The role of carboxymethyl chitosan/Hyaluronic acid embedded gold nanoparticles as hyperlipidemic and leptin resistance agent

Abstract

In this work, hyaluronic acid (HA)/carboxymethyl chitosan (CMCTs) blend, embedded with definite amount of gold nanoparticles (AuNPs), were utilized to mitigate lipid profile and leptin resistance in obese rats. AuNPs were produced through Microwave radiation technique, followed by characterization using the state of art analysis; UV and TEM, Average particle size EDX, XRD and IR. Afterward, 70 male albino rats were divided into two main groups: Group one " n=10 rats " fed healthy diet (negative control). The 2 nd group fed on the high fructose diet (HFD) for 4 weeks to induce hyperlipidemia and obesity. To this end, the 2 nd group is further divided into six sub-groups. The 1 st one (G2) received only HFD (positive control), the 2 nd subgroups (G3) received HFD+CMCTS+HA, the3 rd subgroups (G4) received HFD+ AuNPs, the 4 th ,5 th and 6 th subgroups (G5, G6 and G7) received orally; mixture of both HA and CMCTS in different ratios (3:1; 1:1; 1:3 respectively) embedded all with AuNPs (0.01M), in a dose of 2 mg/kg body weight /day for 4 weeks. The impact of polymers blends with AuNPs on Methicillin-resistant Staphylococcus aureus (MRSA), Klebsiella pneumonias (K. pneumonia) and Candida albicans (ATCC 10231) (C. albicans) was investigated. Results had the best the anti-bacterial and fungal effect for polymers blends in all ratios with AuNPs than for polymers and AuNPs separately. All treated groups (G3, G4, G5, G6 and G7) decreased leptin and lipid profile parameters levels (Serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL) very low-density lipoprotein (VLDL), atherogenic indices (Atherogenic Index (AI), Atherogenic Coefficient (AC) and Cardiogenic Risk Ratio (CRR)) compared to HFD group. Moreover, the mixture of HA/CMCTS (1:3) adorned AuNPs was more potent than other used ratios in attenuating various biochemical and histological abnormalities resulted due to obesity metabolic disorders. Furthermore, all treated subgroups disclosed normal histopathological heart muscle structures.