Adeyanju Anne Adebukola, Akinwunmi Emmanuel Ayomitide, Karigidi Mojisola Esther, Agboola Olubukola Oyebimpe, Elekofehinti Olusola Olalekan
Department of Biological Sciences, Faculty of Applied Sciences, KolaDaisi University, Km 18, Oyo Express Road, Ibadan, Oyo, Nigeria.
Department of Biological Sciences, McPherson University, Seriki Sotayo, Ogun, Nigeria.
Toxicol Rep. 2025 Mar 16;14:101995. doi: 10.1016/j.toxrep.2025.101995. eCollection 2025 Jun.
Bisphenol A (BPA) is regularly used to produce plastic products. Its hepatotoxicity has been unveiled. The effects of cinnamic acid on BPA exposure have not been comprehensively studied, and the key mechanism of action is yet to be unraveled. Rats were allocated into 5 groups. Group 1 (control) was given corn oil. Group 2 received BPA for 14 consecutive days. Group 3 received cinnamic acid at 50 mg/kg in co-administration with BPA while group 4 received cinnamic acid at 100 mg/kg, in co-administration with BPA. Cinnamic acid (CA) only (100 mg/kg) was given to group 5. BPA exposure significantly decreased catalase, glutathione-S-transferase, and superoxide dismutase activities and non-significantly diminished glutathione level. A reduction in the gene expression of catalase accompanied this. Our result showed significant gene elevation at the mRNA level of tumor necrosis factor-α and elevated malondialdehyde by BPA. The significantly elevated alanine transaminase and aspartate transaminase activities in addition to increased levels of total cholesterol, triglycerides, and very low-density lipoprotein with reduced high-density lipoprotein reflected the detrimental effect of BPA in the liver. Our results revealed that cinnamic acid could alleviate the increased pro-inflammatory cytokine level and oxidative stress by downregulating tumor necrosis factor-α gene. The histopathological evaluation confirmed the biochemical results. Hepatic alterations were ameliorated when cinnamic acid was co-administered with BPA. These findings suggest that downregulation of the TNF-α gene induced by cinnamic acid may participate in suppressing the BPA-induced oxidative stress. This offers a new idea to unmask the mechanism underlying cinnamic acid's interference with BPA-induced hepatic damage.
双酚A（BPA）常用于生产塑料制品。其肝毒性已被揭示。肉桂酸对BPA暴露影响的研究尚不全面，关键作用机制仍有待阐明。将大鼠分为5组。第1组（对照组）给予玉米油。第2组连续14天给予BPA。第3组在与BPA联合给药时给予50mg/kg的肉桂酸，而第4组在与BPA联合给药时给予100mg/kg的肉桂酸。第5组仅给予肉桂酸（100mg/kg）。BPA暴露显著降低了过氧化氢酶、谷胱甘肽-S-转移酶和超氧化物歧化酶的活性，谷胱甘肽水平略有下降，同时过氧化氢酶基因表达也随之降低。我们的结果显示，BPA使肿瘤坏死因子-α的mRNA水平显著升高，丙二醛含量增加。此外，丙氨酸转氨酶和天冬氨酸转氨酶活性显著升高，总胆固醇、甘油三酯和极低密度脂蛋白水平升高，高密度脂蛋白水平降低，这反映了BPA对肝脏的有害作用。我们的结果表明，肉桂酸可通过下调肿瘤坏死因子-α基因来减轻促炎细胞因子水平的升高和氧化应激。组织病理学评估证实了生化结果。肉桂酸与BPA联合给药时，肝脏病变得到改善。这些发现表明，肉桂酸诱导的TNF-α基因下调可能参与抑制BPA诱导的氧化应激。这为揭示肉桂酸干扰BPA诱导肝损伤的潜在机制提供了新思路。
