Inhibitory effects and related mechanisms of lycium barbarum polysaccharides on vascular lesions in type 2 diabetes mellitus

Objective: The aim of this study was to investigate the inhibitory effects and related mechanisms of lycium barbarum polysaccharides (LBP) on type 2 diabetes mellitus (T2DM) vascular lesions. Methods: A T2DM rat model was established by intraperitoneal injections of streptozotocin combined with a high-fat diet. Diabetic Sprague-Dawley rats were divided into a control group, T2DM group, experiment A group (group A), and experiment B group (group B). Group A and group B received 20 mg and 40 mg of LBP, respectively. The control group and T2DM group received the same amount of normal saline by gavage. The duration of the experiment was 4 weeks. At the end of the experiment, serum levels of insulin, glycosylated hemoglobin (HbA1c), triglycerides (TG), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), low-density lipoprotein cholesterol (LDL-C), interleukin 4 (IL-4), and interleukin 6 (IL-6) were measured. H&E staining was used to detect pathological changes in vascular structures. MicroRNA and protein levels of p38 mitogen-activated protein kinase (p38MAPK) and intercellular adhesion molecule 1 (ICAM-1) in rat thoracic aortas were analyzed by qRT-PCR and Western blotting, respectively. Results: In group B, serum insulin was significantly increased after large doses of LBP but serum levels of HbA1c, LDL-C, TG, and IL-6 were significantly decreased (all P<0.05). Compared with group A, serum levels of IL-4, SOD, and GSH-PX increased significantly in group B but levels of serum HbA1c, LDL-C, TG, and IL-6 decreased significantly (all P<0.05). H& E staining showed that, compared with T2DM group, the degree of vascular lesions in group A and group B was lower. Compared with group A, mRNA and protein levels of p38MAPK were significantly increased and those of ICAM-1 were decreased in group B (all P<0.05). Conclusion: LBP reduces inflammatory response and vascular lesions induced by T2DM through regulating p38MAPK signaling pathways and increasing antioxidative capacity.