NA

Identification

IUPAC Names

4-methylbenzene-1,2-diol

Molecular Formula
C7H8O2
Mass
NA
Monoisotopic Mass
NA
Charge
NA
InChI
NA
InChIKey
NA
SMILES
NA
Synonyms

1,2-Dihydroxy-4-methylbenzene

1,2-dihydroxy-4-methylbenzene

2-Hydroxy-4-methylphenol

3,4-Dihydroxytoluene

3,4-dihydroxytoluene

4-Methyl-1,2-benzenediol

4-methyl-1,2-benzenediol

4-Methyl-1,2-dihydroxybenzene

4-Methylcatechol

4-methylcatechol

4-Methylpyrocatechol

Homocatechol

Homopyrocatechol

p-Methylcatechol

p-Methylpyrocatechol

Toluene-3,4-diol

Species

homo sapiens

NCBI:txid960622198556

NCBI:txid960624029555

NCBI:txid96066890513

MTBLS136

MTBLS1267

MTBLS106

MTBLS8183

MTBLS5828

MTBLS4967

MTBLS2542

sus scrofa

gallus gallus

mus musculus

ovis aries

reference compound

cladocopium goreaui

Europe PubMed Central results


Anti-inflammatory effects of catechols in lipopolysaccharide-stimulated microglia cells: inhibition of microglial neurotoxicity.

Author: Zheng LT, Ryu GM, Kwon BM, Lee WH, Suk K.

Abstract: Microglial activation plays a pivotal role in the pathogenesis of neurodegenerative diseases by producing various proinflammatory cytokines and nitric oxide (NO). In the present study, the anti-inflammatory and subsequent neuroprotective effects of catechol and its derivatives including 3-methylcatechol, 4-methylcatechol, and 4-tert-butylcatechol were investigated in microglia and neuroblastoma cells in culture. The four catechol compounds showed anti-inflammatory effects with different potency. The catechols significantly decreased lipopolysaccharide (LPS)-induced NO and tumor necrosis factor (TNF)-alpha production in BV-2 microglia cells. The catechols also inhibited the expression of inducible nitric oxide synthase (iNOS) and TNF-alpha at mRNA or protein levels in the LPS-stimulated BV-2 cells. In addition, the catechols inhibited LPS-induced nuclear translocation of p65 subunit of nuclear factor (NF)-kappaB, IkappaB degradation, and phosphorylation of p38 mitogen-activated protein kinase (MAPK) in BV-2 cells. Moreover, the catechols attenuated the cytotoxicity of LPS-stimulated BV-2 microglia toward co-cultured rat B35 neuroblastoma cells. The catechols, however, did not protect B35 cells against H(2)O(2) toxicity, indicating that the compounds exerted the neuroprotective effect by inhibiting the inflammatory activation of microglia in the co-culture. The anti-inflammatory and neuroprotective properties of the catechols in cultured microglia and neuroblastoma cells suggest a therapeutic potential of these compounds for the treatment of neurodegenerative diseases that are associated with an excessive microglial activation.