Oral supplementation of diabetic mice with propolis restores the proliferation capacity and chemotaxis of B and T lymphocytes towards CCL21 and CXCL12 by modulating the lipid profile, the pro-inflammatory cytokine levels and oxidative stress

Journal Article

Garraud, Ahmad A. Al Ghamdi, Gamal Badr, Wael N. Hozzein, Ahmed Allam, Noori S. Al-Waili, Mohammed A. Al-Wadaan and Olivier . 2015

• المجلة \ الصحيفة: BioMed Central
• رقم العدد: 54
• رقم الإصدار السنوي: 16
• الصفحات: 1-14

مستخلص المنشور

Type 1 diabetes mellitus (T1D) is a chronic T-cell–mediated autoimmune disease that results in the destruction of insulin-secreting β-cells [1]. Diabetes is associated with multiple metabolic disorders that are characterized by hyperglycemia, which is accompanied by several complications [2] that result from an absolute or relative deficiency in insulin secretion or action [3]. Dyslipidemia is a common feature of diabetes, which is characterized by elevated triglyceride and low-density lipoprotein (LDL) cholesterol (LDL-C) levels [4]. Hyperglycemia or dyslipidemia easily induces extensive oxidative stress that causes serious cellular dysfunction in diabetic patients [5, 6]. Persistent hyperglycemia increases the production of free radicals, especially reactive oxygen species (ROS), in several tissues [7]. Increased lipid peroxidation, characterized by increases in the levels of malondialdehyde (MDA), results in the formation of crosslinks between single molecules in proteins and the oxidation of LDL particles; oxidized LDL serves as the most common marker of oxidative stress [8, 9].

Inflammation in autoimmune diseases is characterized by an imbalance between pro- and anti-inflammatory cytokines. Pro-inflammatory cytokines deleteriously influence insulin sensitivity and β-cell function [10]. Interestingly, altered levels of cytokines impair insulin secretion in β cells [11], and accumulating evidence supports that diabetes is a disease of the innate immune system [11, 12]. Furthermore, diabetes increases the production of pro-inflammatory cytokines, including IL-1α, IL-1β, IL-6, and CXCL10 [13, 14]. However, the main cytokines involved in diabetes pathogenesis are IL-1, TNF-α, and IL-6 [15]. The impaired production of IL-1, IL-6, TNF-α and IFN-γ and the increased production of IL-10 in type 1 diabetic peripheral blood mononuclear cell (PBMC) cultures may indicate deficiencies in mononuclear cell activation and immune cellular adaptive responses [16].