Caffeic acid phenethyl ester suppresses oxidative stress in Escherichia coli-induced pyelonephritis in rats

Abstract

Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused by Escherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24 h, PYN 48 h, PYN 72 h, CAPE 24 h, CAPE 48 h and CAPE 72 h. E. coli (1 x 10(9) c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten microM/kg-body weight CAPE was injected to the rats in all CAPE groups 24 h before E. coli infection, and injections were repeated at 24-h intervals. Rats were sacrificed 24 h, 48 h and 72 h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated by E. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced by E. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy.

Effects of Cinnamon extract on biochemical enzymes, TNF-α and NF-κB gene expression levels in liver of broiler chickens inoculated with Escherichia coli

“…Helwig et al (2006) and Turkozkan et al (2005) have reported that the exposure with E. coli lead to the inflammatory responses reactions and increase in the concentration of cytokines likes TNF-α and transcription factor NF-κB, which in turn induces the expression of other pro--inflammatory cytokines such as IL-5, IL-2, IL-3, IL-12, and IL-1β (Turkozkan et al 2005, Helwig et al 2006. Furthermore, Celik and colleagues (2007) and Shen and colleagues (2010) have found that infection with E. coli induces the oxidative stress and lipid peroxidation reactions leading to the development of tissue injuries and subsequent detrimental outcomes in the host body (Celik et al 2007, Shen et al 2010). The increased levels of pro-inflammatory mediators and oxidative stress markers due to the inoculation with E. coli may cause cell membrane damages and apoptotic reactions which play crucial roles in cell survival and cell death.…”

“…Exposure to E. coli and its lipopolysaccharide endotoxin results in edema and inflammatory in tissues, elevated levels of acute phase proteins, and increased production of particularly active pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-α) and transcription factor, necrotic factor-kappa B (NF-κB) (Turkozkan et al 2005, Helwig et al 2006, Teo & Tan 2006, Demir et al 2007). E. coli can also lead to increased lipid peroxidation of cell membranes and impaired antioxidant defense of the body, increased vascular permeability and accumulation of proteins and fluid outside cells, and tissue damages (Celik et al 2007, Shen et al 2010. These changes (oxidative stress and inflammatory processes) would be responsible for a variety of diseases in animals and humans.…”

Caffeic acid phenethyl ester inhibits osteoclastogenesis by suppressing NFκB and downregulating NFATc1 and c-Fos

“…It has been reported to have anti-viral, anti-inflammatory, anti-mitogenic, anticarcinogenic, and immuno-modulatory effects [12][13][14][15]. Moreover, CAPE was shown to have anti-oxidant properties like vitamin C, vitamin E and N-acetylcysteine in vivo [16] and to protect inflammation-mediated tissue destruction caused by oxidative stress in rats [13,17]. However, the effect of CAPE on osteoclasts and bone remodeling has not been investigated.…”

Could Pyelonephritic Scarring Be Prevented by Anti-Inflammatory Treatment? An Experimental Model of Acute Pyelonephritis

“…and enterococci, as well as Staphylococci , have been identified [20]. Bacterial inoculation in the tissue, ischemia reperfusion damage, and lysosomal lytic enzyme retention cause renal scar by means of endoxines, cytokines, and chimiotaxy [4].…”