000			03704nam a22001817a 4500
003			OSt
005			20220321135808.0
008			171102b xxu||||| |||| 00| 0 eng d
040			_aMMSU _cULS
100			_9151 _aAlonzo, Trinity Joy E. [and four others]
245			_aThe Potential of Green Grapes (Vitis vinifera) stem extract as anti-anemia in female guinea pigs _cTrinity Joy E. Alonzo [and four others]
260			_c2008
300			_aviii, 59 leaves _c28 cm.
500			_aThesis (Bachelor of Science in Pharmacy) -- Mariano Marcos State University - College of health Sciences, Batac City
504			_aBibliography: leaf 29
520			_bABSTRACT Español, Mavis Maxine A., Galano, Hyacinth Mae E., Jacinto, Victoria Abejoy C., Nebab, Alen O., Paleracio, Bobby F., Peña, Jamyca L., Peralta, Francis U., Undergraduate Thesis. Mariano Marcos State University, College of Health Sciences, Department of Pharmacy, 2906 City of Batac, August 2013. Antioxidant and Hepatoprotective Property of Dippig (Musa Balbisiana) Flower Extract Adviser: Rhian Jaymar D. Ramil, Rph, MS Coadviser: Prof. Janelyn V. Rojas, RPh, MST, MS This is an experimental study on the activity of Dippig (Musa Balbisiana) Flower Extract (DFE) as an antioxidant and hepatoprotective agent. The plant material was obtained from Lasam, Cagayan and oven dried for 24 hours at 50 °C. Extract WAS OBTAINED BY 72-hr maceration with method and rotary evaporation method. The antioxidant activity of methanotic extracts of Dippig (Musa Balbisiana) Flower was evaluated by Total phenotic content by Folin ciocalteu method and DPPH assay with IC50 determination. Total phenolic content was determined by spectrophotometry, using gallic acid as standard. 57.571 microgram total polyphenols as GAE per milligram extract was obtained. DPPH (1,1-diphenyl-2-picryl-hydrazyl) test of DFE showed 78.978% free radical inhibition at a concentration of 200mcg/ml. therefore, the specific DFE concentration that has the capacity to scavenge free radicals in half is 153.62 mcg/ml. for the hepatoprotective activity of DFE, animals were divided into 5 groups of 5 animals each. Group 1 (negative control) received normal saline (5ml/kg, po), for 5 days; Group 2 (positive control) received Silymarin (100mg/kg po) and paracetamol (2g/kg, po) on the 2nd and 3rd day, 30 min after Silymarin administration; Group 3 and 4 received DFE (250mg/kg po and 500mg/kg po), respectively and paracetamol (2g/kg, po) on the 2nd and 3rd day, 30 min after DFE administration; Group 5 (toxic group) was given Paracetamol (2g/kg, po) for 5 days on the 2nd and 3rd day. Alteration in the levels of biochemical markers of hepatic damage like SGPT and SGOT with histopathologic examination of the livers were tested in both treated and untreated group through cardio-puncture collection of blood. Paracetamol increased the SGPT and SGOT levels and showed near normal levels in the dose dependent manner. This was evident in DFE (500mg/kg and positive control, Silymarin, because they showed no significant difference. Histopathological architecture of Paracetamol-induced liver sections showed necrosis and loss of cellular boundaries. However, administration of DFE and Silymarin prevented the further toxic effect of Paracetamol in the liver tissues, showing marked hepatoprotective. Analysis of variance (ANOVA) for data analysis was used to test the significant difference in the treatments. Results of the study showed that in terms of its antioxidant activity, there is a significant difference between Ascorbic acid and DFE while the hepatoprotective activity showed no significant difference between Silymarin and DFE.
942			_2lcc _cTHEDIS
999			_c11800 _d11800