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Eucalyptol

$45

  • Brand : BIOFRON

  • Catalogue Number : AV-P11446

  • Specification : 98%

  • CAS number : 470-82-6

  • Formula : C10H18O

  • Molecular Weight : 154.25

  • PUBCHEM ID : 2758

  • Volume : 0.1ml

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Catalogue Number

AV-P11446

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

154.25

Appearance

Colourless liquid

Botanical Source

Eucalyptus robusta/Occurs in eucalyptus, lavender, sage and many other oils. Detected in the Black Sea bryozoan Conopeum seuratum

Structure Type

Monoterpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1(C2CCC(O1)(CC2)C)C

Synonyms

2-Oxa-1,3,3-trimethylbicyclo(2.2.2)octane/eucalyptol (cineole)/Terpan/2-Oxabicyclo[2.2.2]octane, 1,3,3-trimethyl-/2,2,4-trimethyl-3-oxabicyclo[2.2.2]octane/Eucapur/Zineol/Eukalyptol [Czech]/p-Menthane, 1,8-epoxy-/Eucalyptol/Eucalyptole/1,8-Cineol/1,3,3-Trimethyl-2-oxabicyclo[2.2.2]octane,1,8-Cineole,1,8-Epoxy-p-menthane/1,3,3-Trimethyl-2-oxabicyclo(2.2.2)octane/cineole/Cajeputol/1,3,3-Trimethyl-2-oxabicyclo[2.2.2]octane/1,8-cineole/1,8-Epoxy-p-menthane/limonene oxide/p-Cineole

IUPAC Name

1,3,3-trimethyl-2-oxabicyclo[2.2.2]octane

Applications

Eucalyptol is an inhibitor of 5-HT3 receptor ,potassium channel, TNF-α and IL-1β.

Density

0.9±0.1 g/cm3

Solubility

Chloroform; Ethyl Acetate

Flash Point

50.9±15.3 °C

Boiling Point

174.0±8.0 °C at 760 mmHg

Melting Point

1.5ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:470-82-6) 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

29987888

Abstract

Scope: The maintenance of interpodocyte slit diaphragm is critical in the sieving function of glomerular filtration barrier. Eucalyptol is a natural constituent in aromatic plants with antioxidant properties. This study investigates whether and how eucalyptol inhibits podocyte slit diaphragm malfunction in glucose-exposed podocytes and diabetic mouse kidneys.
Methods and results: Podocytes were incubated in media containing 33 mm glucose with 1-20 μm eucalyptol. The in vivo model employed db/db mice orally administrated with 10 mg kg-1 eucalyptol. Nontoxic eucalyptol enhanced podocyte expression of nephrin, podocin, FAT-1, CD2AP, and α-actinin-4 diminished by glucose. Oral administration of eucalyptol augmented the induction of the slit diaphragm proteins, α-actinin-4, and integrin β1 in diabetic kidneys, and ameliorated glomerular fibrosis and foot process effacement. Eucalyptol counteracted the receptor of advanced glycation end products (RAGE) induction in podocytes with glucose or AGE-BSA, and elevated the reduction of the slit diaphragm proteins by AGE-BSA. Eucalyptol attenuated the RAGE induction and AGE accumulation in diabetic kidneys. The blockade of ERK-c-Myc signaling enhanced the nephrin and CD2AP expression downregulated in AGE-exposed podocytes. These results indicate that eucalyptol blocked glucose-induced AGE-RAGE axis and podocyte injury through disturbing RAGE-ERK-c-Myc signaling.
Conclusion: Eucalyptol may be a potent agent antagonizing diabetes-associated malformation of interpodocyte slit junction and podocyte actin cytoskeleton.

KEYWORDS

ERK signaling; advanced glycation end products; diabetic nephropathy; eucalyptol; podocyte slit diaphragm.

Title

Eucalyptol Inhibits Advanced Glycation End Products-Induced Disruption of Podocyte Slit Junctions by Suppressing Rage-Erk-C-Myc Signaling Pathway

Author

Dong Yeon Kim 1 , Min-Kyung Kang 1 , Eun-Jung Lee 1 , Yun-Ho Kim 1 , Hyeongjoo Oh 1 , Young-Hee Kang 1

Publish date

2018 Oct

PMID

30668445

Abstract

Background: Eucalyptol is a monoterpenoid oil present in many plants, principally the Eucalyptus species, and has been reported to have anti-inflammatory and antioxidative effects.
Hypothesis/purpose: Since the potential effect of eucalyptol on mouse lung repair has not yet been studied, and considering that chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide, the aim of this study was to investigate eucalyptol treatment in emphysematous mice.
Study design: Male mice (C57BL/6) were divided into the following groups: control (sham-exposed), cigarette smoke (CS) (mice exposed to 12 cigarettes a day for 60 days), CS + 1 mg/ml (CS mice treated with 1 mg/ml eucalyptol for 60 days), and CS + 10 mg/ml (CS mice treated with 10 mg/ml eucalyptol for 60 days). Mice in the CS and control groups received vehicle for 60 days. Eucalyptol (or the vehicle) was administered via inhalation (15 min/daily). Mice were sacrificed 24 h after the completion of the 120-day experimental procedure.
Methods: Histology and additional lung morphometric analyses, including analysis of mean linear intercept (Lm) and volume density of alveolar septa (Vv[alveolar septa]) were performed. Biochemical analyses were also performed using colorimetric assays for myeloperoxidase (MPO), malondialdehyde (MDA), and superoxide dismutase (SOD) activity, in addition to using ELISA kits for the determination of inflammatory marker levels (tumor necrosis factor alpha [TNF-α], interleukin-1 beta [IL-1β], interleukin 6 [IL-6], keratinocyte chemoattractant [KC], and tumor growth factor beta 1 [TGF-β1]). Finally, we investigated protein levels by western blotting (nuclear factor (erythroid-derived 2)-like 2 [Nrf2], nuclear factor kappa B [NF-κB], matrix metalloproteinase 12 [MMP-12], tissue inhibitor of matrix metalloproteinase 1 [TIMP-1], neutrophil elastase [NE], and elastin).
Results: Eucalyptol promoted lung repair at the higher dose (10 mg/ml), with de novo formation of alveoli, when compared to the CS group. This result was confirmed with Lm and Vv[alveolar septa] morphometric analyses. Moreover, collagen deposit around the peribronchiolar area was reduced with eucalyptol treatment when compared to the CS group. Eucalyptol also reduced all inflammatory (MPO, TNF-α, IL-1β, IL-6, KC, and TGF-β1) and redox marker levels (MDA) when compared to the CS group (at least p < 0.05). In general, 10 mg/ml eucalyptol was more effective than 1 mg/ml and, at both doses, we observed an upregulation of SOD activity when compared to the CS group (p < 0.001). Eucalyptol upregulated elastin and TIMP-1 levels, and reduced neutrophil elastase (NE) levels, when compared to the CS group. Conclusion: In summary, eucalyptol promoted lung repair in emphysematous mice and represents a potential therapeutic phytomedicine in the treatment of COPD.

KEYWORDS

ERK signaling; advanced glycation end products; diabetic nephropathy; eucalyptol; podocyte slit diaphragm.

Title

Eucalyptol Promotes Lung Repair in Mice Following Cigarette Smoke-Induced Emphysema

Author

Emanuel Kennedy-Feitosa 1 , Isabella Cattani-Cavalieri 1 , Marina Valente Barroso 2 , Bruna Romana-Souza 3 , Lycia Brito-Gitirana 1 , Samuel Santos Valenca 4

Publish date

2019 Mar 1

PMID

29215731

Abstract

This study was conducted to investigate whether eucalyptol plays a role in influencing bacterial growth in cigarette smoke-exposed lungs. Rats were exposed to air (control) and cigarette smoke (smoking) in the presence and absence of eucalyptol (260 mg/day). Morphological analysis of lung structures and status of airway mucous production were observed under microscope. Pathological changes of ciliated columnar epithelium in airways were examined using transmission electron microscopy. MUC5AC protein and messenger RNA (mRNA) expression in bronchoalveolar lavage fluid (BALF) and lungs were determined. Application of eucalyptol reduced pulmonary bullae formation and airway mucus overproduction in the smoke-exposed lungs. Treatment with eucalyptol attenuated ciliated cell damage in cigarette smoke-exposed lungs. Bacterial colonies of lungs were obviously lower in the eucalyptol-treated rats than that in the smoking rats (p < 0.01). Treatment with eucalyptol reduced the counts of bacterial colonization residing in the challenged lungs (p < 0.01). Application of eucalyptol not only decreased MUC5AC protein expression in BALF and tobacco-exposed lungs but also suppressed its mRNA expression in the lungs (all p < 0.05). Intervention of eucalyptol benefits elimination of bacterial organisms from tobacco-exposed lungs through attenuating ciliated cell damage and suppressing MUC5AC expression in the lungs.

KEYWORDS

airway mucus hypersecretion; cigarette smoke; ciliated cells and bacterial colony; eucalyptol.

Title

Eucalyptol Protects Lungs Against Bacterial Invasion Through Attenuating Ciliated Cell Damage and Suppressing MUC5AC Expression

Author

Na Yu 1 , Yi-Tian Sun 2 , Xin-Ming Su 1 , Miao He 3 , Bing Dai 1 , Jian Kang 1

Publish date

2019 May