Most of lipid lowering agents have many

Most of lipid-lowering agents have many therapeutic problems with severe side effects, while dietary fibers as lipid lowering therapy are safer. Chitosan (CS) is a dietary fiber biodegradable, biocompatible and has many health benefits including wound healing, antiinflammatory, anti-cancers, immune-modulator, hemostatic agent, lipid-lowering agent and antioxidants (Xia et al., 2011, Luo and Wang, 2013, Anandan et al., 2013). The lipid-lowering effect of CS is attributed to its binding to fatty acid, cholesterol, and bile salts; this resulted in delaying the digestion and Amadacycline of fat (Xia et al., 2011). Additionally, CS augments lipoprotein lipase activities and influences plasma adipocytokines, which significantly reduce adiposity index. Therefore, CS can regulate the level of circulating triacylglycerol and ameliorates metabolic alterations (Luo and Wang, 2013). CS can help the body maintain the antioxidant activity, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and other antioxidants, which play important roles in counteraction of oxidative stress (Xia et al., 2011, Luo and Wang, 2013).
Materials and methods
Results In the present study, exposure of erythrocytes to HC plasma induced a significant increase of cholesterol inclusion into erythrocytes membrane compared to control ones (P⩽0.01). On the other hand, treatment of HC group with CS or CS plus l-arginine significantly decreased cholesterol loading into cell membranes compared to untreated HC group. Fig. 1 displays these results. In respect of SOD, GPx, and CAT, these results indicated that, treatment of control erythrocytes with CS, l-NAME and l-arginine preserves activity of these enzymes and their ratios (SOD/CAT and SOD/GPx) at values near that of control one. However, a significant (P⩽0.05) decrease in SOD, GPx, and CAT activities was observed in erythrocytes incubated with HC compared to control. Conversely, treatment of HC group with CS, or CS plus l-arginine preserves activity of measured enzymes and their ratios compared to HC group. Table 1 represents these results. In the current work, HC exposure induced marked decrease of GSH/GSSG ratio; however, MDA and PCC were significantly increased compared to control erythrocytes (P⩽0.05). On the other side, treatment of HC with CS or CS plus l-arginine keeps GSH/GSSG, MDA and PCC at values similar to control group, see Table 2. Erythrocytes SA contents were significantly decreased by incubation of cell to HC plasma. However, treatment l-Arginine, CS or CS plus l-arginine prevent HC induces SA loss. Fig. 2 represents these results. Plasma TAC significantly decreased in HC group compared to control. However, no significant difference was noted between control and control treated with CS or CS+l-arginine. Treatment of HC group with CS or Cs+l-arginine prevents HC-induced TAC depletion. Fig. 3 annotates these results. In respect of NO variables, the exposure of erythrocytes to l-NAME caused a significant decrease in NOS activity and NO level compared to control group. A similar result was observed in HC treated group. On the other side, l-arginine treatment induced a significant increase in NOS activity compared to control; however, CS induces a marked but non-significant increase of NOS compared to control group. l-arginine treatment alone fails to prevent HC induced NOS inactivation. However, treatment of HC with l-arginine+CS prevented HC-induced decrease in NOS activity. By contrast, arginase activity was increased by HC exposure; however, CS or CS plus l-arginine treatment prevents HC induced arginase activation. Similar results were observed for arginase/NOS ratio. Table 3 explains these data.
Discussion Previous studies reported that an increase in arginase activity plays a crucial role in the cardiovascular pathobiology, so that the inhibition of arginase may protect against vascular diseases (Rabelo et al., 2015). Therefore, this study was conducted to explore the protective role of CS against HC induced erythrocyte’s arginase activation. HC disrupts erythrocytes cholesterol homeostasis, triggers ROS production and depletes antioxidant capability of cells (Devrim et al., 2008). However, cholesterol-lowering therapy prevents HC induced erythrocytes dysfunction (Franiak-Pietryga et al., 2009, Uydu et al., 2012). Herein, incubation of erythrocytes with cholesterol enriches plasma increased cholesterol inclusion into erythrocytes. Similar results were documented in several previous studies (Uydu et al., 2012, Harisa and Badran, 2015). In contrary, CS prevents cholesterol deposition into erythrocyte membranes; similarly, it has been reported that cholesterol lowering therapy decreases erythrocytes membrane cholesterol (Uydu et al., 2012). The attraction between CS and cholesterol decreases cholesterol inclusion into erythrocytes membrane.