Acute lung injury (ALI) is a serious clinical syndrome with a high rate of mortality. The activation of inflammation is well-recognized as a vital factor in the pathogenesis of lipopolysaccharide (LPS)-induced ALI. Therefore, suppression of the inflammatory response could be an ideal strategy to prevent ALI. Epigallocatechin-3-gallate (EGCG), mainly from green tea, has been shown to have an anti-inflammatory effect. The aim of the study was to explore whether EGCG alleviates inflammation in sepsis-related ALI. Male BALB/C mice were treated with EGCG (10 mg/kg) intraperitoneally (ip) 1 h before LPS injection (10 mg/kg, ip). The results showed that EGCG attenuated LPS-induced ALI as it decreased the changes in blood gases and reduced the histological lesions, wet-to-dry weight ratios, and myeloperoxidase (MPO) activity. In addition, EGCG significantly decreased the expression of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the lung, serum, and bronchoalveolar lavage fluid, and alleviated the expression of TLR-4, MyD88, TRIF, and p-p65 in the lung tissue. In addition, it increased the expression of IκB-α and had no influence on the expression of p65. Collectively, these results demonstrated the protective effects of EGCG against LPS-induced ALI in mice through its anti-inflammatory effect that may be attributed to the suppression of the activation of TLR 4-dependent NF-κB signaling pathways.

1-(2-Hidroxietil)piperidina (HEP) está presente em muitos fármacos e em protótipos de fármacos, mas seus mecanismos de oxidação são mal compreendidos. Assim, a reação de oxidação da HEP pelo bis(hidrogenoperiodato)-argentato(III) ([Ag(HIO6)2]5-;) foi investigada em meio alcalino aquoso. Piperidina e formaldeído foram identificados como principais produtos da reação através da técnica de espectrometria de massa com ionização electrospray. A cinética de oxidação foi acompanhada espectrofotometricamente no intervalo de temperatura de 25,0 a 40,0 ºC, verificando-se que a reação é de primeira ordem em [Ag(III)] e de ordem fracionária em [HEP]. O estudo da dependência das constantes de velocidade k obsd em relação a [OHˉ] e [IO4ˉ]tot (concentração de periodato total) possibilitou estabelecer uma lei de velocidade e propor um mecanismo de reação. O mecanismo envolve a formação do complexo ternário periodato-Ag(III)-HEP, seguido de sua decomposição a Ag(I) através de dois caminhos: um independente e outro facilitado por OH-. As constantes de velocidade e de equilíbrio bem como os parâmetros de ativação correspondentes às etapas determinantes de velocidade foram calculados.

1-(2-Hydroxyethyl)piperidine (HEP) is involved in many drugs and drug leads, but its oxidation mechanisms are poorly understood. The oxidation of HEP by bis(hydrogenperiodato)-argentate(III) ([Ag(HIO6)2]5-;) in aqueous alkaline medium was shown, by electrospray ionization mass spectrometry (ESI-MS), to generate piperidine and formaldehyde as the major products. The reaction was monitored spectrophotometrically in the 25.0 to 40.0 ºC range revealing that the oxidation followed a first-order kinetics in [Ag(III)] and a fractional-order in [HEP]. A rate law and a reaction mechanism were proposed based on the study of the dependency of the pseudo-first-order rate constants, k obsd, on [OHˉ] and on [IO4ˉ]tot (total concentration of periodate). The mechanism involves the formation of a periodato-Ag(III)-HEP ternary complex, whose decomposition generates Ag(I) by means of two pathways: one independent and another facilitated by OHˉ. The reaction rate constants and associated equilibrium constants as well as the activation parameters of the rate-determining steps were calculated.