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Abstract
Type II diabetes is known to cause neuropathy, nephropathy and retinopathy. However, cardiovascular disorders associated with diabetes have been ignored. In traditional medicine, cinnamon (Cinnamomum cassia) bark has been used for its abilities to relieve fever, inflammation and chronic bronchitis. In the present study, the effect of Cinnamomum cassia extract (CN) on the thoracic aorta in an experimental type II diabetes model was investigated. In rats administered with nicotinamide + streptozotocin, significant endothelial dysfunction and oxidative stress were characterised by increased inducible nitric oxide synthase (iNOS) and decreased insulin/proinsulin levels. This impairment was prevented by administering 1000 mg/kg metformin or 500-1000-1500 mg/kg CN. CN administration attenuated the inflammatory response by decreasing the levels of malondialdehyde (MDA), Nitric oxide (NO) and increasing Glutathione peroxidase (GPx), glutathione (GSH). In addition, CN administration was shown to cause down-regulating effects on iNOS in thoracic aorta. These findings reveal that CN could prevent chronic complications of experimentally induced type II diabetes by attenuating inflammation, oxidant/antioxidant imbalance, and normalised contraction and relaxion responses in the thoracic aorta.
Highlights
Diabetes mellitus is associated with numerous complications that are considered as major health problems in the developed world
It has been suggested that endothelial damage may be due to decreased endothelium-derived relaxing factor (EDRF) production and diminished smooth muscle response to EDRF (De Vriese et al, 2000)
Normal pancreas histomorphology was observed in the Normoglycemic Control (NC) group (Figure 1A a)
Summary
Diabetes mellitus is associated with numerous complications that are considered as major health problems in the developed world. It is estimated that more than 75% of deaths in diabetes patients are caused by cardiovascular diseases (Xu, Zou, 2009). Diabetic patients are at an increased risk of three major macrovascular diseases, namely peripheral vascular disease, coronary heart disease, and stroke (Zou, Cohen, Ullrich, 2004; Scirica et al, 2013). It has been suggested that endothelial damage may be due to decreased endothelium-derived relaxing factor (EDRF) production and diminished smooth muscle response to EDRF (De Vriese et al, 2000). Alternative mechanisms that have been suggested include: Deterioration of the vasodilating mechanism of bradykinin (Kiff et al, 1991), abnormalities at the G-protein level and impaired nitric oxide mediated vasodilating mechanism (Williams et al, 1996), and overproduction of endothelium-derived contracting factor (Mayhan, Simmins, Sharpe, 1991)
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