Sodium Pentaborate Attenuates Paracetamol-Induced Splenic Toxicity via Antioxidant, Anti-inflammatory, and Anti-apoptotic Mechanisms

Authors : Tuba Karaaslan, Necati Utlu

Pages : 180-186

Doi:10.31196/huvfd.1739381

View : 51 | Download : 92

Publication Date : 2025-12-24

Article Type : Research Paper

Abstract :Paracetamol (PCM) is a commonly used analgesic and antipyretic drug, yet its overdose may lead to serious organ damage. One of the lesser-explored targets of PCM-induced toxicity is the spleen, a critical immune organ. Boron, a trace element with known biological benefits, has been used therapeutically since ancient times. This study was designed to evaluate the protective effects of boron, administered as sodium pentaborate (50 mg/kg and 100 mg/kg, orally), against paracetamol-induced spleen injury in rats. Male Sprague-Dawley rats were pretreated with sodium pentaborate for six days, followed by a single toxic dose of paracetamol (1 g/kg). Paracetamol exposure led to increased oxidative stress and inflammation in spleen tissue, as evidenced by elevated levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and caspase-3. Additionally, the activities of key antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and the glutathione (GSH) content were significantly reduced. Furthermore, Western blot analysis revealed marked upregulation of nuclear factor-kappa B (NF-κB) and Beclin-1, indicating enhanced inflammatory and autophagic activity in spleen tissue following PCM exposure. Pretreatment with sodium pentaborate significantly ameliorated these biochemical and molecular alterations. Overall, the findings suggest that boron confers protection against paracetamol-induced splenic injury by modulating oxidative stress, inflammation, apoptosis, and autophagy-related pathways.
Keywords : Antioxidant, Apoptosis, Cytokine, Inflammation, Paracetamol, Sodium Pentaborate.

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