6,6'-Di-tert-butyl-4,4'-dimethyl-2,2'-[1,2-phenyl-enebis(nitrilo-methanylyl-idene)]diphenol.

In the title mol-ecule, C(30)H(36)N(2)O(2), the dihedral angles between the central benzene ring and the two benzene rings of the butyl-salicylaldimine groups are 14.3 (2) and 40.6 (2)°. There are two strong intra-molecular O-H⋯N hydrogen bonds which form S(6) rings. The crystal studied was a non-merohedral twin with refined components of 0.270 (4) and 0.730 (4).

Bis-(chloro-acetato-κO)bis(trimethyl-silylmethyl)tin(IV).

In the title complex, [Sn(C(2)H(2)ClO(2))(2)(C(4)H(11)Si)(2)], the Sn(IV) ion is coordinated in a distorted tetra-hedral environment formed by two O atoms from two monodenate chloro-acetato ligands and two C atoms from two trimethyl silyl ligands. Two further weak intra-molecular Sn⋯O contacts [2.744 (2) and 2.655 (2) Å] are formed by the chloro-acetato ligands.

Veratric Acid Inhibits LPS-Induced IL-6 and IL-8 Production in Human Gingival Fibroblasts.

Veratric acid, one of the major benzoic acid isolated from vegetables and fruits, has been reported to have anti-inflammatory activity. The purpose of this study was to investigate the anti-inflammatory effects of veratric acid on lipopolysaccharide (LPS)-induced inflammatory response in human gingival fibroblasts (HGFs). HGFs were pretreated with veratric acid 1 h before LPS stimulation. The productions of IL-6 and IL-8 were detected by ELISA. The expression of iNOS, COX-2, PI3K, AKT, and NF-κB were detected by western blotting. The results showed that veratric acid inhibited LPS-induced IL-6 and IL-8 production, as well as iNOS and COX-2 expression. Veratric acid also inhibited LPS-induced NF-κB activation. In addition, veratric acid was found to suppress LPS-induced PI3K and AKT phosphorylation. In conclusion, the anti-inflammatory mechanism of veratric acid is due to its ability to inhibit PI3K/Akt/NF-κB signaling pathway.