Decreasing serum homocysteine and hypocholesterolemic effects of bovine lactoferrin in male rat fed with high-cholesterol diet

Abstract

Introduction: Lipid metabolism disorder or hyperlipidemia is known as a risk factor for cardiovascular disease, the increase in serum homocysteine and leptin are associated with atherosclerotic disease. The purpose of the present study was to examine the effects of bovine lactoferrin (bLF) on serum homocysteine (Hcy), apolipoproteinA-I (ApoA-I) and B (ApoB), leptin and lipid profile changes in high-cholesterol-diet (HCD) fed rats. Methods: The Healthy Adult Sprague-Dawley (SD) male rats were randomly assigned into three experimental groups. Each group consisted of eleven male rats including control group, HCD rats and hypercholesterolemic rats, which were treated with bLF (HCD+bLF). bLF was given by gavage (200 mg/kg/d). After 4 weeks of feeding and overnight fasting, total blood samples were collected. Results: The results showed the elevated level of Hcy, leptin, total cholesterol, low density lipoprotein cholesterol (LDL-C), ApoB and decrease in ApoA-I in non-treated HCD group compared to the control rats. Administration of bLF significantly ameliorated the Hcy and leptin levels with decrease in LDL-C and total cholesterol in rats fed with a high-cholesterol diet. bLF also tended to increase low serum concentration of ApoA-I and high density lipoprotein cholesterol (HDL-C) in HCD rats. Meanwhile, upon bLF-treated rats, there was a significant decrease in ApoB in HCD group. Conclusion: The findings indicated that bLF can improve the alteration of serum Hcy, leptin, apolipproteins and lipid changes in male rats fed with high-cholesterol diet. So, bLF can counteract with HCD elicited hyper-homocysteinemia and hyper-leptinemia, suggesting it to have the useful therapeutic potential in patients with atherosclerosis and lipid disorder.

Lactoferrin suppresses LPS-induced expression of HMGB1, microRNA 155, 146, and TLR4/MyD88/NF-кB pathway in RAW264.7 cells

“…It has been suggested that lactoferrin (LF), one of the major antioxidants in human milk, has potential pharmacological activities, could reduce tissue in ammatory response in T cells [15]. Our previous ndings and other reports have suggested that LF inhibit the in ammatory response to the high-fat dietinduced in ammation and metabolic stress in rat [16,17]. It was also informed that LF signi cantly attenuates the catecholamine-induced cardiotoxicity by inhibition of reactive oxygen species (ROS) [18].…”

Lactoferrin Suppresses LPS-Induced Expression of HMGB1, microRNA 155, 146, and TLR4/MyD88/NF-кB Pathway in RAW264.7 Cells

“…It has been suggested that lactoferrin (LF), one of the major antioxidants in human milk, has potential pharmacological activities, could reduce tissue in ammatory response in T cells [17]. Our previous ndings and other reports have suggested that LF inhibit the in ammatory response to the high-fat dietinduced in ammation and metabolic stress in rat [18,19]. It was also informed that LF signi cantly attenuates the catecholamine-induced cardiotoxicity by inhibition of reactive oxygen species (ROS) [20].…”

Cardioprotective effects of enteral vs. parenteral lactoferrin administration on myocardial ischemia-reperfusion injury in a rat model of stunned myocardium

“…Maekawa et al [34] reported that lactoferrin administered to rats by intraperitoneal injection increased GLP-1 in plasma. Adipocytokines such as omentin, apelin, and adiponectin could also be substances induced or activated by enteral lactoferrin, considering that enteral lactoferrin is transported to the mesenteric fat tissue [24] and is associated with lipid metabolism [35,36]. Ikoma-Seki et al [37] reported that lactoferrin induced lipolysis via the cyclic adenosine monophosphate-protein kinase A signaling pathway in rat adipocytes isolated from mesenteric fat.…”