Home Neuronal Signaling GABA Receptor modulator (+)-Borneol

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(+)-Borneol GABA Receptor modulator

Cat.No.S3959

(+)-Borneol is one of enantiomers of borneol which is a valuable medical material, senior aromatic spice, and chemical material and has been used in food and also folk medicine.
(+)-Borneol GABA Receptor modulator Chemical Structure

Chemical Structure

Molecular Weight: 154.25

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Quality Control

Batch: S395901 DMSO]30 mg/mL]false]]]false]]]false Purity: 98%
98

Chemical Information, Storage & Stability

Molecular Weight 154.25 Formula

C10H18O

 Storage (From the date of receipt)
CAS No. 464-43-7 -- Storage of Stock Solutions

Synonyms N/A Smiles CC1(C2CCC1(C(C2)O)C)C

Solubility

In vitro
Batch:

DMSO : 30 mg/mL (194.48 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

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Mass Concentration Volume Molecular Weight

In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

In vitro
(+)-borneol significantly inhibits the expression of iNOS and TNF-α in a dose-dependent manner in the LPS-stimulated BV-2 cells[1]. Aβ-induced cell cytotoxicity is inhibited by 100 μM of (−) and (+) borneol treatment. Treatment of borneol significantly decreases ROS generation. The expression of HO-1 and nuclear translocation of Nrf2 are increased by Aβ treatment. This nuclear translocation of Nrf2 is further increased by administration of borneol. Compared with the Aβ treated group, the (+) borneol treated group significantly increases Bcl-2 expression with decreased expression of Bax. Thus, Borneol protects SH-SY5Y cells against Aβ-induced toxicity, exerts an antioxidative effect and suppresses apoptosis[2].
In vivo
In the rat model of permanent cerebral ischemia, (+)-borneol (1.0 mg/kg) significantly ameliorates infarct size and neurological scoresvia reducing the expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α) in a dose dependent manner. Notably, (+)-borneol shows long-term effects on the improvement of sensorimotor functions in the photothrombotic model of stroke, which decreases the number of foot faults in the grid-walking task and forelimb asymmetry scores in the cylinder task, at least in part through reducing loss of dendritic spines in the length, brunch number and density. (+)-Borneol obviously loosens the intercellular tight junction in the blood-brain barrier (BBB) and enhances the distribution of drugs in the brain tissue, as it could increase number and volume of pinocytotic vesicles in BBB cells and then promotes the transportation of substance by cell pinocytosis. It contributes to neuroprotection and reduces pro-inflammatory cytokine expression and promotes functional recovery from permanent stroke with a long-term effect in the acute phase of focal permanent cerebral ischemia[1].
References

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