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Notoginsenoside R2 (20(S)-Notoginsenoside R2; Ginsenoside Ng-R2) is an orally active notoginsenoside. Notoginsenoside R2 activates P90RSK and Nrf2 via the MEK1/2-ERK1/2 pathway to inhibit 6-OHDA-induced apoptotic damage in nerve cells. Notoginsenoside R2 upregulates SOX8/β-catenin by reducing miR-27a, thereby suppressing Aβ25-35-induced neuronal apoptosis and inflammatory responses. Notoginsenoside R2 alleviates lipid accumulation and mitochondrial dysfunction in diabetic nephropathy by inhibiting c-Src. Notoginsenoside R2 alleviates hepatic fibrosis by inducing hepatic stellate cell senescence and inhibiting the inflammatory microenvironment via JAK/STAT3 suppression. Notoginsenoside R2 can be used in research related to Parkinson's disease, Alzheimer's disease, diabetic nephropathy and hepatic fibrosis.
Notoginsenoside R2 (20(S)-Notoginsenoside R2; Ginsenoside Ng-R2) is an orally active notoginsenoside. Notoginsenoside R2 activates P90RSK and Nrf2 via the MEK1/2-ERK1/2 pathway to inhibit 6-OHDA-induced apoptotic damage in nerve cells. Notoginsenoside R2 upregulates SOX8/β-catenin by reducing miR-27a, thereby suppressing Aβ25-35-induced neuronal apoptosis and inflammatory responses. Notoginsenoside R2 alleviates lipid accumulation and mitochondrial dysfunction in diabetic nephropathy by inhibiting c-Src. Notoginsenoside R2 alleviates hepatic fibrosis by inducing hepatic stellate cell senescence and inhibiting the inflammatory microenvironment via JAK/STAT3 suppression. Notoginsenoside R2 can be used in research related to Parkinson's disease, Alzheimer's disease, diabetic nephropathy and hepatic fibrosis[1][2][3][4][5].
In Vitro
Notoginsenoside R2 (20 μM; 24 h) protects SH-SY5Y cells against 6-OHDA (HY-B1081)-induced cell death, with reduced counts of TUNEL-positive cells and decreased overall apoptosis rate[1]. Notoginsenoside R2 (20 μM; 24 h) reduces 6-OHDA-induced LDH release in SH-SY5Y cells, PC12 cells, and primary cortical neurons[1]. Notoginsenoside R2 (20 μM; 24 h) inhibits 6-OHDA-induced oxidative stress in SH-SY5Y cells, as evidenced by decreased intracellular ROS production and MDA levels, and reverses mitochondrial membrane depolarization in cells[1]. Notoginsenoside R2 (20 μM) increases the activities of HO-1, GSH-PX and GR in SH-SY5Y cells, and pre-incubation for 24 h reverses the 6-OHDA-induced decreases in the activities of these enzymes and the reduced nuclear accumulation level of Nrf2[1]. Notoginsenoside R2 (20 μM; 4-24 h) activates the MEK1/2-ERK1/2 signaling pathway in SH-SY5Y cells, thereby inducing the activation of downstream P90RSK and Nrf2. The latter mediates the inhibition of 6-OHDA-induced apoptotic protein expression. Notably, the activation of the aforementioned pathway depends on MEK1/2-ERK1/2 signal transduction, but is independent of JNK, p38 or PI3K/Akt signal transduction[1]. Notoginsenoside R2 (10-30 μM) dose-dependently attenuates Aβ25-35 (HY-P0128)-induced apoptosis of primary rat cortical neurons, reduces the expression levels of activated caspase-3 and miR-27a, downregulates COX-2 expression, upregulates the mRNA and protein expression of SOX8, and increases the expression of total β-catenin protein and nuclear β-catenin protein[2]. Notoginsenoside R2 (10-40 μM; 24 h) attenuates lipid accumulation, oxidative stress, mitochondrial dysfunction and apoptosis in HK-2 cells stimulated with high glucose and palmitic acid (HGPA) by inhibiting c-Src activation[3]. Notoginsenoside R2 (10-100 μM; 24 h) inhibits the proliferation of HSC-T6 cells[5]. Notoginsenoside R2 (20-30 μM; 24 h) downregulates the mRNA and protein expressions of α-SMA and COL-I in HSC-T6 cells[5]. Notoginsenoside R2 (20 μM; 24 h) downregulates fibrosis markers (α-SMA, COL-I, Desmin, TIMP-1) and upregulates senescence markers (p16, p21, p53) in HSC-T6 cells[5]. Notoginsenoside R2 (20 μM; 24 h) inhibits the JAK/STAT3 signaling pathway in HSC-T6 cells[5]. Notoginsenoside R2 (20 μM; 24 h) inhibits the mRNA expression of proinflammatory cytokines in HSC-T6 cells[5]. Notoginsenoside R2 (20 μM; 24 h) upregulates the mRNA expression of SASP components in HSC-T6 cells[5]. Notoginsenoside R2 (20 μM; 24 h) reduces intracellular ROS levels in HSC-T6 cells[5]. Notoginsenoside R2 (20 μM; 24 h) induces senescence in HSC-T6 cells[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Significantly reduced the number of TUNEL-positive cells and the overall apoptosis rate induced by 6-OHDA. Had no effect on apoptosis rate or TUNEL-positive cell count when treated alone.
Increased phosphorylation of P90RSK, BAD, MEK1/2, and ERK1/2, and enhanced nuclear Nrf2 accumulation in a time-dependent manner when treated alone, with MEK1/2 phosphorylation peaking at 16 h and ERK1/2 phosphorylation peaking at 20 h. Blocked 6-OHDA-induced increases in cytochrome c release, cleaved caspase-9, and cleaved caspase-3, and reversed 6-OHDA-induced reductions in p-BAD levels when pre-incubated for 24 h. Induced P90RSK phosphorylation and nuclear Nrf2 accumulation were prevented by pre-incubation with MEK1/2 inhibitor PD98059, while JNK, p38, or PI3K/Akt inhibitors had no effect. Induced phosphorylation of ERK1/2, P90RSK, and BAD, as well as nuclear Nrf2 accumulation and increases in HO-1, GSH-PX, and GR activities were blocked by MEK1/2 or ERK1/2 siRNA transfection. Induced increases in HO-1, GSH-PX, and GR activities were blocked by Nrf2 siRNA transfection.
Suppressed HSC-T6 cell proliferation in a dose-dependent manner at concentrations of 40-100 μM. Caused statistically significant reductions in cell viability at 80 μM and 100 μM relative to the normal control.
Caused a marked reduction in mRNA expression of α-SMA relative to the normal control. Caused a marked reduction in mRNA expression of COL-I relative to the normal control.
Significantly decreased the area of α-SMA staining in HSC-T6 cells relative to the normal control. Significantly decreased the area of COL-I staining in HSC-T6 cells relative to the normal control.
Significantly reduced protein expression of α-SMA relative to the normal control. Significantly reduced protein expression of COL-I) relative to the normal control. Significantly reduced protein expression of Desmin relative to the normal control. Significantly reduced protein expression of TIMP-1 relative to the normal control. Significantly increased protein expression of p16 relative to the normal control. Significantly increased protein expression of p21 relative to the normal control. Significantly increased protein expression of p53 relative to the normal control.\nSignificantly reduced the phosphorylation of JAK relative to the normal control. Significantly reduced the phosphorylation of STAT3 relative to the normal control. Left total JAK and STAT3 protein levels unchanged.
Significantly reduced mRNA expression of pro-inflammatory mediators including IL-6, IL-1β, CCL2, IL-8, and TNF-α relative to the normal control.\nSignificantly upregulated mRNA expression of SASP components including p16, p21, p53, and MMP10 relative to the normal control.
In Vivo
Notoginsenoside R2 (250 mg/kg, i.p., once daily for 20 consecutive weeks) improves cognitive function, reduces hippocampal neuronal apoptosis, and regulates the expression of apoptosis- and inflammation-related proteins in SAMP8 mice, a spontaneous Alzheimer's disease model[2]. Notoginsenoside R2 (250 mg/kg; i.p.; once daily; for 20 consecutive weeks) improves cognitive function in Alzheimer's disease rats induced by Aβ25-35, reduces hippocampal neuronal apoptosis, and regulates the expression of apoptosis- and inflammation-related proteins[2]. Notoginsenoside R2 (20-40 mg/kg, oral administration daily for 8 weeks) improves renal dysfunction, histopathological damage, lipid accumulation, oxidative stress, mitochondrial dysfunction and apoptosis in db/db mice, a model of diabetic nephropathy. This effect is partially achieved by inhibiting the activation of c-Src[3]. Notoginsenoside R2 (6.25-25 μM; administered 72 hours after TAA pretreatment) alleviates TAA (HY-Y0698)-induced liver fibrosis in zebrafish in a dose-dependent manner by reducing oxidative stress, suppressing inflammatory responses, and inducing hepatic stellate cell senescence via a STAT3-dependent pathway[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Reduced learning reaction time to 25.23 s. Reduced learning error time to 4.52. Increased memory reaction time to 180 s. Reduced memory error time to 5.41. Alleviated hippocampal neuronal disorganization and loss of pyramidal cells. Reduced TUNEL-positive apoptotic cells compared to the AD group. Decreased cleaved caspase-3 and COX-2 protein expression compared to the AD group. Increased SOX8 and β-catenin protein expression compared to the AD group.
Animal Model:
Sprague-Dawley (male, 18-20 months-old, 200-220 g, Aβ25-35-induced Alzheimer's disease model via bilateral hippocampal injection); Sprague-Dawley (male, 3-6 months-old, control)[2]
Dosage:
250 mg/kg
Administration:
i.p.; daily; 20 consecutive weeks
Result:
Reduced learning reaction time to 25.23 s. Reduced learning error time to 3.98. Increased memory reaction time to 182.32 s. Reduced memory error time to 6.23. Restored hippocampal neuronal structure compared to the Aβ25-35-treated group. Reduced TUNEL-positive apoptotic cells compared to the Aβ25-35-treated group. Decreased cleaved caspase-3 and COX-2 protein expression compared to the Aβ25-35-treated group. Increased SOX8 and β-catenin protein expression compared to the Aβ25-35-treated group.
Reduced urine albumin-to-creatinine ratios (ACR) levels compared to untreated db/db mice, with 40 mg/kg dose causing greater reduction than positive control Losartan. Significantly lowered serum creatinine (Scr) and blood urea nitrogen (BUN) levels relative to untreated db/db mice at 40 mg/kg dose; significantly reduced Scr levels at 20 mg/kg dose. Significantly reduced serum total cholesterol (TC) levels compared to untreated db/db mice at 20 mg/kg dose; reduced TC levels to a greater, statistically significant extent at 40 mg/kg dose. Left serum triglyceride (TG) levels unchanged with either dose. Unaffected liver function markers (ALT, AST), indicating no liver toxicity. Ameliorated renal histopathological abnormalities including mesangial expansion, glycogen deposition, collagen fiber deposition, and podocyte foot process effacement, and significantly reduced renal expression of fibrosis-related proteins (fibronectin, vimentin, α-SMA) at both doses. Significantly reduced intrarenal lipid accumulation (measured by Oil Red O staining and renal triglyceride content), and suppressed renal expression of phosphorylated c-Src (Tyr416), phosphorylated JNK, phosphorylated STAT1, and CD36 at both doses. Reduced renal malondialdehyde (MDA) levels, increased superoxide dismutase (SOD), glutathione (GSH), glutathione reductase (GR), catalase (CAT), and ATP levels relative to untreated db/db mice at both doses. Downregulated renal expression of mitochondrial fission proteins Drp1 and Fis1, and upregulated the mitochondrial fusion protein Mfn2 at both doses. Reduced renal TUNEL-positive apoptotic cells, lowered expression of pro-apoptotic proteins (Bax, cleaved-caspase-3), and increased expression of the anti-apoptotic protein Bcl-2 at both doses.
Animal Model:
wild-type AB strain; transgenic Tg(lfabp10α:eGFP) strain (2-day post-fertilization larvae)[5]
administered following 72-hour TAA preconditioning
Result:
Caused no notable morphological abnormalities, developmental delays, or hatching rate differences compared to untreated controls at 6.25 μM, 12.5 μM, and 25 μM. Significantly mitigated TAA-induced hepatic damage (reduced intercellular gaps, hepatocellular enlargement, and vacuolation) as observed via H&E staining, and dose-dependently reduced mRNA levels of fibrotic markers α-SMA and COL-I at 6.25 μM, 12.5 μM, and 25 μM. Significantly reduced hepatic reactive oxygen species (ROS) levels, reduced mRNA expression of pro-inflammatory cytokines (IL-6, IL-1β, CCL2, IL-8, TNF-α), reduced STAT3 protein levels and JAK/STAT3 pathway gene expression, and significantly upregulated protein and mRNA levels of senescence biomarkers p16 and p21, plus SASP components including p53 at 25 μM. Lost antifibrotic effects in STAT3-knockdown zebrafish: no longer mitigated hepatic vacuolation/tissue disorganization, failed to reduce α-SMA and COL-I mRNA levels, showed diminished ROS suppression, lost anti-inflammatory activity, and no longer upregulated senescence biomarkers p16 and p21 or SASP components at 25 μM.
DMSO : 100 mg/mL (129.70 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
1.2970 mL
6.4852 mL
12.9703 mL
5 mM
0.2594 mL
1.2970 mL
2.5941 mL
10 mM
0.1297 mL
0.6485 mL
1.2970 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (3.24 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (3.24 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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