Sanguinarine CAS NO.2447-54-3

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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.

Chemical Properties of Sanguinarine

Cas No.	2447-54-3	SDF
PubChem ID	72619	Appearance	Powder
Formula	C20H14NO4	M.Wt	332.3
Type of Compound	Alkaloids	Storage	Desiccate at -20°C
Synonyms	Pseudochelerythrine; Sanguinarin
Solubility	Limited solubility
SMILES	C[N+]1=C2C(=C3C=CC4=C(C3=C1)OCO4)C=CC5=CC6=C(C=C52)OCO6.[N+](=O)([O-])[O-]
Standard InChIKey	RBKBIPRGKKUAFZ-UHFFFAOYSA-N
Standard InChI	InChI=1S/C20H14NO4.NO3/c1-21-8-15-12(4-5-16-20(15)25-10-22-16)13-3-2-11-6-17-18(24-9-23-17)7-14(11)19(13)21;2-1(3)4/h2-8H,9-10H2,1H3;/q+1;-1
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 Sanguinarine

The herbs of Chelidonium majus

Biological Activity of Sanguinarine

Description	Sanguinarine possesses anticancer, antimicrobial, anti-inflammatory, and antioxidant properties, it has therapeutic potential in preventing the neurodegenerative diseases, it may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure and shows protective effects on teeth and alveolar bone health. Sanguinarine can inhibit osteoclast formation and bone resorption via suppressing RANKL-induced activation of NF-κB and ERK signaling pathways, and can protect against cardiac hypertrophy and fibrosis via inhibiting NF-κB activation.
Targets	Akt | NF-kB | ROS | Bcl-2/Bax | Caspase | HIF | PARP | HO-1 | Nrf2 | ERK | Calcium Channel | ATPase | DNA/RNA Synthesis
In vitro	Differential antiproliferative and apoptotic response of sanguinarine for cancer cells versus normal cells.[Pubmed: 10778985] Clin Cancer Res. 2000 Apr;6(4):1524-8. Sanguinarine, derived from the root of Sanguinaria canadendid, has been shown to possess antimicrobial, anti-inflammatory, and antioxidant properties. Here we compared the antiproliferative and apoptotic potential of Sanguinarine against human epidermoid carcinoma (A431) cells and normal human epidermal keratinocytes (NHEKs). METHODS AND RESULTS: Sanguinarine treatment was found to result in a dose-dependent decrease in the viability of A431 cells as well as NHEKs albeit at different levels because Sanguinarine-mediated loss of viability occurred at lower doses and was much more pronounced in the A431 carcinoma cells than in the normal keratinocytes. DNA ladder assay demonstrated that compared to vehicle-treated control, Sanguinarine treatment of A431 cells resulted in an induction of apoptosis at 1-, 2-, and 5-microM doses. Sanguinarine treatment did not result in the formation of a DNA ladder in NHEKs, even at the very high dose of 10 microM. The induction of apoptosis by Sanguinarine was also evident by confocal microscopy after labeling the cells with annexin V. This method also identified necrotic cells, and Sanguinarine treatment also resulted in the necrosis of A431 cells. The NHEKs showed exclusively necrotic staining at high doses (2 and 5 microM). We also explored the possibility of cell cycle perturbation by Sanguinarine in A431 cells. The DNA cell cycle analysis revealed that Sanguinarine treatment did not significantly affect the distribution of cells among the different phases of the cell cycle in A431 cells. CONCLUSIONS: We suggest that Sanguinarine could be developed as an anticancer drug. Molecular signatures of sanguinarine in human pancreatic cancer cells: A large scale label-free comparative proteomics approach.[Pubmed: 25929337] Oncotarget. 2015 Apr 30;6(12):10335-49. Pancreatic cancer remains one of the most lethal of all human malignancies with its incidence nearly equaling its mortality rate. Therefore, it's crucial to identify newer mechanism-based agents and targets to effectively manage pancreatic cancer. Plant-derived agents/drugs have historically been useful in cancer therapeutics. Sanguinarine is a plant alkaloid with anti-proliferative effects against cancers, including pancreatic cancer. This study was designed to determine the mechanism of Sanguinarine's effects in pancreatic cancer with a hope to obtain useful information to improve the therapeutic options for the management of this neoplasm. METHODS AND RESULTS: We employed a quantitative proteomics approach to define the mechanism of Sanguinarine's effects in human pancreatic cancer cells. Proteins from control and Sanguinarine-treated pancreatic cancer cells were digested with trypsin, run by nano-LC/MS/MS, and identified with the help of Swiss-Prot database. Results from replicate injections were processed with the SIEVE software to identify proteins with differential expression. We identified 37 differentially expressed proteins (from a total of 3107), which are known to be involved in variety of cellular processes. Four of these proteins (IL33, CUL5, GPS1 and DUSP4) appear to occupy regulatory nodes in key pathways. Further validation by qRT-PCR and immunoblot analyses demonstrated that the dual specificity phosphatase-4 (DUSP4) was significantly upregulated by Sanguinarine in BxPC-3 and MIA PaCa-2 cells. Sanguinarine treatment also caused down-regulation of HIF1α and PCNA, and increased cleavage of PARP and Caspase-7. CONCLUSIONS: Taken together, Sanguinarine appears to have pleotropic effects, as it modulates multiple key signaling pathways, supporting the potential usefulness of Sanguinarine against pancreatic cancer. Involvement of heme oxygenase-1 in neuroprotection by sanguinarine against glutamate-triggered apoptosis in HT22 neuronal cells.[Pubmed: 25299846] Environ Toxicol Pharmacol. 2014 Nov;38(3):701-10. Sanguinarine is a natural compound isolated from the roots of Macleaya cordata and M. microcarpa, has been reported to possess several biological activities such as anti-inflammatory and anti-oxidant effects. METHODS AND RESULTS: In the present study, we demonstrated that Sanguinarine markedly induces the expression of HO-1 which leads to a neuroprotective response in mouse hippocampus-derived neuronal HT22 cells from apoptotic cell death induced by glutamate. Sanguinarine significantly attenuated the loss of mitochondrial function and membrane integrity associated with glutamate-induced neurotoxicity. Sanguinarine protected against glutamate-induced neurotoxicity through inhibition of HT22 cell apoptosis. JC-1 staining, which is a well-established measure of mitochondrial damage, was decreased after treatment with Sanguinarine in glutamate-challenged HT22cells. In addition, Sanguinarine diminished the intracellular accumulation of ROS and Ca(2+). Sanguinarine also induced HO-1, NQO-1 expression via activation of Nrf2. Additionally, we found that si RNA mediated knock-down of Nrf2 or HO-1 significantly inhibited Sanguinarine-induced neuroprotective response. CONCLUSIONS: These findings revealed the therapeutic potential of Sanguinarine in preventing the neurodegenerative diseases.
In vivo	Sanguinarine protects against pressure overload?induced cardiac remodeling via inhibition of nuclear factor-κB activation.[Pubmed: 24804701] Mol Med Rep. 2014 Jul;10(1):211-6. Cardiac remodeling is a major determinant of heart failure characterized by cardiac hypertrophy and fibrosis. Sanguinarine exerts widespread pharmacological effects, including antitumor and anti?inflammatory responses. In the present study, the effect of Sanguinarine on cardiac hypertrophy, fibrosis and heart function was determined using the model induced by aortic banding (AB) in mice. METHODS AND RESULTS: AB surgery and sham surgery were performed on male wild?type C57 mice, aged 8?10 weeks, with or without administration of Sanguinarine from one week after surgery for an additional seven weeks. Sanguinarine protected against the cardiac hypertrophy, fibrosis and dysfunction induced by AB, as assessed by the heart weight/body weight, lung weight/body weight and heart weight/tibia length ratios, echocardiographic and hemodynamic parameters, histological analysis, and the gene expression levels of hypertrophic and fibrotic markers. The inhibitory effect of Sanguinarine on cardiac remodeling was mediated by inhibiting nuclear factor (NF)?κB signaling pathway activation. CONCLUSIONS: The findings indicated that Sanguinarine protected against cardiac hypertrophy and fibrosis via inhibiting NF?κB activation. These findings may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure. Sanguinarine inhibits osteoclast formation and bone resorption via suppressing RANKL-induced activation of NF-κB and ERK signaling pathways.[Pubmed: 23261473 ] Biochem Biophys Res Commun. 2013 Jan 18;430(3):951-6. Sanguinarine is a natural plant extract that has been supplemented in a number of gingival health products to suppress the growth of dental plaque. However, whether Sanguinarine has any effect on teeth and alveolar bone health is still unclear. METHODS AND RESULTS: In this study, we demonstrated for the first time that Sanguinarine could suppress osteoclastic bone resorption and osteoclast formation in a dose-dependent manner. Sanguinarine diminished the expression of osteoclast marker genes, including TRAP, cathepsin K, calcitonin receptor, DC-STAMP, V-ATPase d2, NFATc1 and c-fos. Further investigation revealed that Sanguinarine attenuated RANKL-mediated IκBα phosphorylation and degradation, leading to the impairment of NF-κB signaling pathway during osteoclast differentiation. In addition, Sanguinarine also affected the ERK signaling pathway by inhibiting RANKL-induced ERK phosphorylation. CONCLUSIONS: Collectively, this study suggested that Sanguinarine has protective effects on teeth and alveolar bone health.

Protocol of Sanguinarine

Kinase Assay

Biochemical activities of berberine, palmatine and sanguinarine mediating chemical defence against microorganisms and herbivores.[Pubmed: 9004542] Phytochemistry. 1997 Jan;44(2):257-66. The alkaloids berberine, palmatine and Sanguinarine are toxic to insects and vertebrates and inhibit the multiplication of bacteria, fungi and viruses. Biochemical properties which may contribute to these allelochemical activities were analysed. Acetylcholine esterase, butyrylcholinesterase, choline acetyl transferase, alpha 1- and alpha 2-adrenergic, nicotinergic, muscarinergic and serotonin2 receptors were substantially affected. Sanguinarine appears to be the most effective inhibitor of choline acetyl-transferase (IC50 284 nM), while the protoberberines were inactive at this target. Berberine and palmatine were most active at the alpha 2-receptor (binding with IC50 476 and 956 nM, respectively). Furthermore, berberine and Sanguinarine intercalate DNA, inhibit DNA synthesis and reverse transcriptase. In addition, Sanguinarine (but not berberine) affects membrane permeability and berberine protein biosynthesis. In consequence, these biochemical activities may mediate chemical defence against microorganisms, viruses and herbivores in the plants producing these alkaloids.

Cell Research

BCL2 promotor methylation and miR-15a/16-1 upregulation is associated with sanguinarine-induced apoptotic death in rat HSC-T6 cells[Pubmed: 25704029] J Pharmacol Sci. 2015 Jan;127(1):135-44. Previous studies show that several pathways are involved in Sanguinarine-induced apoptotic cell death, including AKT downregulation, inhibition of NF-kB activation, mediation of ROS production, downregulation of anti-apoptosis proteins XIAP and cIAP-1, upregulation of BAX, and downregulation of BCL2. METHODS AND RESULTS: Sanguinarine-induced rat hepatic stellate T6 cells (HSC-T6 cells) apoptosis was correlated with the generation of increased ROS, which was followed by the activation of caspase-8 (-3, -6, and -9), and the decreasing in the miltochondrial membrane potential (MMP) and the down-regulation of anti-apoptotic protein Bcl-2. We showed that Sanguinarine-induced down regulation of BCL2 was associated with the increased methylation rate of BCL2 promotor district and the increased expression of miR-15a/16-1. HSC-T6 cells treatment with 5-Aza-2'-deoxycytidine (5'-Aza-CdR) impeded Sanguinarine-induced BCL2 promotor district methylation and recovered BCL2's expression. Over expression of BCL2 using pEGFP-N1 vector decreased Sanguinarine-induced HSC-T6 cells apoptotic death significantly but not completely. CONCLUSIONS: These observations clearly showed that BCL2 down regulation was associated with its promoter methylation and miR-15a/16-1 upregulation in Sanguinarine-induced Rat HSC-T6 cells.

Preparing Stock Solutions of Sanguinarine

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	3.0093 mL	15.0466 mL	30.0933 mL	60.1866 mL	75.2332 mL
5 mM	0.6019 mL	3.0093 mL	6.0187 mL	12.0373 mL	15.0466 mL
10 mM	0.3009 mL	1.5047 mL	3.0093 mL	6.0187 mL	7.5233 mL
50 mM	0.0602 mL	0.3009 mL	0.6019 mL	1.2037 mL	1.5047 mL
100 mM	0.0301 mL	0.1505 mL	0.3009 mL	0.6019 mL	0.7523 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.

References on Sanguinarine

Molecular signatures of sanguinarine in human pancreatic cancer cells: A large scale label-free comparative proteomics approach.[Pubmed:25929337]

Oncotarget. 2015 Apr 30;6(12):10335-48.

Pancreatic cancer remains one of the most lethal of all human malignancies with its incidence nearly equaling its mortality rate. Therefore, it's crucial to identify newer mechanism-based agents and targets to effectively manage pancreatic cancer. Plant-derived agents/drugs have historically been useful in cancer therapeutics. Sanguinarine is a plant alkaloid with anti-proliferative effects against cancers, including pancreatic cancer. This study was designed to determine the mechanism of Sanguinarine's effects in pancreatic cancer with a hope to obtain useful information to improve the therapeutic options for the management of this neoplasm. We employed a quantitative proteomics approach to define the mechanism of Sanguinarine's effects in human pancreatic cancer cells. Proteins from control and Sanguinarine-treated pancreatic cancer cells were digested with trypsin, run by nano-LC/MS/MS, and identified with the help of Swiss-Prot database. Results from replicate injections were processed with the SIEVE software to identify proteins with differential expression. We identified 37 differentially expressed proteins (from a total of 3107), which are known to be involved in variety of cellular processes. Four of these proteins (IL33, CUL5, GPS1 and DUSP4) appear to occupy regulatory nodes in key pathways. Further validation by qRT-PCR and immunoblot analyses demonstrated that the dual specificity phosphatase-4 (DUSP4) was significantly upregulated by Sanguinarine in BxPC-3 and MIA PaCa-2 cells. Sanguinarine treatment also caused down-regulation of HIF1alpha and PCNA, and increased cleavage of PARP and Caspase-7. Taken together, Sanguinarine appears to have pleotropic effects, as it modulates multiple key signaling pathways, supporting the potential usefulness of Sanguinarine against pancreatic cancer.

Biochemical activities of berberine, palmatine and sanguinarine mediating chemical defence against microorganisms and herbivores.[Pubmed:9004542]

Phytochemistry. 1997 Jan;44(2):257-66.

The alkaloids berberine, palmatine and Sanguinarine are toxic to insects and vertebrates and inhibit the multiplication of bacteria, fungi and viruses. Biochemical properties which may contribute to these allelochemical activities were analysed. Acetylcholine esterase, butyrylcholinesterase, choline acetyl transferase, alpha 1- and alpha 2-adrenergic, nicotinergic, muscarinergic and serotonin2 receptors were substantially affected. Sanguinarine appears to be the most effective inhibitor of choline acetyl-transferase (IC50 284 nM), while the protoberberines were inactive at this target. Berberine and palmatine were most active at the alpha 2-receptor (binding with IC50 476 and 956 nM, respectively). Furthermore, berberine and Sanguinarine intercalate DNA, inhibit DNA synthesis and reverse transcriptase. In addition, Sanguinarine (but not berberine) affects membrane permeability and berberine protein biosynthesis. In consequence, these biochemical activities may mediate chemical defence against microorganisms, viruses and herbivores in the plants producing these alkaloids.

Differential antiproliferative and apoptotic response of sanguinarine for cancer cells versus normal cells.[Pubmed:10778985]

Clin Cancer Res. 2000 Apr;6(4):1524-8.

Sanguinarine, derived from the root of Sanguinaria canadendid, has been shown to possess antimicrobial, anti-inflammatory, and antioxidant properties. Here we compared the antiproliferative and apoptotic potential of Sanguinarine against human epidermoid carcinoma (A431) cells and normal human epidermal keratinocytes (NHEKs). Sanguinarine treatment was found to result in a dose-dependent decrease in the viability of A431 cells as well as NHEKs albeit at different levels because Sanguinarine-mediated loss of viability occurred at lower doses and was much more pronounced in the A431 carcinoma cells than in the normal keratinocytes. DNA ladder assay demonstrated that compared to vehicle-treated control, Sanguinarine treatment of A431 cells resulted in an induction of apoptosis at 1-, 2-, and 5-microM doses. Sanguinarine treatment did not result in the formation of a DNA ladder in NHEKs, even at the very high dose of 10 microM. The induction of apoptosis by Sanguinarine was also evident by confocal microscopy after labeling the cells with annexin V. This method also identified necrotic cells, and Sanguinarine treatment also resulted in the necrosis of A431 cells. The NHEKs showed exclusively necrotic staining at high doses (2 and 5 microM). We also explored the possibility of cell cycle perturbation by Sanguinarine in A431 cells. The DNA cell cycle analysis revealed that Sanguinarine treatment did not significantly affect the distribution of cells among the different phases of the cell cycle in A431 cells. We suggest that Sanguinarine could be developed as an anticancer drug.

Sanguinarine protects against pressure overloadinduced cardiac remodeling via inhibition of nuclear factor-kappaB activation.[Pubmed:24804701]

Mol Med Rep. 2014 Jul;10(1):211-6.

Cardiac remodeling is a major determinant of heart failure characterized by cardiac hypertrophy and fibrosis. Sanguinarine exerts widespread pharmacological effects, including antitumor and antiinflammatory responses. In the present study, the effect of Sanguinarine on cardiac hypertrophy, fibrosis and heart function was determined using the model induced by aortic banding (AB) in mice. AB surgery and sham surgery were performed on male wildtype C57 mice, aged 810 weeks, with or without administration of Sanguinarine from one week after surgery for an additional seven weeks. Sanguinarine protected against the cardiac hypertrophy, fibrosis and dysfunction induced by AB, as assessed by the heart weight/body weight, lung weight/body weight and heart weight/tibia length ratios, echocardiographic and hemodynamic parameters, histological analysis, and the gene expression levels of hypertrophic and fibrotic markers. The inhibitory effect of Sanguinarine on cardiac remodeling was mediated by inhibiting nuclear factor (NF)kappaB signaling pathway activation. The findings indicated that Sanguinarine protected against cardiac hypertrophy and fibrosis via inhibiting NFkappaB activation. These findings may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure.

Sanguinarine inhibits osteoclast formation and bone resorption via suppressing RANKL-induced activation of NF-kappaB and ERK signaling pathways.[Pubmed:23261473]

Biochem Biophys Res Commun. 2013 Jan 18;430(3):951-6.

Sanguinarine is a natural plant extract that has been supplemented in a number of gingival health products to suppress the growth of dental plaque. However, whether Sanguinarine has any effect on teeth and alveolar bone health is still unclear. In this study, we demonstrated for the first time that Sanguinarine could suppress osteoclastic bone resorption and osteoclast formation in a dose-dependent manner. Sanguinarine diminished the expression of osteoclast marker genes, including TRAP, cathepsin K, calcitonin receptor, DC-STAMP, V-ATPase d2, NFATc1 and c-fos. Further investigation revealed that Sanguinarine attenuated RANKL-mediated IkappaBalpha phosphorylation and degradation, leading to the impairment of NF-kappaB signaling pathway during osteoclast differentiation. In addition, Sanguinarine also affected the ERK signaling pathway by inhibiting RANKL-induced ERK phosphorylation. Collectively, this study suggested that Sanguinarine has protective effects on teeth and alveolar bone health.

BCL2 promotor methylation and miR-15a/16-1 upregulation is associated with sanguinarine-induced apoptotic death in rat HSC-T6 cells.[Pubmed:25704029]

J Pharmacol Sci. 2015 Jan;127(1):135-44.

Previous studies show that several pathways are involved in Sanguinarine-induced apoptotic cell death, including AKT downregulation, inhibition of NF-kB activation, mediation of ROS production, downregulation of anti-apoptosis proteins XIAP and cIAP-1, upregulation of BAX, and downregulation of BCL2. In this study, we found out that the quenching of ROS generation by N-acetyl-l-cysteine (NAC), a scavenger of ROS, reversed Sanguinarine-induced apoptosis effects, also we found out that Sanguinarine-induced rat hepatic stellate T6 cells (HSC-T6 cells) apoptosis was correlated with the generation of increased ROS, which was followed by the activation of caspase-8 (-3, -6, and -9), and the decreasing in the miltochondrial membrane potential (MMP) and the down-regulation of anti-apoptotic protein Bcl-2. It is not clear whether BCL2's downregulation relates to its promoter methylation and miR-15a/16-1 expression which can bind to BCL2 3'-UTR (un-translation reagon). We showed that Sanguinarine-induced down regulation of BCL2 was associated with the increased methylation rate of BCL2 promotor district and the increased expression of miR-15a/16-1. HSC-T6 cells treatment with 5-Aza-2'-deoxycytidine (5'-Aza-CdR) impeded Sanguinarine-induced BCL2 promotor district methylation and recovered BCL2's expression. Over expression of BCL2 using pEGFP-N1 vector decreased Sanguinarine-induced HSC-T6 cells apoptotic death significantly but not completely. These observations clearly showed that BCL2 down regulation was associated with its promoter methylation and miR-15a/16-1 upregulation in Sanguinarine-induced Rat HSC-T6 cells.

Involvement of heme oxygenase-1 in neuroprotection by sanguinarine against glutamate-triggered apoptosis in HT22 neuronal cells.[Pubmed:25299846]

Environ Toxicol Pharmacol. 2014 Nov;38(3):701-10.

Sanguinarine is a natural compound isolated from the roots of Macleaya cordata and M. microcarpa, has been reported to possess several biological activities such as anti-inflammatory and anti-oxidant effects. In the present study, we demonstrated that Sanguinarine markedly induces the expression of HO-1 which leads to a neuroprotective response in mouse hippocampus-derived neuronal HT22 cells from apoptotic cell death induced by glutamate. Sanguinarine significantly attenuated the loss of mitochondrial function and membrane integrity associated with glutamate-induced neurotoxicity. Sanguinarine protected against glutamate-induced neurotoxicity through inhibition of HT22 cell apoptosis. JC-1 staining, which is a well-established measure of mitochondrial damage, was decreased after treatment with Sanguinarine in glutamate-challenged HT22cells. In addition, Sanguinarine diminished the intracellular accumulation of ROS and Ca(2+). Sanguinarine also induced HO-1, NQO-1 expression via activation of Nrf2. Additionally, we found that si RNA mediated knock-down of Nrf2 or HO-1 significantly inhibited Sanguinarine-induced neuroprotective response. These findings revealed the therapeutic potential of Sanguinarine in preventing the neurodegenerative diseases.

Description

Sanguinarine, a benzophenanthridine alkaloid derived from the root of Sanguinaria Canadensis, can stimulate apoptosis via activating the production of reactive oxygen species (ROS). Sanguinarine-induced apoptosis is associated with the activation of JNK and NF-κB.