Department of Biotechnology, School of Biotechnology and Health Sciences, Karunya University, Karunya Nagar, Coimbatore, Tamil Nadu, India.
Biol Trace Elem Res. 2013 Jan;151(1):85-91. doi: 10.1007/s12011-012-9534-2. Epub 2012 Nov 14.
The present study is aimed to evaluate the protective effect of ferulic acid (FA) on fluoride-induced oxidative hepatotoxicity in male Wistar rats. Fluoride (25 mg/L) was given orally to induce hepatotoxicity for 12 weeks. Hepatic damage were assessed using status of pathophysiological markers like serum marker enzymes like aspartate transaminase, alanine transaminase, alkaline phosphatase, acid phosphatase, gamma glutamyl transferase, lactate dehydrogenase, bilirubin, lipid profile, total protein content levels, and histopathological studies. Treatment with FA significantly reduced the degree of histological aberrations and rescued lipid peroxidation, as observed from reduced levels of lipid hydroperoxides, nitric oxide, restored levels of enzymic and non-enzymic antioxidants, and total protein content, with a concomitant decline in the levels of marker enzymes and lipid profile in fluoride-induced rats. These results suggest that ferulic acid has the ability to protect fluoride-induced hepatic damage.
本研究旨在评估阿魏酸（FA）对雄性 Wistar 大鼠氟诱导的氧化性肝毒性的保护作用。通过口服给予氟（25mg/L）12 周诱导肝毒性。使用血清标志物酶（如天冬氨酸转氨酶、丙氨酸转氨酶、碱性磷酸酶、酸性磷酸酶、γ-谷氨酰转移酶、乳酸脱氢酶、胆红素、脂质谱、总蛋白含量水平）等生理病理标志物的状态评估肝损伤。FA 的治疗显著降低了组织学异常的程度，并从脂质过氧化物水平的降低中挽救了脂质过氧化，观察到一氧化氮水平降低，酶和非酶抗氧化剂以及总蛋白含量的水平得到恢复，同时氟诱导大鼠的标记酶和脂质谱水平下降。这些结果表明，阿魏酸具有保护氟诱导的肝损伤的能力。
