Catalogue Number
BD-D1352
Analysis Method
HPLC,NMR,MS
Specification
98%(HPLC)
Storage
2-8℃
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
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
2932990000
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.
29987888
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.
ERK signaling; advanced glycation end products; diabetic nephropathy; eucalyptol; podocyte slit diaphragm.
Eucalyptol Inhibits Advanced Glycation End Products-Induced Disruption of Podocyte Slit Junctions by Suppressing Rage-Erk-C-Myc Signaling Pathway
Dong Yeon Kim 1 , Min-Kyung Kang 1 , Eun-Jung Lee 1 , Yun-Ho Kim 1 , Hyeongjoo Oh 1 , Young-Hee Kang 1
2018 Oct
30668445
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.
ERK signaling; advanced glycation end products; diabetic nephropathy; eucalyptol; podocyte slit diaphragm.
Eucalyptol Promotes Lung Repair in Mice Following Cigarette Smoke-Induced Emphysema
Emanuel Kennedy-Feitosa 1 , Isabella Cattani-Cavalieri 1 , Marina Valente Barroso 2 , Bruna Romana-Souza 3 , Lycia Brito-Gitirana 1 , Samuel Santos Valenca 4
2019 Mar 1
29215731
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.
airway mucus hypersecretion; cigarette smoke; ciliated cells and bacterial colony; eucalyptol.
Eucalyptol Protects Lungs Against Bacterial Invasion Through Attenuating Ciliated Cell Damage and Suppressing MUC5AC Expression
Na Yu 1 , Yi-Tian Sun 2 , Xin-Ming Su 1 , Miao He 3 , Bing Dai 1 , Jian Kang 1
2019 May