In vitro and in vivo anticancer efficacy potential of Quercetin loaded polymeric nanoparticles.

Quercetin (QCT) is a flavonoid, abundantly present in plants and has gained considerable interest for its antioxidant property and chemo preventive activity. Bioavailability of QCT is very low due to its poor aqueous solubility and instability. Researchers are working on the application of nanotechnology to target chemotherapeutic drugs to the tumour site. The aim of the present study was to develop quercetin loaded chitosan nanoparticles (QCT-CS NPs) with enhanced encapsulation efficiency and sustained release property. We prepared biocompatible NPs with small size (<200 nm) and encapsulation efficiency of 79.78%. In vitro drug release study exhibited a cumulative amount of 67.28% release of QCT over a period of 12 h. at pH 7.4. In vitro cytotoxicity assay showed significantly reduced IC50 value of QCT-CS NPs as compared to free QCT (p < 0.05). Intra venous treatment of QCT-CS NPs in tumour xenograft mice with A549 and MDA MB 468 cells exerted significant reduction of tumour volume in comparison to disease control groups (p < 0.05). Serum anti oxidant enzyme superoxide dismutase (SOD) level markedly increased in QCT-CS NPs treated tumour bearing mice than free QCT treated group. In summary, the recent investigations reported successful encapsulation of QCT in chitosan (CS) NPs to target the tumour microenvironment and exhibited enhanced efficacy of QCT-CS NPs in cancer therapy.

Curcumin, a component of turmeric, efficiently prevents diclofenac sodium-induced gastroenteropathic damage in rats: A step towards translational medicine.

There is a need to find/discover novel leads to treat complex and/or multi-factorial disease(s). Curcumin (CUR) is one of the promising lead molecules which need its further evaluation against NSAID-induced gastroenteropathy. Hence, the aim of the present study was to explore the pharmaco-mechanistic efficacy of CUR against NSAID-induced gastroenteropathy. Rats were treated twice daily with CUR (25, 50 and 100 mg kg-1 peroral) or vehicle for 10 days. In some experiments, diclofenac sodium (DIC; 9 mg kg-1) was administered orally twice daily for the final 5 days of CUR/vehicle administration. After the last dose on 9th day, rats were fasted. 12 h after the last dose on 10th day, rats were euthanized and their GI tracts were assessed for haemorrhagic lesions, lipid peroxidation, intestinal permeability and GI luminal pH alterations along with haemato-biochemical estimations. The macroscopic, biochemical, haematological and histological evidences suggested that co-administration of CUR resulted in dose dependent attenuation of the NSAID-induced gastroenteropathic damage and the mechanisms may be related to its ability to prevent the NSAID-induced alterations in the GI luminal pH, lipid peroxidation/oxidative stress, GI blood loss and intestinal permeability alteration. Based on these pharmaco-mechanistic results we propose it as a promising lead to treat NSAID-gastroenteropahty.