Formulation and evaluation of folic acid conjugated gliadin nanoparticles of curcumin for targeting colon cancer cells.

Preparation of folic acid (FA) conjugated (FA-CUR-GNPs) and non-conjugated (CUR-GNPs) gliadin nanoparticles of curcumin were successfully formulated by desolvation method for oral delivery of drug for targeting colon cancer cell. F1, F3, F5 (conjugated) and F2, F4, F6 (Non-conjugated) were formulated using various drug-polymer ratio (1:2). They were further characterized by FTIR, Mass spectroscopy, NMR, solubility studies, entrapment efficiency, TEM, particle size, surface charge, In-vitro release studies, In vivo toxicity studies and simultaneously evaluated. F3 (curcumin 10mg, gliadin 20mg and FA 5mg) and F4 (curcumin 10mg and gliadin 20 mg) were found as the optimized formulation among both the categories. For F3 and F4 formulations; average particle size (168.1 and 195.7nm), zeta potential (-16.5 and -24.4mV), cumulative % drug release (92.92 and 94%) and In vivo toxicity studies were conducted and compared with the control (phosphate-buffer saline, pH 6.8) reveals no toxicity. From the characterization and evaluation studies it was identified that F4 (FA-CUR-GNPs) had better solubility, In vitro release profile and no specified In-vivo toxicity than F3 (CUR-GNPs) formulation with nano-range particle size throughout the experiment. Improved bioavailability and increase targeting capacity toward colon cancer tumor cells were successfully achieved.

Effects of IL-18 and IL-10 pre-treatment on the alteration of endogenous cytokines in liver and spleen of mice with experimental endotoxemia.

Mechanisms of interleukin-18 (IL-18) and interleukin-10 (IL-10) in lipopolysaccharide (LPS) induced endotoxemia are not clear; their protective role is being investigated so that they may effectively modulate the host cytokine levels during endotoxemia. The aim of the study was to evaluate protective effects of IL-18 and IL-10 in experimentally induced endotoxemia in mice correlating the changes in tissue anti-oxidant enzymes and circulating cytokines. Liver injury was determined by estimation of serum glutamate oxalate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT), serum nitric oxide (NOx), hepatic anti-oxidant enzyme and cytokine content in LPS (250 g/kg) induced endotoxemic mice receiving either IL-18 (500 ng/mouse) or IL-10 (600 ng/mouse) treatment. Mice (87% of IL-10 treated and 74% of IL-18 treated) survived when administered prior to LPS challenge. Pre-treatment of mice with either IL-10 or IL-18 followed by LPS, lead to reduction in SGPT and SGOT level, serum NOx, and altered hepatic anti-oxidant enzymes activity and myeloperoxidase activity than the only LPS treated group. Marked reduction in the amounts of LPS-induced hepatic and splenic TNF- content has been observed after IL-10 pre-treatment. Results suggested that attenuating the induction of TNF- and IFN- and subsequent induction of nitric oxide formation in response to LPS may in part account for efficient protection by IL-18 and IL-10 in the reduction of LPS-induced liver injury.