Anti-inflammatory, anti-oxidant and hepatoprotective effects of lactoferrin in rats
Anti-inflammatory, anti-oxidant and hepatoprotective effects of lactoferrin in rats
复制标题
DOI：
10.1080/01480545.2019.1585868
复制
发表时间：
2021-05-04
影响因子：
2.6
通讯作者：
Abdelhiee, Ehab Yahya
中科院分区：
文献类型：
--
作者：
Farid, Ayman Samir;El Shemy, Mona A.;Abdelhiee, Ehab Yahya
四氯化碳（CCl4）是一种强肝毒性物质。在给予四氯化碳（CCl4）的Wistar大鼠模型中，检查抗炎剂乳铁蛋白（LF）减轻肝脏炎症的能力。雄性Wistar大鼠30只，随机分为5组：对照组、LF组（300 mg/kg B. CCl 4组（1 ml CCl 4/kg B. LF保护组（300 mg LF/kg B. wt每日1次，持续3周，随后为1 mL CCl4/kg B. LF治疗组（1 mL CCl4/kg B. wt，1次口服，随后300 mg LF/kg B.每天口服三周）。测定红细胞、白细胞、氧化应激标志物（超氧化物歧化酶[SOD]、谷胱甘肽过氧化物酶[GPx]和丙二醛[MDA]）的活性以及肝对氧磷酶-1（PON1）、白细胞介素（IL）-1 β和IL-10 mRNA的表达。对肝组织进行组织学检查。CCl4引起肝损伤，肝脏SOD和GPx抗氧化活性丧失，血清丙二醛水平显著升高。此外，CCl4诱导肝促炎因子（IL-1 β）上调，抗炎因子（IL-10和PON1）下调。根据组织病理学检查，肝组织有严重的炎症和损伤。然而，LF减轻肝损伤，氧化应激和肝毒性引起的四氯化碳。总体而言，这些结果表明，LF介导的免疫机制减轻四氯化碳诱导的肝毒性，并提供了一个新的观点LF的潜在用途，在治疗肝脏疾病的预防和治疗应用。
Carbon tetrachloride (CCl4) is a strong hepatotoxic agent. The ability of the anti-inflammatory agent, lactoferrin (LF), to alleviate hepatic inflammation in a Wistar rat model administered with carbon tetrachloride (CCl4) was examined. Thirty male Wistar rats were segregated into 5 groups (6 rats per group): Control group, LF group (300 mg LF/kg b. wt daily for three weeks), CCl4 group (1 ml CCl4/kg b. wt once orally), LF-protected group (300 mg LF/kg b. wt daily for 3 weeks followed by 1 mL CCl4/kg b. wt once orally), and LF-treated group (1 mL CCl4/kg b.wt once orally followed by 300 mg LF/kg b. wt orally every day for three weeks). Erythrogram, leukogram, activity of oxidative stress markers (Superoxide dismutase [SOD], Glutathione peroxidase [GPx], and Malondialdehyde [MDA]), and expression of hepatic paraoxonase-1 (PON1), interleukin (IL)-1 beta, and IL-10 mRNA were determined. Histopathological examination of the hepatic tissue was carried out. CCl4 caused liver injury, loss of liver antioxidant activity of SOD and GPx, and a significant increase in the level of malondialdehyde in the serum. Moreover, CCl4 induced up-regulation of hepatic pro-inflammatory (IL-1 beta) factors, and down-regulation of anti-inflammatory (IL-10 and PON1) factors. Based on histopathological examination, the hepatic tissues had severe inflammation and were damaged. However, LF mitigated the liver damage, oxidative stress, and hepatotoxicity caused by CCl4. Overall, these results suggest that LF-mediated immunological mechanisms alleviate CCl4-induced hepatic toxicity and provide a novel perspective on the potential use of LF for prophylactic and therapeutic applications in treating liver diseases.