Abstract
ObjectiveIncreased inflammatory response may be associated with adverse clinical outcomes, especially in the neonatal period. The aims of this study were to determine whether N-acetyl-cysteine (NAC), an anti-inflammatory agent, attenuates the inflammatory response in young rats and to determine the most effective route of administration.MethodsFour groups of Sprague-Dawley rats (in each group four rats) were studied at 30 days of age. One hour following intraperitoneal (IP) injection of lipopolysaccharide 50 μg/kg, the rats were randomized to subcutaneous (SC), per os (PO), or intraperitoneal (IP) injection of NAC 300 mg/kg, or saline. The control group received saline injection (IP). Three hours following the N-acetyl-cysteine injection the rats were sacrificed, then serum tumor necrosis factor-α (TNF-α) and IL-6 levels were determined by ELISA.ResultsLipopolysaccharide significantly increased the neonatal serum IL-6 and TNF-α (2051.0±349 and 147.0±25.8 pg/mL, respectively; P<0.01) levels compared to 10 pg/mL in the controls. N-acetyl-cysteine administered one hour following lipopolysaccharide injection significantly attenuated the inflammatory response. Intraperitoneal administration of NAC decreased IL-6 and TNF-α concentration to 294.6 and 17.1 pg/mL, respectively, and was more effective than SC or PO administration.ConclusionsN-acetyl-cysteine attenuated the inflammatory response in the neonatal rats, and IP was the most effective administration route.
Highlights
The inflammatory response to infection is the host’s most important initial defense mechanism against pathogens
Lipopolysaccharide significantly increased the neonatal serum IL-6 and tumor necrosis factor-α (TNF-α) (2051.0±349 and 147.0±25.8 pg/mL, respectively; P
Tissue damage associated with the infection is a consequence of increased proinflammatory response rather than directly from the bacteria.[2]
Summary
The inflammatory response to infection is the host’s most important initial defense mechanism against pathogens. An imbalance between the pro- and antiinflammatory responses may have adverse effects on the host. Severe postnatal infections lead to a systemic inflammatory response with excessive release of cytokines (interleukin-1 [IL-1], IL-8, and tumor necrosis factor [TNF]-α), which can be a stressful event for the newborn. Inflammation is associated with the generation of a large quantity and variety of free radicals and reactive oxygen species (FR/ROS) that increase the production and secretion of the cytokines.[1] In the neonatal period, infants are more vulnerable to infections. Tissue damage associated with the infection is a consequence of increased proinflammatory response rather than directly from the bacteria.[2] There is imbalance between the pro- and anti-inflammatory responses in newborns and neonates that may further increase the risk of infection in early life. Each year more than a million infants are estimated to die in their first four weeks from infections, and Gram-negative rods account for the majority of deaths.[3]
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