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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

symptoms such as anxiety, depression, attention deficit hyperactivity disorder, and
irritability associated with ASD (Hellings, 2023).

Infliximab, a chimeric monoclonal antibody targeting tumor necrosis factor-alpha
(TNF-α), is used to treat various pathological conditions, especially inflammatory diseases

(Alacabey et al., 2022). Recent studies have demonstrated that infliximab possesses not

only anti-inflammatory but also antioxidative properties. By blocking TNF-α, infliximab
reduces reactive oxygen species (ROS) production, thereby limiting oxidative stress-

induced cellular damage (Zhou et al., 2021). Widely used in the treatment of rheumatoid
arthritis, psoriatic arthritis, ankylosing spondylitis, spondyloarthropathies, Crohn’s

disease, and ulcerative colitis, infliximab has recently been reported to alleviate cognitive
impairment, depression, and anxiety symptoms secondary to various diseases and

improve quality of life (Rahmati-Dehkordi et al., 2025).

The present study aims to investigate the effects of infliximab administration on
oxidative stress parameters in the temporal cortex of a propionic acid-induced

experimental autism model. We hypothesize that infliximab treatment may modulate
oxidative stress markers in this model, potentially influencing antioxidant defense

mechanisms and inflammatory pathways associated with ASD pathophysiology.

MATERIAL AND METHODS
This study was conducted in accordance with the ethical approval granted by the

Van Yüzüncü Yıl University Local Animal Experiments Ethics Committee, dated
26.06.2025, decision number 719521. A total of 32 male Wistar Albino rats, aged 3–5

weeks and weighing approximately 125–175 g, were randomly divided into four groups,

with 8 rats per group. The animals were obtained from the Experimental Medicine
Application and Research Center of Yüzüncü Yıl University (YÜDETAM) and housed under

standard laboratory conditions (12 h light:12 h dark cycle, 24±3°C), with ad libitum
access to standard pellet feed and water. The experimental period lasted for 35 days.

The groups were as follows:
1. Control group: Rats received 0.5 ml phosphate buffer (0.2 M, pH 7.2) via oral

gavage for 3 consecutive days. From day 4 onwards, they were administered 0.1 ml saline
intraperitoneally once weekly for 5 weeks.

2. Autism group: To induce the experimental ASD model, rats were administered 0.5
ml of 250 mg/kg propionic acid (PPA) dissolved in phosphate buffer (0.2 M, pH 7.2) via oral
gavage for 3 consecutive days (El-Ansary et al., 2018; Mirza and Sharma, 2018; Alsubaiei et

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