Linarin

CAS# 480-36-4

Linarin

Catalog No. BCN5554----Order now to get a substantial discount!

Product Name & Size Price Stock
Linarin: 5mg $35 In Stock
Linarin: 10mg Please Inquire In Stock
Linarin: 20mg Please Inquire Please Inquire
Linarin: 50mg Please Inquire Please Inquire
Linarin: 100mg Please Inquire Please Inquire
Linarin: 200mg Please Inquire Please Inquire
Linarin: 500mg Please Inquire Please Inquire
Linarin: 1000mg Please Inquire Please Inquire

Quality Control of Linarin

Number of papers citing our products

Chemical structure

Linarin

3D structure

Chemical Properties of Linarin

Cas No. 480-36-4 SDF Download SDF
PubChem ID 5317025 Appearance White-yellowish powder
Formula C28H32O14 M.Wt 592.6
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms Acacetin 7-O-rutinoside; Acaciin; Buddleoflavonoloside; Buddleoside; 5,7-Dihydroxy 4'-methoxyflavone 7-rutinoside; Linarigenin glycoside
Solubility Soluble in DMSO
Chemical Name 5-hydroxy-2-(4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxychromen-4-one
SMILES CC1C(C(C(C(O1)OCC2C(C(C(C(O2)OC3=CC(=C4C(=C3)OC(=CC4=O)C5=CC=C(C=C5)OC)O)O)O)O)O)O)O
Standard InChIKey YFVGIJBUXMQFOF-PJOVQGMDSA-N
Standard InChI InChI=1S/C28H32O14/c1-11-21(31)23(33)25(35)27(39-11)38-10-19-22(32)24(34)26(36)28(42-19)40-14-7-15(29)20-16(30)9-17(41-18(20)8-14)12-3-5-13(37-2)6-4-12/h3-9,11,19,21-29,31-36H,10H2,1-2H3/t11-,19+,21-,22+,23+,24-,25+,26+,27+,28+/m0/s1
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 Linarin

1 Daphne sp. 2 Linaria sp. 3 Monarda sp. 4 Peganum sp. 5 Robinia sp.

Biological Activity of Linarin

DescriptionLinarin possesses analgesic, antipyretic, anti-acetylcholinesterase, hepatoprotective ,anti-inflammatory and neuroprotective activities, it prevents Aβ(25-35)-induced neurotoxicity through the activation of PI3K/Akt, which subsequently inhibits GSK-3β and up-regulates Bcl-2. Linarin can protect osteoblasts against hydrogen peroxide-induced osteoblastic dysfunction and may exert anti-resorptive actions, at least in part, via the reduction of RANKL and oxidative damage; it also can treat postmenopausal osteoporosis,it induces the osteogenic differentiation and mineralization of MC3T3-E1 osteoblastic cells by activating the BMP-2/RUNX2 pathway through PKA signalingin vitroand protected against OVX-induced bone lossin vivo.
TargetsLTR | Caspase | TNF-α | STAT | AChR | IL Receptor | PI3K | Akt | PKA | Beta Amyloid | GSK-3 | NF-kB | Bcl-2/Bax
In vitro

Protective effect of linarin against D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure.[Pubmed: 24877692]

Eur J Pharmacol. 2014 Sep 5;738:66-73.

Linarin was isolated from Chrysanthemum indicum L. Fulminant hepatic failure is a serious clinical syndrome that results in massive inflammation and hepatocyte death. Apoptosis is an important cellular pathological process in d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury, and regulation of liver apoptosis might be an effective therapeutic method for fulminant hepatic failure.
METHODS AND RESULTS:
This study examined the cytoprotective mechanisms of Linarin against GalN/LPS-induced hepatic failure. Mice were given an oral administration of Linarin (12.5, 25 and 50mg/kg) 1h before receiving GalN (800 mg/kg)/LPS (40 μg/kg). Linarin treatment reversed the lethality induced by GalN/LPS. After 6h of GalN/LPS injection, the serum levels of alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor (TNF)-α, interleukin-6 and interferon-γ were significantly elevated. GalN/LPS increased toll-like receptor 4 and interleukin-1 receptor-associated kinase protein expression. These increases were attenuated by Linarin. Linarin attenuated the increased expression of Fas-associated death domain and caspase-8 induced by GalN/LPS, reduced the cytosolic release of cytochrome c and caspase-3 cleavage induced by GalN/LPS, and reduced the pro-apoptotic Bim phosphorylation induced by GalN/LPS. However, Linarin increased the level of anti-apoptotic Bcl-xL and phosphorylation of STAT3.
CONCLUSIONS:
Our results suggest that Linarin alleviates GalN/LPS-induced liver injury by suppressing TNF-α-mediated apoptotic pathways.

Linarin promotes osteogenic differentiation by activating the BMP-2/RUNX2 pathway via protein kinase A signaling.[Pubmed: 26935542 ]

Int J Mol Med. 2016 Apr;37(4):901-10.

Linarin (LIN), a flavonoid which exerts both anti-inflammatory and antioxidative effects, has been found to promote osteogenic differentiation. However, the molecular mechanism of its effect on osteoblast differentiation was unclear.
METHODS AND RESULTS:
In the present study, LIN from Flos Chrysanthemi Indici (FCI) was isolated in order to investigate the underlying mechanisms of LIN on MC3T3-E1 cells (a mouse osteoblastic cell line) and the osteoprotective effect of LIN in mice which had undergone an ovariectomy (OVX). The results revealed that LIN enhanced osteoblast proliferation and differentiation in MC3T3-E1 cells dose‑dependently, with enhanced alkaline phosphatase (ALP) activity and mineralization of extracellular matrix. LIN upregulated osteogenesis-related gene expression, including that of ALP, runt‑related transcription factor 2 (RUNX2), osteocalcin (OCN), bone sialoprotein (BSP), and type I collagen (COL‑I). Pretreatment with noggin, a bone morphogenetic protein-2 (BMP-2) antagonist, meant that LIN-induced gene expression levels of COL-1, ALP, OCN, BSP and RUNX2 were significantly reduced, as shown by RT-qPCR. Western blot analysis showed that LIN dose‑dependently increased the protein levels of BMP-2 and RUNX2 and enhanced the phosphorylation of SMAD1/5. In addition, LIN dose‑dependently upregulated protein kinase A (PKA) expression. H-89 (a PKA inhibitor) partially blocked the LIN-induced protein increase in BMP-2, p-SMAD1/5 and RUNX2. We noted that LIN preserved the trabecular bone microarchitecture of ovariectomized mice in vivo. Moreover, pretreatment with LIN significantly lowered serum levels of ALP and OCN in ovariectomized mice.
CONCLUSIONS:
Our data indicated that LIN induced the osteogenic differentiation and mineralization of MC3T3-E1 osteoblastic cells by activating the BMP-2/RUNX2 pathway through PKA signaling in vitro and protected against OVX-induced bone loss in vivo. The results strongly suggest that LIN is a useful natural alternative for the management of postmenopausal osteoporosis.

Linarin isolated from Buddleja officinalis prevents hydrogen peroxide-induced dysfunction in osteoblastic MC3T3-E1 cells.[Pubmed: 21420072]

Cell Immunol. 2011;268(2):112-6.

The flowers and leaves buds of Buddleja officinalis MAXIM (Buddlejaceae) are used to treat eye troubles, hernia, gonorrhea and liver troubles in Asia.
METHODS AND RESULTS:
To elucidate the protective effects of Linarin isolated from B. officinalis on the response of osteoblast to oxidative stress, osteoblastic MC3T3-E1 cells were pre-incubated with Linarin for 1h before treatment with 0.3mM H(2)O(2) for 48h, and markers of osteoblast function and oxidative damage were examined. Linarin significantly (P<0.05) increased cell survival, alkaline phosphatase (ALP) activity, collagen content, calcium deposition, and osteocalcin secretion and decreased the production of receptor activator of nuclear factor-kB ligand (RANKL), protein carbonyl (PCO), and malondialdehyde (MDA) of osteoblastic MC3T3-E1 cells in the presence of hydrogen peroxide.
CONCLUSIONS:
These results demonstrate that Linarin can protect osteoblasts against hydrogen peroxide-induced osteoblastic dysfunction and may exert anti-resorptive actions, at least in part, via the reduction of RANKL and oxidative damage.

Protocol of Linarin

Kinase Assay

Linarin Inhibits the Acetylcholinesterase Activity In-vitro and Ex-vivo.[Pubmed: 26330885 ]

Iran J Pharm Res. 2015 Summer;14(3):949-54.

Linarin is a flavone glycoside in the plants Flos chrysanthemi indici, Buddleja officinalis, Cirsium setosum, Mentha arvensis and Buddleja davidii, and has been reported to possess analgesic, Linarin is a flavone glycoside in the plants Flos chrysanthemi indici, Buddleja officinalis, Cirsium setosum, Mentha arvensis and Buddleja davidii, and has been reported to possess analgesic, antipyretic, anti-inflammatory and neuroprotective activities.
METHODS AND RESULTS:
In this paper, Linarin was investigated for its AChE inhibitory potential both in-vitro and ex-vivo. Ellman's colorimetric method was used for the determination of AChE inhibitory activity in mouse brain. In-vitro assays revealed that Linarin inhibited AChE activity with an IC50 of 3.801 ± 1.149 μM. Ex-vivo study showed that the AChE activity was significantly reduced in both the cortex and hippocampus of mice treated intraperitoneally with various doses of Linarin (35, 70 and 140 mg/Kg). The inhibition effects produced by high dose of Linarin were the same as that obtained after huperzine A treatment (0.5 mg/Kg). Molecular docking study revealed that both 4'-methoxyl group and 7-O-sugar moiety of Linarin played important roles in ligand-receptor binding and thus they are mainly responsible for AChE inhibitory activity.
CONCLUSIONS:
In view of its potent AChE inhibitory activity, Linarin may be a promising therapeutic agent for the treatment of some diseases associated with AChE, such as glaucoma, myasthenia gravis, gastric motility and Alzheimer's disease.

Cell Research

Neuroprotective effects of linarin through activation of the PI3K/Akt pathway in amyloid-β-induced neuronal cell death.[Pubmed: 21652214 ]

Phytochemical linarin enriched in the flower of Chrysanthemum indicum inhibits proliferation of A549 human alveolar basal epithelial cells through suppression of the Akt-dependent signaling pathway.[Pubmed: 24117095]

J Med Food. 2013 Dec;16(12):1086-94.


METHODS AND RESULTS:
In this study, we report the anti-proliferative effect and molecular mechanism of Chrysanthemum indicum (C. indicum) on A549 human alveolar basal epithelial cells. We also analyzed the changes in C. indicum component profiles due to modifications of predrying process, flower size, and extraction method. Among the varieties of modifications tested, high-temperature heat dry (HTD) of small flower biotype followed by the methanolic extraction resulted in the strongest anti-proliferative activity of C. indicum extract in A549 cells. High-performance liquid chromatography of C. indicum revealed that the levels of acacetin 7-O-rutinoside (Linarin) are markedly increased by heat treatment, especially HTD. Finally, we showed that Linarin-mediated inhibition of cell proliferation is associated with suppression of Akt activation and induction of cyclin-dependent kinase inhibitor p27(Kip1) as evidenced by cell cycle analysis and treatment with LY294002, an inhibitor of phosphatidylinositol 3-kinase/Akt pathway.
CONCLUSIONS:
Taken together, these findings suggest the need for further development and evaluation of Linarin from C. indicum for the treatment and prevention of lung cancer.

Bioorg Med Chem. 2011 Jul 1;19(13):4021-7.

Linarin, a natural occurring flavanol glycoside derived from Mentha arvensis and Buddleja davidii is known to have anti-acetylcholinesterase effects.
METHODS AND RESULTS:
The present study intended to explore the neuroprotective effects of Linarin against Aβ(25-35)-induced neurotoxicity with cultured rat pheochromocytoma cells (PC12 cells) and the possible mechanisms involved. For this purpose, PC12 cells were cultured and exposed to 30 μM Aβ(25-35) in the absence or presence of Linarin (0.1, 1.0 and 10 μM). In addition, the potential contribution of the PI3K/Akt neuroprotective pathway in Linarin-mediated protection against Aβ(25-35)-induced neurotoxicity was also investigated. The results showed that Linarin dose-dependently increased cell viability and reduced the number of apoptotic cells as measured by MTT assay, Annexin-V/PI staining, JC-1 staining and caspase-3 activity assay. Linarin could also inhibit acetylcholinesterase activity induced by Aβ(25-35) in PC12 cells. Further study revealed that Linarin induced the phosphorylation of Akt dose-dependently. Treatment of PC12 cells with the PI3K inhibitor LY294002 attenuated the protective effects of Linarin. Furthermore, Linarin also stimulated phosphorylation of glycogen synthase kinase-3β (GSK-3β), a downstream target of PI3K/Akt. Moreover, the expression of the anti-apoptotic protein Bcl-2 was also increased by Linarin treatment.
CONCLUSIONS:
These results suggest that Linarin prevents Aβ(25-35)-induced neurotoxicity through the activation of PI3K/Akt, which subsequently inhibits GSK-3β and up-regulates Bcl-2. These findings raise the possibility that Linarin may be a potent therapeutic compound against Alzheimer's disease acting through both acetylcholinesterase inhibition and neuroprotection.

Linarin Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Linarin Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Linarin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.6875 mL 8.4374 mL 16.8748 mL 33.7496 mL 42.187 mL
5 mM 0.3375 mL 1.6875 mL 3.375 mL 6.7499 mL 8.4374 mL
10 mM 0.1687 mL 0.8437 mL 1.6875 mL 3.375 mL 4.2187 mL
50 mM 0.0337 mL 0.1687 mL 0.3375 mL 0.675 mL 0.8437 mL
100 mM 0.0169 mL 0.0844 mL 0.1687 mL 0.3375 mL 0.4219 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.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
  • Eugenin

    Catalog No.:BCN2921
    CAS No.:480-34-2
  • Mellein

    Catalog No.:BCN4785
    CAS No.:480-33-1
  • Orobol

    Catalog No.:BCN5553
    CAS No.:480-23-9
  • Aromadendrin

    Catalog No.:BCN5552
    CAS No.:480-20-6
  • Isorhamnetin

    Catalog No.:BCN5551
    CAS No.:480-19-3
  • Taxifolin

    Catalog No.:BCN5550
    CAS No.:480-18-2
  • Morin

    Catalog No.:BCN1028
    CAS No.:480-16-0
  • Izalpinine

    Catalog No.:BCN3682
    CAS No.:480-14-8
  • Oroxylin A

    Catalog No.:BCN5363
    CAS No.:480-11-5
  • Astragalin

    Catalog No.:BCN5549
    CAS No.:480-10-4
  • Eleutherol

    Catalog No.:BCN8480
    CAS No.:480-00-2
  • CP-809101

    Catalog No.:BCC1498
    CAS No.:479683-64-2
New Products
 

References on Linarin

Linarin promotes osteogenic differentiation by activating the BMP-2/RUNX2 pathway via protein kinase A signaling.[Pubmed:26935542]

Int J Mol Med. 2016 Apr;37(4):901-10.

Linarin (LIN), a flavonoid which exerts both anti-inflammatory and antioxidative effects, has been found to promote osteogenic differentiation. However, the molecular mechanism of its effect on osteoblast differentiation was unclear. In the present study, LIN from Flos Chrysanthemi Indici (FCI) was isolated in order to investigate the underlying mechanisms of LIN on MC3T3-E1 cells (a mouse osteoblastic cell line) and the osteoprotective effect of LIN in mice which had undergone an ovariectomy (OVX). The results revealed that LIN enhanced osteoblast proliferation and differentiation in MC3T3-E1 cells dosedependently, with enhanced alkaline phosphatase (ALP) activity and mineralization of extracellular matrix. LIN upregulated osteogenesis-related gene expression, including that of ALP, runtrelated transcription factor 2 (RUNX2), osteocalcin (OCN), bone sialoprotein (BSP), and type I collagen (COLI). Pretreatment with noggin, a bone morphogenetic protein-2 (BMP-2) antagonist, meant that LIN-induced gene expression levels of COL-1, ALP, OCN, BSP and RUNX2 were significantly reduced, as shown by RT-qPCR. Western blot analysis showed that LIN dosedependently increased the protein levels of BMP-2 and RUNX2 and enhanced the phosphorylation of SMAD1/5. In addition, LIN dosedependently upregulated protein kinase A (PKA) expression. H-89 (a PKA inhibitor) partially blocked the LIN-induced protein increase in BMP-2, p-SMAD1/5 and RUNX2. We noted that LIN preserved the trabecular bone microarchitecture of ovariectomized mice in vivo. Moreover, pretreatment with LIN significantly lowered serum levels of ALP and OCN in ovariectomized mice. Our data indicated that LIN induced the osteogenic differentiation and mineralization of MC3T3-E1 osteoblastic cells by activating the BMP-2/RUNX2 pathway through PKA signaling in vitro and protected against OVX-induced bone loss in vivo. The results strongly suggest that LIN is a useful natural alternative for the management of postmenopausal osteoporosis.

Phytochemical linarin enriched in the flower of Chrysanthemum indicum inhibits proliferation of A549 human alveolar basal epithelial cells through suppression of the Akt-dependent signaling pathway.[Pubmed:24117095]

J Med Food. 2013 Dec;16(12):1086-94.

In this study, we report the anti-proliferative effect and molecular mechanism of Chrysanthemum indicum (C. indicum) on A549 human alveolar basal epithelial cells. We also analyzed the changes in C. indicum component profiles due to modifications of predrying process, flower size, and extraction method. Among the varieties of modifications tested, high-temperature heat dry (HTD) of small flower biotype followed by the methanolic extraction resulted in the strongest anti-proliferative activity of C. indicum extract in A549 cells. High-performance liquid chromatography of C. indicum revealed that the levels of acacetin 7-O-rutinoside (Linarin) are markedly increased by heat treatment, especially HTD. Finally, we showed that Linarin-mediated inhibition of cell proliferation is associated with suppression of Akt activation and induction of cyclin-dependent kinase inhibitor p27(Kip1) as evidenced by cell cycle analysis and treatment with LY294002, an inhibitor of phosphatidylinositol 3-kinase/Akt pathway. Taken together, these findings suggest the need for further development and evaluation of Linarin from C. indicum for the treatment and prevention of lung cancer.

Linarin Inhibits the Acetylcholinesterase Activity In-vitro and Ex-vivo.[Pubmed:26330885]

Iran J Pharm Res. 2015 Summer;14(3):949-54.

Linarin is a flavone glycoside in the plants Flos chrysanthemi indici, Buddleja officinalis, Cirsium setosum, Mentha arvensis and Buddleja davidii, and has been reported to possess analgesic, antipyretic, anti-inflammatory and neuroprotective activities. In this paper, Linarin was investigated for its AChE inhibitory potential both in-vitro and ex-vivo. Ellman's colorimetric method was used for the determination of AChE inhibitory activity in mouse brain. In-vitro assays revealed that Linarin inhibited AChE activity with an IC50 of 3.801 +/- 1.149 muM. Ex-vivo study showed that the AChE activity was significantly reduced in both the cortex and hippocampus of mice treated intraperitoneally with various doses of Linarin (35, 70 and 140 mg/Kg). The inhibition effects produced by high dose of Linarin were the same as that obtained after huperzine A treatment (0.5 mg/Kg). Molecular docking study revealed that both 4'-methoxyl group and 7-O-sugar moiety of Linarin played important roles in ligand-receptor binding and thus they are mainly responsible for AChE inhibitory activity. In view of its potent AChE inhibitory activity, Linarin may be a promising therapeutic agent for the treatment of some diseases associated with AChE, such as glaucoma, myasthenia gravis, gastric motility and Alzheimer's disease.

Neuroprotective effects of linarin through activation of the PI3K/Akt pathway in amyloid-beta-induced neuronal cell death.[Pubmed:21652214]

Bioorg Med Chem. 2011 Jul 1;19(13):4021-7.

Linarin, a natural occurring flavanol glycoside derived from Mentha arvensis and Buddleja davidii is known to have anti-acetylcholinesterase effects. The present study intended to explore the neuroprotective effects of Linarin against Abeta(25-35)-induced neurotoxicity with cultured rat pheochromocytoma cells (PC12 cells) and the possible mechanisms involved. For this purpose, PC12 cells were cultured and exposed to 30 muM Abeta(25-35) in the absence or presence of Linarin (0.1, 1.0 and 10 muM). In addition, the potential contribution of the PI3K/Akt neuroprotective pathway in Linarin-mediated protection against Abeta(25-35)-induced neurotoxicity was also investigated. The results showed that Linarin dose-dependently increased cell viability and reduced the number of apoptotic cells as measured by MTT assay, Annexin-V/PI staining, JC-1 staining and caspase-3 activity assay. Linarin could also inhibit acetylcholinesterase activity induced by Abeta(25-35) in PC12 cells. Further study revealed that Linarin induced the phosphorylation of Akt dose-dependently. Treatment of PC12 cells with the PI3K inhibitor LY294002 attenuated the protective effects of Linarin. Furthermore, Linarin also stimulated phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), a downstream target of PI3K/Akt. Moreover, the expression of the anti-apoptotic protein Bcl-2 was also increased by Linarin treatment. These results suggest that Linarin prevents Abeta(25-35)-induced neurotoxicity through the activation of PI3K/Akt, which subsequently inhibits GSK-3beta and up-regulates Bcl-2. These findings raise the possibility that Linarin may be a potent therapeutic compound against Alzheimer's disease acting through both acetylcholinesterase inhibition and neuroprotection.

Linarin isolated from Buddleja officinalis prevents hydrogen peroxide-induced dysfunction in osteoblastic MC3T3-E1 cells.[Pubmed:21420072]

Cell Immunol. 2011;268(2):112-6.

The flowers and leaves buds of Buddleja officinalis MAXIM (Buddlejaceae) are used to treat eye troubles, hernia, gonorrhea and liver troubles in Asia. To elucidate the protective effects of Linarin isolated from B. officinalis on the response of osteoblast to oxidative stress, osteoblastic MC3T3-E1 cells were pre-incubated with Linarin for 1h before treatment with 0.3mM H(2)O(2) for 48h, and markers of osteoblast function and oxidative damage were examined. Linarin significantly (P<0.05) increased cell survival, alkaline phosphatase (ALP) activity, collagen content, calcium deposition, and osteocalcin secretion and decreased the production of receptor activator of nuclear factor-kB ligand (RANKL), protein carbonyl (PCO), and malondialdehyde (MDA) of osteoblastic MC3T3-E1 cells in the presence of hydrogen peroxide. These results demonstrate that Linarin can protect osteoblasts against hydrogen peroxide-induced osteoblastic dysfunction and may exert anti-resorptive actions, at least in part, via the reduction of RANKL and oxidative damage.

Protective effect of linarin against D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure.[Pubmed:24877692]

Eur J Pharmacol. 2014 Sep 5;738:66-73.

Linarin was isolated from Chrysanthemum indicum L. Fulminant hepatic failure is a serious clinical syndrome that results in massive inflammation and hepatocyte death. Apoptosis is an important cellular pathological process in d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury, and regulation of liver apoptosis might be an effective therapeutic method for fulminant hepatic failure. This study examined the cytoprotective mechanisms of Linarin against GalN/LPS-induced hepatic failure. Mice were given an oral administration of Linarin (12.5, 25 and 50mg/kg) 1h before receiving GalN (800 mg/kg)/LPS (40 mug/kg). Linarin treatment reversed the lethality induced by GalN/LPS. After 6h of GalN/LPS injection, the serum levels of alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor (TNF)-alpha, interleukin-6 and interferon-gamma were significantly elevated. GalN/LPS increased toll-like receptor 4 and interleukin-1 receptor-associated kinase protein expression. These increases were attenuated by Linarin. Linarin attenuated the increased expression of Fas-associated death domain and caspase-8 induced by GalN/LPS, reduced the cytosolic release of cytochrome c and caspase-3 cleavage induced by GalN/LPS, and reduced the pro-apoptotic Bim phosphorylation induced by GalN/LPS. However, Linarin increased the level of anti-apoptotic Bcl-xL and phosphorylation of STAT3. Our results suggest that Linarin alleviates GalN/LPS-induced liver injury by suppressing TNF-alpha-mediated apoptotic pathways.

Description

Linarin (Buddleoside), isolated from the flower extract of Mentha arvensis, shows selective dose dependent inhibitory effect on acetylcholinesterase (AChE).

Keywords:

Linarin,480-36-4,Acacetin 7-O-rutinoside; Acaciin; Buddleoflavonoloside; Buddleoside; 5,7-Dihydroxy 4'-methoxyflavone 7-rutinoside; Linarigenin glycoside,Natural Products, buy Linarin , Linarin supplier , purchase Linarin , Linarin cost , Linarin manufacturer , order Linarin , high purity Linarin

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: