 20 μg/ml ginsenoside M1 and 50 μM CDDP, but not 10 μg/ml ginsenoside M1 significantly increased the percentage of OECM-1 cells with PI/Annexin V double positive staining (FIG. 3C). These results indicated that ginsenoside M1 induced human oral cancer cells OECM-1 apoptosis significantly at concentration of 20 μg/ml. The apoptosis induction activity of ginsenoside M1 in human oral cancer SAS cells was confirmed as ginsenoside M1 induced a decrease of the precursors of caspase-3 and caspase-9 in a dose-dependent manner, indicating that caspase 3 and caspase-9 were activated by ginsenoside M1 (FIG. 3D). The data were expressed as mean±SD; n=3. ** and *** indicate a significant difference at the level of p<0.01 and p<0.001, respectively, compared to vehicle-control cells. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
4
Ginsenoside M1 Inhibits Oral Cancer Xenografts
Not available on PMC !

Example 6

To evaluate the anti-cancer activity of ginsenoside M1 in vivo, human oral cancer xenografts were used. Six-week-old male congenital athymic BALB/c nude (nu/nu) mice were purchased from BioLASCO Taiwan Co., Ltd (Ilan, Taiwan), and housed in a room under controlled temperature (23±3° C.) and relative humidity (50±5%). Animal experiments were performed with the approval of the Institutional Animal Care and Use Committee of the National Ilan University (approval number: No. 106-13) according to the NIH Guide for the Care and Use of Laboratory Animals. Xenografts mice were established by subcutaneous (SC) injection of 2×106 human oral cancer cells SAS (in 75 μl PBS+75 μl Matrigel) on the backs of the nude mice. After the tumor has reached about 40˜60 mm3 in size, the mice were randomized into six groups (six mice each): (1) oral vehicle control; (2) oral 30 mg/kg ginsenoside M1; (3) oral 60 mg/kg ginsenoside M1; (4) oral 90 mg/kg ginsenoside M1; (5) SC vehicle control; (6) SC 20 mg/kg ginsenoside M1. The mice were given a daily oral administration or SC injection of either vehicle or ginsenoside M1 for 5 successive days. The mice were scarified at 24 h after received the last dose of ginsenoside M1 or vehicle. The tumor volume (TV) was determined by measurement of the length (L) and width (W) of the tumor. The TV on day n (TVn) was calculated as TV (mm3)=(L×W2)/2. The relative tumor volume on day n (RTVn) versus day 0 was expressed according to the following formula: RTVn=TVn/TV0. We found that oral administration of ginsenoside M1 at 90 mg/kg significantly reduced the tumor size compared to vehicle control group; however, oral administration of ginsenoside M1 at 30 and 60 mg/kg did not significant reduce the tumor size (FIG. 6A) and tumor weight (FIG. 6B). Oral administration of ginsenoside M1 did not significantly affect the body weight of mice (FIG. 6C). The data were expressed as mean±SD; n=6. ** and *** indicate a significant difference at the level of p<0.01 and p<0.001, respectively, compared to vehicle-control mice. (One-way ANOVA with Dunnett's multiple comparisons test).

In addition, SC injection of 20 mg/kg ginsenoside M1 also significantly reduced the tumor size (FIG. 7A) and tumor weight (FIG. 7B) compared to vehicle control group. SC injection of ginsenoside M1 did not significantly affect the body weight of mice (FIG. 7C). The data were expressed as mean±SD; n=6. ** indicates a significant difference at the level of p<0.01, compared to vehicle-control mice. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
5
Comparative Cytotoxicity of Ginsenosides
Not available on PMC !

Example 2

Plate 5×105 normal human gingival epithelioid cell line SG per 6-cm dish in 2 ml of culture medium and were grown overnight at 37° C. in a 5% CO2 incubator. The cells were incubated for 24 h with ginsenoside M1 (5˜20 μg/ml), ginsenoside Rh2 (5˜20 μg/ml) or vehicle. Each group contains a final DMSO concentration of 0.1%. Thereafter, the cell numbers were counted by Trypan blue exclusion method. We found that ginsenoside M1 showed less toxic to SG cells than ginsenoside Rh2 (FIG. 2). Ginsenoside Rh2 at 20 μg/ml completely killed the SG cells; however, ginsenoside M1 at 20 μg/ml only reduced 50% cell number compared to control cells (namely at least 50% normal cells were preserved) (FIG. 2). The data were expressed as mean±SD; n=3. ** and *** indicate a significant difference at the level of p<0.01 and p<0.001, respectively, compared to vehicle-control cells. (One-way ANOVA with Dunnett's multiple comparisons test).

US11524021B2. Use of ginsenoside M1 for manufacturing medicament for treating oral cancer (2022-12-13). None [TW]. Inventors: Sheau-Long Lee [TW], Kuo-Feng Hua [TW], Yu-Chieh Lee [TW].
Full text: Click here
Patent 2022
Cell Lines Cells Culture Media Epithelioid Cells Gingiva Ginsenoside ginsenoside Rh2 Homo sapiens Hyperostosis, Diffuse Idiopathic Skeletal neuro-oncological ventral antigen 2, human Sulfoxide, Dimethyl Trypan Blue

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More about "Ginsenoside M1"

Ginsenoside M1 is a natural compound derived from the ginseng plant root.
It has garnered increasing research interest due to its potential therapeutic benefits, including anti-inflammatory, antioxidant, and neuroprotective effects.
PubCompare.ai's AI-driven protocols can optimize your Ginsenoside M1 research by locating relevant protocols from literature, preprints, and patents, and using advanced AI comparisons to identify the best protocols and products.
This can simplify your research and accelerate your discoveries around this important compound.
Ginsenoside M1, also known as 20(S)-Ginsenoside Rh1, is a triterpenoid saponin that can be extracted from the Panax ginseng plant.
It has been the subject of numerous studies exploring its pharmacological properties and potential applications in various medical fields.
Research has indicated that Ginsenoside M1 may possess anti-inflammatory, antioxidant, and neuroprotective effects, making it a promising candidate for the treatment of conditions such as neurodegenerative diseases, cancer, and metabolic disorders.
To optimize your research on Ginsenoside M1, PubCompare.ai's AI-driven protocols can help you locate relevant experimental protocols from the literature, preprints, and patents.
These protocols may include methods for the extraction and purification of Ginsenoside M1, as well as in vitro and in vivo assays to evaluate its biological activities.
The AI-driven comparisons can help you identify the most effective and efficient protocols, saving you time and resources in your research.
In addition to locating relevant protocols, PubCompare.ai's tools can also help you identify the best products and reagents for your Ginsenoside M1 research.
This may include 3H-thymidine for cell proliferation assays, the ABI 7500 system for gene expression analysis, Dihydroethidium (DHE) for oxidative stress measurement, the FACSCalibur analyzer for flow cytometry, and antibodies such as anti-mouse CD3 for immunological studies.
By streamlining your access to these essential research tools, PubCompare.ai can help you accelerate your discoveries around Ginsenoside M1 and its potential therapeutic applications.
Furthermore, PubCompare.ai's platform can provide insights into the latest research trends and developments related to Ginsenoside M1, including the identification of key subtopics such as the role of β-actin, SIRT3, and 2′,7′-dichlorofluorescein diacetate in Ginsenoside M1-mediated cellular processes.
This information can help you stay up-to-date with the latest advancements in the field and inform the direction of your own research.
In summary, PubCompare.ai's AI-driven protocols can be a valuable resource for optimizing your Ginsenoside M1 research.
By locating relevant protocols, identifying the best products and reagents, and providing insights into the latest research trends, PubCompare.ai can simplify your research process and accelerate your discoveries around this important natural compound.