Almohawes Zakiah Nasser, Okail Hanan A, Al-Megrin Wafa A, El-Khadragy Manal F, Ibrahim Mona A, Fathalla Ayah S, Soliman Doaa, Mohamed Sherif R
Department of Biology, College of Science, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia.
Department of Zoology, Faculty of Science, Sohag University, Sohag, Egypt.
Front Vet Sci. 2025 May 19;12:1590722. doi: 10.3389/fvets.2025.1590722. eCollection 2025.
Thioacetamide (TAA) is widely used as an experimental drug in liver disease studies and has been shown to exert toxicity across multiple organs. It has been linked to oxidative stress, inflammation, apoptosis, fibrosis, and epigenetic modifications. Whey protein (WP) provides an abundant supply of essential and non-essential amino acids that are vital for the human body. It is highly valued for its nutritional and biological properties, benefiting the immune, digestive, cardiovascular, neurological, and endocrine systems. This research sought to evaluate the possible protective effects of WP against TAA-induced cardiotoxicity in rats, emphasizing its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.
A total of forty male rats were randomly divided into four groups, with each group containing ten rats: the control group, the TAA-treated group (100 mg/kg body weight), the WP-treated group (300 mg/kg body weight), and the WP + TAA group. The treatments were administered for three consecutive weeks.
The findings revealed that TAA exposure significantly reduced cardiac tissue activities of glutathione, superoxide dismutase, and catalase while markedly increasing malondialdehyde and nitric oxide activities. Additionally, TAA administration led to a significant elevation in inflammatory markers (TNF-α and IL-1β) and apoptotic markers (Bax and Bcl-2), along with increased caspase-3 gene expression in heart tissue. Serum levels of lactate dehydrogenase were also notably higher in the TAA-intoxicated group, accompanied by significant histopathological alterations, increased collagen fiber deposition, and a pronounced immunopositive reaction for TGF-β1 and NF-κB in heart tissue. However, pre-treatment with WP significantly alleviated TAA-induced cardiotoxicity by reducing oxidative stress, inflammatory response, and apoptotic markers in cardiac tissue.
The results indicate that WP supplementation offers protective effects and mitigates the cardiotoxicity triggered by TAA.
硫代乙酰胺（TAA）在肝脏疾病研究中被广泛用作实验药物，已被证明会对多个器官产生毒性。它与氧化应激、炎症、细胞凋亡、纤维化和表观遗传修饰有关。乳清蛋白（WP）提供了丰富的必需和非必需氨基酸，这些氨基酸对人体至关重要。它因其营养和生物学特性而受到高度重视，对免疫、消化、心血管、神经和内分泌系统有益。本研究旨在评估WP对TAA诱导的大鼠心脏毒性的可能保护作用，重点关注其抗氧化、抗炎和抗凋亡机制。
总共40只雄性大鼠被随机分为四组，每组10只：对照组、TAA处理组（100mg/kg体重）、WP处理组（300mg/kg体重）和WP+TAA组。连续三周进行治疗。
研究结果显示，TAA暴露显著降低了心脏组织中谷胱甘肽、超氧化物歧化酶和过氧化氢酶的活性，同时显著增加了丙二醛和一氧化氮的活性。此外，TAA给药导致炎症标志物（TNF-α和IL-1β）和凋亡标志物（Bax和Bcl-2）显著升高，同时心脏组织中caspase-3基因表达增加。TAA中毒组的血清乳酸脱氢酶水平也明显更高，同时伴有明显的组织病理学改变、胶原纤维沉积增加以及心脏组织中TGF-β1和NF-κB的明显免疫阳性反应。然而，WP预处理通过降低心脏组织中的氧化应激、炎症反应和凋亡标志物，显著减轻了TAA诱导的心脏毒性。
结果表明，补充WP具有保护作用，并减轻了TAA引发的心脏毒性。
