Farahat Yomna A, El-Sayed Norhan M, Hazem Reem M, Mehanna Eman T, Radwan Asmaa
Department of Pharmacology & Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt.
Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt.
Biomedicines. 2025 Apr 28;13(5):1065. doi: 10.3390/biomedicines13051065.
: Cadmium (Cd) is a harmful metal commonly used in industry. Numerous clinical diseases, including osteomalacia, testicular damage, renal and hepatic failure, and pulmonary edema, are associated with Cd exposure. The current study evaluated the protective effect of Sinapic acid (SA) against Cd-induced hepatotoxicity by investigating different mechanistic pathways interfering with Cd-related liver injury. : Forty rats were randomly assigned to four groups as follows; group 1 served as negative control and received saline, group 2 received saline for 14 days and CdCl (3.5 mg/kg IP) as a single dose on day 14, groups 3 and 4 were treated with SA (20, 40 mg/kg PO), respectively, for 14 days and injected with CdCl (3.5 mg/kg IP) on day 14. Serum was collected to evaluate liver function. Liver samples were collected for histopathological examination and the assessment of markers related to oxidative stress, inflammation, and apoptosis. : Acute Cd administration elevated liver enzymes and induced pathological changes in liver specimens, with the concurrent release of inflammatory markers and reduced antioxidant capabilities. Pretreatment with SA improved liver function and Cd-induced histopathological changes and elevated the activities of antioxidant enzymes. SA ameliorated inflammation, as evidenced by decreased expression of NF-κB, TNF-α, TLR-4, and COX-2, iNOS, and IL-1β levels along with suppression of mTOR, JNK, ERK, BAX, and Bcl-2. : The present data suggest that SA represents a promising protective agent against Cd-induced hepatic injury by attenuating oxidative stress, inflammation, and apoptosis.
镉（Cd）是一种工业中常用的有害金属。许多临床疾病，包括骨软化症、睾丸损伤、肾衰竭和肝衰竭以及肺水肿，都与镉暴露有关。本研究通过研究干扰镉相关肝损伤的不同机制途径，评估了芥子酸（SA）对镉诱导的肝毒性的保护作用。
40只大鼠被随机分为四组，如下所示：第1组作为阴性对照，接受生理盐水；第2组接受14天生理盐水，在第14天接受单次剂量的CdCl（3.5mg/kg腹腔注射）；第3组和第4组分别用SA（20、40mg/kg口服）治疗14天，并在第14天注射CdCl（3.5mg/kg腹腔注射）。收集血清以评估肝功能。收集肝脏样本进行组织病理学检查以及评估与氧化应激、炎症和凋亡相关的标志物。
急性给予镉会升高肝酶并在肝脏标本中诱导病理变化，同时释放炎症标志物并降低抗氧化能力。SA预处理改善了肝功能和镉诱导的组织病理学变化，并提高了抗氧化酶的活性。SA减轻了炎症，表现为NF-κB、TNF-α、TLR-4和COX-2、iNOS以及IL-1β水平的表达降低，同时抑制了mTOR、JNK、ERK、BAX和Bcl-2。
目前的数据表明，SA通过减轻氧化应激、炎症和凋亡，是一种有前景的抗镉诱导肝损伤的保护剂。
