Abstract
Type II diabetes (T2D) is a pandemic characterized by pathological circulating inflammatory markers, high-glucose levels and oxidative stress. The hematological system is especially vulnerable to these aberrant circulating molecules, and erythrocytes (RBCs) show aberrant rheology properties, owing to the direct contact with these molecules. Pathological levels of circulating inflammatory markers in T2D therefore have a direct effect on the molecular and cellular structure of RBCs. Previous research has suggested that antioxidants may reduce oxidative stress that results from the pathological inflammatory markers. Particularly, polyphenol antioxidants like oligomeric proanthocyanidins (OPCs) may act as a hydroxyl mopping agent, and may have a positive effect on the deformability and membrane protein structure of RBCs from T2D. In this paper, we look at the effect of one such agent, Pinus massoniana bark extract (standardized to 95% oligomeric proanthicyanidins), on the RBC membrane structures and RBC shape changes of T2D, after laboratory exposure at physiological levels. Our methods of choice were atomic force microscopy and scanning electron microscopy to study RBC elasticity and ultrastructure. Results showed that in our hands, this OPC could change both the eryptotic nature of the RBCs, as viewed with scanning electron microscopy, as well as the elasticity. We found a significant difference in variation between the elasticity measurement values between the RBCs before and after OPC exposure (P-value <0.0001). In conclusion, the data from both these techniques therefore suggest that OPC usage might contribute to the improvement of RBC functioning.
Highlights
Type II diabetes (T2D) is commonly associated with comorbidities including dyslipidaemia[1,2,3,4] and hypertension.[4,5] The main cause of morbidity and mortality in individuals with type II diabetes (T2D) is cardiovascular disease (CVD), with up to 80% of diabetes subjects dying as a result of cardiovascular complications.[1,3,6] The risk of atherothrombotic events is comparable to individuals without diabetes but with a history of ischemic heart disease.[1]
The main cause of morbidity and mortality in individuals with T2D is cardiovascular disease (CVD), with up to 80% of diabetes subjects dying as a result of cardiovascular complications.[1,3,6]
Oxidative stress and chronic inflammation, all lead to a pathophysiological coagulation system that is characterized by hypercoagulability
Summary
Type II diabetes (T2D) is commonly associated with comorbidities including dyslipidaemia[1,2,3,4] and hypertension.[4,5] The main cause of morbidity and mortality in individuals with T2D is cardiovascular disease (CVD), with up to 80% of diabetes subjects dying as a result of cardiovascular complications.[1,3,6] The risk of atherothrombotic events is comparable to individuals without diabetes but with a history of ischemic heart disease.[1]. Oxidative stress and chronic (systemic) inflammation, all lead to a pathophysiological coagulation system that is characterized by hypercoagulability. Systemic inflammation has a fundamental role in many chronic conditions, including T2D and CVD.[8,9,10,11,12] CVD and vascular dysfunction are fundamental parts of the etiology of T2D and this condition is known to have a changed coagulation system. All these factors serve as early indicators of vascular dysfunction. There are important links between oxidative stress, a changed inflammatory marker profile and inflammation, the progression of T2D and vascular dysfunction.[4]
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