Senegenin

CAS# 2469-34-3

Senegenin

Catalog No. BCN5899----Order now to get a substantial discount!

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Quality Control of Senegenin

Number of papers citing our products

Chemical structure

Senegenin

3D structure

Chemical Properties of Senegenin

Cas No. 2469-34-3 SDF Download SDF
PubChem ID 200662 Appearance White powder
Formula C30H45ClO6 M.Wt 537.14
Type of Compound Triterpenoids Storage Desiccate at -20°C
Solubility DMSO : 100 mg/mL (186.17 mM; Need ultrasonic)
Chemical Name 13-(chloromethyl)-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-2,3,4a,5,6,7,8,9,10,12,12a,13,14,14a-tetradecahydro-1H-picene-4,8a-dicarboxylic acid
SMILES CC1(CCC2(CCC3=C(C2C1)C(CC4C3(CCC5C4(CC(C(C5(C)C(=O)O)O)O)C)C)CCl)C(=O)O)C
Standard InChIKey CWHJIJJSDGEHNS-UHFFFAOYSA-N
Standard InChI InChI=1S/C30H45ClO6/c1-26(2)10-11-30(25(36)37)9-6-17-22(18(30)13-26)16(15-31)12-21-27(17,3)8-7-20-28(21,4)14-19(32)23(33)29(20,5)24(34)35/h16,18-21,23,32-33H,6-15H2,1-5H3,(H,34,35)(H,36,37)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Senegenin

The root of Polygala tenuifolia Willd

Biological Activity of Senegenin

DescriptionSenegenin has anti-apoptotic,anti-oxidative,and neuroprotective activities, it might be a potential agent for prevention and treatment of postoperative cognitive dysfunction (POCD) or other neurodegenerative diseases. It also be a potential therapeutic agent against sepsis. Senegenin decreased the levels of TNF-α ,IL-1β, NF-κB.
TargetsTNF-α | IL Receptor | NF-kB | JNK
In vitro

Neurotrophic effects of senegenin.[Pubmed: 24620696]

Zhong Yao Cai. 2013 Sep;36(9):1477-80.

To study the neurotrophic effects of Senegenin on the expression of MAP2 mRNA and BDNF mRNA in cultured cerebral cortical neurons.
METHODS AND RESULTS:
The newborn rat cerebral cortex neurons were cultured in vitro. LDH assay was used to investigate the effect of Senegenin on the neuronal viability and reverse transcription polymerase chain reaction (RT-PCR) was carried out to determine the expression level of MAP2 mRNA and BDNF mRNA. LDH assay showed that Senegenin at the concentration of 0. 5 micromol/L,1 micromol/L and 2 micromol/L could obviously enhance the survival of cells and the survival rates were in dose-dependent manner to some extent. Moreover, the low, medium and high concentrations of Senegenin significantly increased the expression of MAP2 mRNA and BDNF mRNA.
CONCLUSIONS:
The study suggests that suitable dose of Senegenin can increase the expression of MAP2 mRNA and BDNF mRNA in cultured cerebral cortical neurons, and its mechanism needs further study.

In vivo

Senegenin Ameliorate Acute Lung Injury Through Reduction of Oxidative Stress and Inhibition of Inflammation in Cecal Ligation and Puncture-Induced Sepsis Rats.[Pubmed: 26945584 ]

Inflammation. 2016 Apr;39(2):900-6.

The purpose of this study was to assess the protective effect of Senegenin on acute lung injury (ALI) in rats induced by sepsis.
METHODS AND RESULTS:
Rat ALI model was reproduced by cecal ligation and puncture (CLP). All rats were randomly divided into five groups: group 1 (control), group 2 (CLP), group 3 (CLP + Senegenin 15 mg/kg), group 4 (CLP + Senegenin 30 mg/kg), and group 5 (CLP + Senegenin 60 mg/kg). CLP + Senegenin groups received Senegenin by gavage daily for consecutive 5 days, respectively, while the mice in control and CLP groups were given an equivalent volume of saline. We detected the lung wet/dry weight ratios and the histopathology of the lung. The levels of lung tissue myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were determined. Meanwhile, the nuclear factor-kappa B (NF-κB) activation, tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β) levels were studied. The results demonstrated that Senegenin treatment significantly attenuated CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and MPO activity. In addition, Senegenin markedly decreased MDA content and increased SOD activity and GSH level. Serum levels of TNF-α and IL-1β were also decreased by Senegenin administration. Furthermore, Senegenin administration inhibited the nuclear translocation of NF-κB in the lungs.
CONCLUSIONS:
These findings indicate that Senegenin exerts protective effects on CLP-induced septic rats. Senegenin may be a potential therapeutic agent against sepsis.

Protocol of Senegenin

Cell Research

Senegenin Inhibits Hypoxia/Reoxygenation-Induced Neuronal Apoptosis by Upregulating RhoGDIα[Pubmed: 25367882]

Mol Neurobiol. 2014 Nov 4.

Neuronal apoptosis is an important event in hypoxia/reoxygenation (H/R)-induced neuronal injury. Senegenin (Sen), the predominant and most active component in Radix Polygalae root extracts, displays anti-apoptotic and anti-oxidative properties. Sen protects against H/R-induced neuronal apoptosis of highly differentiated PC12 cells and primary cortical neurons. Sen has also been investigated as a source of potential therapeutic targets.
METHODS AND RESULTS:
In this study, a proteomic approach was used to identify Sen-regulated proteins in PC12 cells. We found that Sen protected against H/R-induced neuronal apoptosis by upregulating RhoGDIα protein expression. The regulatory functions of RhoGDIα were investigated by knocking down RhoGDIα expression in PC12 cells using small interfering RNA (siRNA), followed by quantification of apoptosis and then altering the expression levels of apoptosis-related proteins. Our data show that after silencing RhoGDIα, the neuroprotective effects of Sen on H/R-induced PC12 cell apoptosis were absent. Furthermore, RhoGDIα silencing alleviated the Sen-mediated inhibition of the JNK pathway.
CONCLUSIONS:
Therefore, these findings indicated that Sen attenuates H/R-induced neuronal apoptosis by upregulating RhoGDIα expression and inhibiting the JNK pathway. In addition to the mechanism underlying neuroprotective effects of Sen, RhoGDIα was identified as a putative target of Sen based on a primary rat cortical neuron model of H/R-induced injury.

Animal Research

Protective effect of senegenin on splenectomy-induced postoperative cognitive dysfunction in elderly rats.[Pubmed: 24660030]

Exp Ther Med. 2014 Apr;7(4):821-826. Epub 2014 Jan 24.

Postoperative cognitive dysfunction (POCD) is common in elderly patients. Senegenin, an active component of extracts from Polygala tenuifolia root, a traditional Chinese medicine, has neuroprotective and neuroregenerative effects. However, the mechanism underlying the effects of Senegenin against postoperative cognitive impairment in elderly individuals has yet to be elucidated.
METHODS AND RESULTS:
The aim of this study was to investigate the protective effects of Senegenin on the cognitive functions of elderly rats with splenectomy-induced POCD. Results from a Morris water maze test suggested that splenectomy induced a transient cognitive deficiency in the elderly rats; however, when the rats were treated with Senegenin, the cognitive impairment was notably attenuated. Further experiments showed that Senegenin significantly inhibited the mRNA and protein expression of several key pro-inflammatory cytokines, specifically, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-8, in the hippocampal tissues of elderly rats following splenectomy. In order to investigate the molecular mechanism involved, the expression and activity of the Toll-like receptor 4 (TLR4) signaling pathway was assessed. On day 1 postoperatively, it was observed that Senegenin markedly suppressed the mRNA and protein expression of TLR4, myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor-inducing interferon-β (TRIF). Furthermore, the phosphorylation levels of nuclear factor-κB (NF-κB) p65 and inhibitor of NF-κB (IκBα) were also decreased following Senegenin treatment on the first day subsequent to surgery. These results suggest that Senegenin suppressed splenectomy-induced transient cognitive impairment in elderly rats, possibly by downregulating two signaling pathways involved in inflammation, TLR4/MyD88/NF-κB and TLR4/TRIF/NF-κB, to further inhibit the expression of key pro-inflammatory cytokines, specifically, TNF-α, IL-1β, IL-6 and IL-8, and ultimately the neuroinflammation in the hippocampal tissues.
CONCLUSIONS:
In conclusion, the present study revealed that Senegenin exhibited neuroprotective effects against splenectomy-induced transient cognitive impairment in elderly rats, which indicated that Senegenin may be a promising agent for the treatment of POCD.

Senegenin Dilution Calculator

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Preparing Stock Solutions of Senegenin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.8617 mL 9.3086 mL 18.6171 mL 37.2342 mL 46.5428 mL
5 mM 0.3723 mL 1.8617 mL 3.7234 mL 7.4468 mL 9.3086 mL
10 mM 0.1862 mL 0.9309 mL 1.8617 mL 3.7234 mL 4.6543 mL
50 mM 0.0372 mL 0.1862 mL 0.3723 mL 0.7447 mL 0.9309 mL
100 mM 0.0186 mL 0.0931 mL 0.1862 mL 0.3723 mL 0.4654 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Senegenin

Senegenin attenuates hepatic ischemia-reperfusion induced cognitive dysfunction by increasing hippocampal NR2B expression in rats.[Pubmed:23029109]

PLoS One. 2012;7(9):e45575.

BACKGROUND: The root of Polygala tenuifolia, a traditional Chinese medicine, has been used to improve memory and intelligence, while the underlying mechanisms remain largely unknown. In this study, we investigated the protective effects of Senegenin, an component of Polygala tenuifolia root extracts, on cognitive dysfunction induced by hepatic ischemia-reperfusion. METHODOLOGY/PRINCIPAL FINDINGS: Initially, we constructed a rat model of hepatic ischemia-reperfusion (HIR) and found that the memory retention ability of rats in the step-down and Y maze test was impaired after HIR, paralleled by a decrease of N-methyl-D-aspartate (NMDA) receptor NR2B subunit mRNA and protein expressions in hippocampus. Furthermore, we found that administration of Senegenin by gavage attenuated HIR-induced cognitive impairment in a dose and time dependent manner, and its mechanisms might partly due to the increasing expression of NR2B in rat hippocampus. CONCLUSIONS/SIGNIFICANCE: Cognitive dysfunction induced by HIR is associated with reduction of NR2B expression. Senegenin plays a neuroprotective role in HIR via increasing NR2B expression in rat hippocampus. These findings suggest that Senegenin might be a potential agent for prevention and treatment of postoperative cognitive dysfunction (POCD) or other neurodegenerative diseases.

Senegenin Inhibits Hypoxia/Reoxygenation-Induced Neuronal Apoptosis by Upregulating RhoGDIalpha.[Pubmed:25367882]

Mol Neurobiol. 2015 Dec;52(3):1561-1571.

Neuronal apoptosis is an important event in hypoxia/reoxygenation (H/R)-induced neuronal injury. Senegenin (Sen), the predominant and most active component in Radix Polygalae root extracts, displays anti-apoptotic and anti-oxidative properties. Sen protects against H/R-induced neuronal apoptosis of highly differentiated PC12 cells and primary cortical neurons. Sen has also been investigated as a source of potential therapeutic targets. In this study, a proteomic approach was used to identify Sen-regulated proteins in PC12 cells. We found that Sen protected against H/R-induced neuronal apoptosis by upregulating RhoGDIalpha protein expression. The regulatory functions of RhoGDIalpha were investigated by knocking down RhoGDIalpha expression in PC12 cells using small interfering RNA (siRNA), followed by quantification of apoptosis and then altering the expression levels of apoptosis-related proteins. Our data show that after silencing RhoGDIalpha, the neuroprotective effects of Sen on H/R-induced PC12 cell apoptosis were absent. Furthermore, RhoGDIalpha silencing alleviated the Sen-mediated inhibition of the JNK pathway. Therefore, these findings indicated that Sen attenuates H/R-induced neuronal apoptosis by upregulating RhoGDIalpha expression and inhibiting the JNK pathway. In addition to the mechanism underlying neuroprotective effects of Sen, RhoGDIalpha was identified as a putative target of Sen based on a primary rat cortical neuron model of H/R-induced injury.

Protective effect of senegenin on splenectomy-induced postoperative cognitive dysfunction in elderly rats.[Pubmed:24660030]

Exp Ther Med. 2014 Apr;7(4):821-826.

Postoperative cognitive dysfunction (POCD) is common in elderly patients. Senegenin, an active component of extracts from Polygala tenuifolia root, a traditional Chinese medicine, has neuroprotective and neuroregenerative effects. However, the mechanism underlying the effects of Senegenin against postoperative cognitive impairment in elderly individuals has yet to be elucidated. The aim of this study was to investigate the protective effects of Senegenin on the cognitive functions of elderly rats with splenectomy-induced POCD. Results from a Morris water maze test suggested that splenectomy induced a transient cognitive deficiency in the elderly rats; however, when the rats were treated with Senegenin, the cognitive impairment was notably attenuated. Further experiments showed that Senegenin significantly inhibited the mRNA and protein expression of several key pro-inflammatory cytokines, specifically, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), IL-6 and IL-8, in the hippocampal tissues of elderly rats following splenectomy. In order to investigate the molecular mechanism involved, the expression and activity of the Toll-like receptor 4 (TLR4) signaling pathway was assessed. On day 1 postoperatively, it was observed that Senegenin markedly suppressed the mRNA and protein expression of TLR4, myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor-inducing interferon-beta (TRIF). Furthermore, the phosphorylation levels of nuclear factor-kappaB (NF-kappaB) p65 and inhibitor of NF-kappaB (IkappaBalpha) were also decreased following Senegenin treatment on the first day subsequent to surgery. These results suggest that Senegenin suppressed splenectomy-induced transient cognitive impairment in elderly rats, possibly by downregulating two signaling pathways involved in inflammation, TLR4/MyD88/NF-kappaB and TLR4/TRIF/NF-kappaB, to further inhibit the expression of key pro-inflammatory cytokines, specifically, TNF-alpha, IL-1beta, IL-6 and IL-8, and ultimately the neuroinflammation in the hippocampal tissues. In conclusion, the present study revealed that Senegenin exhibited neuroprotective effects against splenectomy-induced transient cognitive impairment in elderly rats, which indicated that Senegenin may be a promising agent for the treatment of POCD.

Senegenin Ameliorate Acute Lung Injury Through Reduction of Oxidative Stress and Inhibition of Inflammation in Cecal Ligation and Puncture-Induced Sepsis Rats.[Pubmed:26945584]

Inflammation. 2016 Apr;39(2):900-6.

The purpose of this study was to assess the protective effect of Senegenin on acute lung injury (ALI) in rats induced by sepsis. Rat ALI model was reproduced by cecal ligation and puncture (CLP). All rats were randomly divided into five groups: group 1 (control), group 2 (CLP), group 3 (CLP + Senegenin 15 mg/kg), group 4 (CLP + Senegenin 30 mg/kg), and group 5 (CLP + Senegenin 60 mg/kg). CLP + Senegenin groups received Senegenin by gavage daily for consecutive 5 days, respectively, while the mice in control and CLP groups were given an equivalent volume of saline. We detected the lung wet/dry weight ratios and the histopathology of the lung. The levels of lung tissue myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were determined. Meanwhile, the nuclear factor-kappa B (NF-kappaB) activation, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) levels were studied. The results demonstrated that Senegenin treatment significantly attenuated CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and MPO activity. In addition, Senegenin markedly decreased MDA content and increased SOD activity and GSH level. Serum levels of TNF-alpha and IL-1beta were also decreased by Senegenin administration. Furthermore, Senegenin administration inhibited the nuclear translocation of NF-kappaB in the lungs. These findings indicate that Senegenin exerts protective effects on CLP-induced septic rats. Senegenin may be a potential therapeutic agent against sepsis.

Description

Tenuigenin is a major active component isolated from the root of the Chinese herb Polygala tenuifolia. Tenuigenin protects against S.aureus-induced pneumonia by inhibiting NF-κB activation. Tenuigenin has anti-inflammatory effect.

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