Zakiah Nasser Almohawes, Hanan A Okail, Wafa A Al-Megrin, Manal F El-Khadragy, Mona A Ibrahim, Ayah S Fathalla, Doaa Soliman, Sherif R Mohamed
{"title":"乳清蛋白通过抗氧化、抗炎和抗凋亡作用对抗硫代乙酰胺诱导的雄性白化大鼠的心脏保护作用。","authors":"Zakiah Nasser Almohawes, Hanan A Okail, Wafa A Al-Megrin, Manal F El-Khadragy, Mona A Ibrahim, Ayah S Fathalla, Doaa Soliman, Sherif R Mohamed","doi":"10.3389/fvets.2025.1590722","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Discussion: </strong>The results indicate that WP supplementation offers protective effects and mitigates the cardiotoxicity triggered by TAA.</p>","PeriodicalId":12772,"journal":{"name":"Frontiers in Veterinary Science","volume":"12 ","pages":"1590722"},"PeriodicalIF":2.6000,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12127417/pdf/","citationCount":"0","resultStr":"{\"title\":\"The cardioprotective effect of whey protein against thioacetamide-induced toxicity through its antioxidant, anti-inflammatory, and anti-apoptotic effects in male albino rats.\",\"authors\":\"Zakiah Nasser Almohawes, Hanan A Okail, Wafa A Al-Megrin, Manal F El-Khadragy, Mona A Ibrahim, Ayah S Fathalla, Doaa Soliman, Sherif R Mohamed\",\"doi\":\"10.3389/fvets.2025.1590722\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Discussion: </strong>The results indicate that WP supplementation offers protective effects and mitigates the cardiotoxicity triggered by TAA.</p>\",\"PeriodicalId\":12772,\"journal\":{\"name\":\"Frontiers in Veterinary Science\",\"volume\":\"12 \",\"pages\":\"1590722\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2025-05-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12127417/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in Veterinary Science\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://doi.org/10.3389/fvets.2025.1590722\",\"RegionNum\":2,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"VETERINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Veterinary Science","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.3389/fvets.2025.1590722","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
The cardioprotective effect of whey protein against thioacetamide-induced toxicity through its antioxidant, anti-inflammatory, and anti-apoptotic effects in male albino rats.
Introduction: 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.
Methods: 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.
Results: 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.
Discussion: The results indicate that WP supplementation offers protective effects and mitigates the cardiotoxicity triggered by TAA.
期刊介绍：
Frontiers in Veterinary Science is a global, peer-reviewed, Open Access journal that bridges animal and human health, brings a comparative approach to medical and surgical challenges, and advances innovative biotechnology and therapy.
Veterinary research today is interdisciplinary, collaborative, and socially relevant, transforming how we understand and investigate animal health and disease. Fundamental research in emerging infectious diseases, predictive genomics, stem cell therapy, and translational modelling is grounded within the integrative social context of public and environmental health, wildlife conservation, novel biomarkers, societal well-being, and cutting-edge clinical practice and specialization. Frontiers in Veterinary Science brings a 21st-century approach—networked, collaborative, and Open Access—to communicate this progress and innovation to both the specialist and to the wider audience of readers in the field.
Frontiers in Veterinary Science publishes articles on outstanding discoveries across a wide spectrum of translational, foundational, and clinical research. The journal''s mission is to bring all relevant veterinary sciences together on a single platform with the goal of improving animal and human health.
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