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Boldine

$220

  • Brand : BIOFRON

  • Catalogue Number : BD-D0650

  • Specification : HPLC≥98%

  • CAS number : 476-70-0

  • Formula : C19H21NO4

  • Molecular Weight : 327.37

  • PUBCHEM ID : 10154

  • Volume : 20mg

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Catalogue Number

BD-D0650

Analysis Method

HPLC,NMR,MS

Specification

HPLC≥98%

Storage

2-8°C

Molecular Weight

327.37

Appearance

White crystalline powder

Botanical Source

Peumus boldus Molina

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

CN1CCC2=CC(=C(C3=C2C1CC4=CC(=C(C=C43)OC)O)OC)O

Synonyms

Boldine chloroform/4H-Dibenzo[de,g]quinoline-2,9-diol, 5,6,6a,7-tetrahydro-1,10-dimethoxy-6-methyl-/Boldin/2,6-dihydroxy-3,5-dimethoxyaporphine/5,6,6a,7-Tetrahydro-1,10-dimethoxy-6-methyl-4H-dibenzo[de,g]quinoline-2,9-diol/1,10-dimethoxy-2,9-dihydroxyaporphine/Uniboldina/2,9-Dihydroxy-1,10-dimethoxyaporphine/1,10-Dimethoxy-6aa-aporphine-2,9-diol/dl-Boldine/Boldine/1,10-Dimethoxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinoline-2,9-diol

IUPAC Name

(6aS)-1,10-dimethoxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinoline-2,9-diol

Applications

Boldine is an aporphine isoquinoline alkaloid extracted from the root of Litsea cubeba and also possesses these properties, including antioxidant, anti-inflammatory and cytoprotective effects. Boldine suppresses osteoclastogenesis, improves bone destruction by down-regulating the OPG/RANKL/RANK signal pathway and may be a potential therapeutic agent for rheumatoid arthritis[1].

Density

1.3±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

273.9±30.1 °C

Boiling Point

529.3±50.0 °C at 760 mmHg

Melting Point

162-164ºC

InChl

InChI=1S/C19H21NO4/c1-20-5-4-10-7-15(22)19(24-3)18-12-9-16(23-2)14(21)8-11(12)6-13(20)17(10)18/h7-9,13,21-22H,4-6H2,1-3H3/t13-/m0/s1

InChl Key

LZJRNLRASBVRRX-ZDUSSCGKSA-N

WGK Germany

RID/ADR

HS Code Reference

2939800000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:476-70-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

31593341

Abstract

Discovering the utmost effective and targeted chemotherapy for hepatocellular carcinoma is still a significant challenge. In the present study, diethylnitrosamine was used as a liver carcinogen and boldine a compound of boldo. We anticipated the hypothesis that boldine endow antiproliferative and promote apoptosis on hepatocarcinoma rats. We analyzed that boldine alters the tumor biomarkers and liver markers enzyme levels. Also, we determined boldine modulate the enzymatic and nonenzymatic antioxidant activities, as well as messenger RNA and protein expressions of Bcl2, Bax, and cleaved caspase 3 by reverse transcription polymerase chain reaction and Western blot analysis, respectively. It was also manifested by histopathology studies in liver tissues of HCC rats. Our finding suggested that boldine has antioxidant activity, and moreover, also contributes apoptotic nature by upregulating the protein expression of Bax, and cleaved caspase 3. Our data accomplishes that boldine a candidate drug has dynamic therapeutic activity and suitable for the treatment of HCC.

© 2019 Wiley Periodicals, Inc.

KEYWORDS

HCC; antioxidant; antiproliferative; boldine; caspase-dependent mitochondrial intrinsic apoptosis pathway

Title

Hepatoprotective effect of boldine against diethylnitrosamine-induced hepatocarcinogenesis in wistar rats.

Author

Subramaniam N1, Kannan P2, K A3, Thiruvengadam D1.

Publish date

2019 Dec

PMID

30081409

Abstract

Boldine is a natural antioxidant that exhibits some important pharmacological properties, which is due to its free radical scavenging effects. And at the same time, reactive oxygen species (ROS) has an important role in pathogenesis of seizure; hence, reducing it via antioxidants like boldine seems to be effective in treating seizure. This study was designed to investigate whether acute treatment with boldine could alter seizures induced by pentylenetetrazole or electroshock in mice. We also evaluated to see if boldine’s antioxidant properties play a role in its anti-convulsant activity. Boldine acute administration increased time latencies to the onset of myoclonic jerks and clonic seizures induced by intraperitoneal pentylenetetrazole model. Moreover, boldine increased seizure threshold induced by intravenous infusion of pentylenetetrazole. Additionally, acute doses of boldine reduced the duration of tonic hind-limb extension in the electroshock-induced seizure model. Non-effective dose of vitamin C (as an antioxidant agent) and boldine had anti-convulsant effect in intraperitoneal pentylenetetrazole, intravenous pentylenetetrazole and electroshock models. Boldine administration increased glutathione and superoxide dismutase levels in mice whole brain. The result showed boldine anti-seizure properties, which might be due to its antioxidant activity.

© Georg Thieme Verlag KG Stuttgart · New York.

Title

Acute Boldine Treatment Induces Anti-convulsant Effects in Mice through its Antioxidant Activity.

Author

Moezi L1,2, Yahosseini S3, Jamshizadeh A2,3, Pirsalami F1.

Publish date

2019 Apr

PMID

29941815

Abstract

Boldine, a major aporphine alkaloid found in the Chilean boldo tree, is a potent antioxidant. Oxidative stress plays a detrimental role in the pathogenesis of kidney damage in renovascular hypertension (RVH). The activation of the renin-angiotensin system (RAS) is crucial to the development and progression of hypertensive renal damage and TGF-β is closely associated with the activation of RAS. In the present study, we assessed the effect of boldine on the progression of kidney disease using the 2K1C hypertension model and identifying mediators in the RAS, such as TGF-β, that could be modulated by this alkaloid. Toward this hypothesis, rats (n = 5/group) were treated with boldine (50 mg/kg/day, gavage) for six weeks after 2K1C surgery (pressure ≥ 180 mmHg). Kidney function was evaluated by measuring of proteinuria/creatininuria ratio (U prot/U Crea), oxidative stress (OS) by measuring thiobarbituric acid reactive substances (TBARS). The evolution of systolic blood pressure (SBP) was followed weekly. Alpha-smooth muscle actin (α-SMA) and Col III were used as markers of kidney damage; ED-1 and osteopontin (OPN) were used as markers of inflammation. We also explored the effect in RAS mediators, such as ACE-1 and TGF-β. Boldine treatment reduced the UProt/UCrea ratio, plasma TBARS, and slightly reduced SBP in 2K1C hypertensive rats, producing no effect in control animals. In 2K1C rats treated with boldine the levels of α-SMA, Col III, ED-1, and OPN were lower when compared to 2K1C rats. Boldine prevented the increase in ACE-1 and TGF-β in 2K1C rats, suggesting that boldine reduces kidney damage. These results suggest that boldine could potentially be used as a nutraceutic.

KEYWORDS

(S)-2,9-dihydroxy-1,10-dimethoxy-aporphine; chronic kidney disease; fibrosis; oxidative stress; renovascular hypertension

Title

Boldine Improves Kidney Damage in the Goldblatt 2K1C Model Avoiding the Increase in TGF-β.

Author

Gomez GI1,2, Velarde V3.

Publish date

2018 Jun 25