Typhoid fever (TF) is an acute systemic infection caused by Salmonella Typhi, Salmonella Para Typhi A and Salmonella Para Typhi B. It is transmitted by the fecal oral route mainly via contaminated food and water. The developing countries have high rate of morbidity and mortality due to Typhoid fever, epidemics take place in developed world also. There are increased incidences of multi drug resistant in S. typhi strains that has further complicated its management and only a few antibiotics are now effective in treatment of typhoid. We report that the aqueous extracts of fruit peel Citrus sinensis (L.) confer anti typhoid activity against Salmonella Typhi, Salmonella Para Typhi A and Salmonella Para Typhi B respectively on comparison with ciprofloxacin.
Key words: Typhoid fever, Salmonella Typhi, Salmonella Para Typhi A , Salmonella Para Typhi B, anti typhoid activity, Citrus sinensis.
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INTERNATIONAL JOURNAL OF PHARMACEUTICAL RESEARCH AND DEVELOPMENT
December - 2010 / Volume - 2/Issue - 10
( Total Articles =17 )
December 2010 Issue
Article No 15
December - 2010 / Volume - 2 / Issue - 10 /Article No - 10 / Research Article
APOPTOSIS INDUCING ACTIVITY OF LUFFA ACUTANGULA FRUIT IN LEUKEMIA CELLS (HL-60)
B. Purushotham Reddy1*,
A. Raghuram Reddy2 , B. Srinivas Reddy3 ,
S Venkata Mohan1, P.N Sarma1
1Bioengineering and Environmental Centre,
Indian Institute of Chemical Technology
Hyderabad 500 607, India
1Medicinal Chemistry Research Division, UCPSc,
Kakatiya University, Warangal-506009, India
1Biomedical Science Department,, Texas tech University
Health Sciences Cernter, Amarillo 79106, Texas, USA.
In the present study we evaluated the apoptosis inducing activity of Luffa acutangula fruit extracts in leukemia model. Our results show that partially purified methanolic extract, F-3, dose dependently induced apoptosis in leukemia cell line HL-60. Initially apoptosis inducing activity of fraction F-3 was evaluated by observing morphological changes in HL-60, our results show that F-3 fraction treated HL-60 cells show characteristic morphology of apoptosis such as nuclear bebbling and budding of apoptosis bodies. In addition, F-3 fraction treated HL-60 cells have shown increased sub G0/G1 population and DNA fragment ladder as compared to control cells. To delineate the molecular mechanism F-3 treated cells were subjected to western blotting. Further more, FACS analysis show increased population in annexine positive in F-3 treated cells. Our results show that antiapoptotic protein Bcl2 expression was down regulated whereas, proapoptotic protein Bax was up regulated as compared to control cells. Apoptosis markers, cleaved caspase3 and PARP were dose dependently up regulated by F-3 treatment. Finally to test whether fraction F-3 induced apoptosis is mediated by extrinsic or intrinsic pathway, F-3 fraction treated HL-60 cells were analyzed for mitochondrial membrane depolarization and our results show that F-3 fraction significantly depolarizing the mitochondrial membrane in HL-60 cells indicating apoptosis induction by F-3 fraction is mediated may be by intrinsic pathway.
Key words: Human Leukemia, Cytosolic Condensation, Nuclear fragmentation, Caspase and Annexin