Effects of gallic acid on acrylamide-induced endoplasmic reticulum stress, neuroinflammation and neuronal apoptosis in rats
Rizvanoglu, Omer Faruk, Yildirim, Serkan, Kiliclioglu, Metin, Tekin, Samet, Sengul, Emin, Tulobaev, Askarbek, Cinar, Ali
(ACR)-induced neurotoxicity, focusing on oxidative stress, endoplasmic reticulum (ER) stress, neuroinflammation, and apoptosis mechanisms. Fifty male Sprague-Dawley rats were divided into five groups: Control, ACR, GA50 +ACR, GA100 +ACR, and GA100. GA (50 and & micro;mg/kg) and ACR (50 mg/kg) were administered intraperitoneally for 14 days. ACR exposure significantly decreased antioxidant enzyme activities (SOD, GSH, GPx, CAT) and increased malondialdehyde (MDA) levels, pro-inflammatory cytokines (TNF-alpha, IL-1 beta, IL-6), neuronal nitric oxide synthase (nNOS), and apoptosis-related gene expression (Bax and caspase-3). Histopathological analysis revealed neuronal degeneration and vascular hyperemia, while BDNF, Nrf2, and HO-1 immunoreactivity decreased in the ACR group. GA treatment, particularly at 100 mg/kg, markedly ameliorated these biochemical, molecular, and histopathological alterations. These findings indicate that GA exerts significant neuroprotective effects against ACR-induced brain injury by modulating oxidative stress, ER stress, inflammatory, and apoptotic pathways.
- Dergi
- NEUROTOXICOLOGY
- Yıl
- 2026
- Cilt
- 114
- ISSN
- 0161-813X
- eISSN
- 1872-9711
- DOI
- 10.1016/j.neuro.2026.103431
- WoS UID
- WOS:001722528800001