ABSTRACT
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.
ABSTRACT
Background: For spinal anesthesia there are drugs which can increase the level and quality of analgesia. Any drug which decreases sensory block level in spinal anesthesia is of great concern as it may need analgesic, sedative, supplement or even conversion to general anesthesia. Ondansetron is one such drug which has been reported to decrease the height of sensory block achieved after subarachnoid administration of bupivacaine. In this prospective observational study, we studied the effect of administration of ondansetron on the level of the sensory block achieved after subarachnoid blockade. Methods: In Group II, 4 mg ondansetron was given and 15 mins before giving spinal anesthesia Group II against control group receiving 2 ml saline intravenous (Group I). 15 mins before giving spinal anesthesia. Both groups received 3.5 ml of bupivacaine heavy was given intrathecally. Sensory and motor block was assessed 5, 15, and 30 mins. We analyzed both highest spinal block level achieved and time to regress to L1 level. Results: We found that in Group II both highest level of sensory block (T6 by median method) duration to regress to L1 level (1.43±0.22 hrs) was lesser as compared to group I and Group III T4 by median method and time to regress from T6 to L1 Group I 2.03±0.06 hrs Group III 1.84±0.27 hrs. Motor block did not differ between groups. Conclusions: We concluded that probably ondansetron was responsible for lower spinal block level and early recovery from spinal anesthesia after intrathecal bupivacaine and should not be given empirically for nausea and vomiting.