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1860797397655879680
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| building |
INTELEK Repository
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| collection |
Online Access
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| collectionurl |
https://intelek.unisza.edu.my/intelek/pages/search.php?search=!collection407072
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| date |
2024-08-27 12:21:23
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| format |
Restricted Document
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12552
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UniSZA
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| internalnotes |
[1] S Srinivasan; LPari,J Fun Foods.,2013,5, 484-492. [2] P Misra; RPUpadhyay; PAMisra; KAnand,Diabetes Res ClinPract.,2011,92, 303-311. [3] HMohan.Textbook of pathology.5th Edition, New Delhi,Jaypee Brothers Medical Publishers,2005, 850. [4] SGenuth; KGAlberti;PBennett; JBuse; RDefronzo; RKahn,Diab Care.,2003,2, 3160-3167. [5] IDF, 2012, Diabetes Atlas, 5th Edition, http://www.idf.org/diabetesatlas/5e/the-global-burden (accessed 08.11.12). [6] JHDoughari;AMEl-Mahmood; ITyoyina,Afr J Pharm Pharmacol.,2008,2, 7-13. [7] AV Khan; QU Ahmed; IShukla; AA Khan,Asian Pacific journal of tropical biomedicine.,2012,2, 189-194. [8] DArcanjo; A Albuquerque;BMelo-Neto;LSantana; M Medeiros; ACitó,Braz J Biol.,2012,72, 505-509. [9] MV Vijayakumar;SSingh; RRChhipa; MKBhat,Brit J pharmacol.,2005,146, 41-48. [10] M Eddouks; HJouad;M Maghrani; A Lemhadri; R Burcelin,Phytomedicine.,2003,10, 594-599. [11] LLi; CZheng; Y Fu; D Wu;XYang; HShen;Biol Trace Elem Res.,2012,145, 101-108. [12] RDARibeiro; F de Barros; F de Melo; C Muniz; SChieia; MWanderley; G Trolin,J.Ethnopharmacol.,1988,24, 19-29. [13] KV Prasad; KBharathi;KKSrinivasan,Indian JPharmacol.,1993,37, 337-341. [14] DJ Newman; GM Cragg; KM Snader,J Nat Prod.,2003,66, 1022-1037. [15] CMarie-Magdeleine;LUdino; LPhilibert; BBocage; HArchimede;Res Vet Sci.,2014,96,127-132. [16] GETrease; WCEvans;Trease and Evan’s Textbook of Pharmacognosy.13th Edition, Cambridge University Press, London, 1989,546. [17] NRakieten; MRakieten; MNadkarni,Cancer ChemotherRep.,1962,29, 91–98. [18] MEddouks; DChattopadhyay;NAZeggwagh, Evidence-Based Complementary and Alternative Medicine.,2012. [19] PTrinder,Ann ClinBiochem.,1969,6, 24-27. [20] DLDrabkin; JHAustin,J Biol Chem.,1932,98, 719–733. [21] SSNayak; TNPattabiraman,ClinChimActa.,1981,109, 267–274. [22] JKing. The transaminases: alanine and aspartate transaminases. In: Practical clinical enzymology, 1st Edition, Van NostrandReinhold, London, 1965a,363–395. [23] JKing. The hydorlases-acid and alkaline phosphatases. In: Practical clinical enzymology, 1st Edition, VanNostrand Reinhold, London, 1965b, 199–208. [24] OH Lowry; NJ Rosebrough; AL Farr; RJRandall,J Biol Chem.,1951,193,265–275. [25] J Brod; JHSirota,J Clin Invest.,1948,27, 645. [26] SNatelson; MLScott; CABeffa,Amer J Clin Pat.,1951,21, 275-76. [27] WTCaraway. Uric acid. D. Seligson 1st Edition, Standard Methods of Clinical Chemistry, Vol. 4, Academic Press, New York,1963, 239–247. [28] WT Friedewald; RI Levy; DSFredrickson,Clin Chem.,1972,18, 499–502. [29] P Bradbury; KCGordon. Theory and practice of histological techniques. Connective tissue and stains. 3rd Edition, Edinburgh London Melbourne and New York, Churchill Livingstone Inc, 1990, 119-142. [30] MRao; SSubramanian, Med Chem Res.,2009,18, 443-446. [31] JAOjewole,Phytomedicine.,2003,10, 675-681. [32] RJKoeing; CMPeterson; CKilo;Diabete.,1976,25, 230–240. [33] GC Sheela; KT Augusti,IndianJ Exp Biol.,1992,30, 523–526. [34] EHHarris,ClinDiab.,2005,23,115-119. [35]AScott.2012 The management of hypersmolar hypoglycemic state in adults withdiabetes.iLondon:iDiabetesiUK;i[online]iAvailableifrom: https://www.diabetes.org.UK/Aboutus/What-we-say.What-we say/ Improving-diabetes-health-care/Management-ofthe-hypersmolar-hypoglycemicstate-HHS-inadults-with-diabetes/ [accesed on 16th April, 2014). [36] MKaleem; PMedha; QUAhmed; MAsif; BBano,Singapore Med J.,2008,49(10), 800. [37] SS Lal; YSukla; ASingh; EAAndriyas; AMLall,Asian J Med Sci.,2009,1, 33-34. [38] JYu; PJCui; WLZeng; XLXie; WJLiang; GBLin; LZeng,Food Chem.,2009,117, 42–47. [39] RP Agrawal; P Sharma; M Pal; A Kochar; DKKochar,Diabetes Res ClinPract.,2006,73, 211–214. [40] MNWoo; SHBok; MKLee; HJKim; SMJeon; GMDo; SKShin; TYHa; MSChoi,J Med Food.,2008,11, 169– 178. [41] DJHausenloy;DMYellon,CurrOpinCardiol.,2009,24, 473–482. [42] JJ Badimon; BIbanez,RevEspCardiol.,2010, 63, 323–333. [43] MAMironova; RLKlein; GTVirella; MFLopes-Virella,Diabetes.,2000,49, 1033-1049.
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6859-01-FH02-FP-15-04236.pdf
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| person |
Hamendra ji
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| recordtype |
oai_dc
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| resourceurl |
https://intelek.unisza.edu.my/intelek/pages/view.php?ref=12552
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| spelling |
12552 https://intelek.unisza.edu.my/intelek/pages/view.php?ref=12552 https://intelek.unisza.edu.my/intelek/pages/search.php?search=!collection407072 Restricted Document Article Journal application/pdf Adobe Acrobat Pro DC 20 Paper Capture Plug-in with ClearScan 11 1.6 Hamendra ji 2024-08-27 12:21:23 6859-01-FH02-FP-15-04236.pdf UniSZA Private Access Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice Journal of Chemical and Pharmaceutical Research The use of medicinal plants as source of remedies for the treatment of many diseases dated back to prehistory and people of all continents have this old tradition. I the present study, methanolic tepal extract (MTE) of Musa paradisiaca was evaluated for phytochemical screening, andin vivo antidiabetic therapeutic efficacy in streptozotocin (STZ)-induced diabetic mice. Diabetic mice were administered 500 mg/kg per day of MTE orally for one month. The mice were sacrificed and blood collected for key biochemical parameters such as, blood glucose, insulin, hemoglobin and glycosylated hemaoglin (HbA 1c), creatinine, urea, uric acid, total protein, lipid profile, aminotransferases and alkaline phosphatase. The histopathological studies of pancreas, liver and kidney was also performed. Preliminary phytochemical screening reveals the presence of phenolics, flavonoids, glycosides, terpenoids, tannins and alkaloids. Elevated blood glucose, HbA1c creatinine, urea and uric acid and decreased level s of plasma insulin and hemoglobin were significantly (p<0.05) reverted back to near normal in STZ-induced diabetic mice after oral administration of MTE. Plasma protein, lipid profile, transaminases and alkaline phosphatase were also significantly normalized (p<0.05) after the treatment. Histopathological analysis indicated tissue damages in the diabetic untreated mice. MTE treated groups shows the tissue protection (of pancreas and liver) against peroxidation damage, thus signifying tissue integrity maintenance of MTE. It can be inferred that thein vivo antidiabetic therapeutic efficacy of tepals of Musa paradisiaca may be attributed to the presence of phytochemicals such as phenolics, flavonoids, alkaloids etc. 7 8 837-846 [1] S Srinivasan; LPari,J Fun Foods.,2013,5, 484-492. [2] P Misra; RPUpadhyay; PAMisra; KAnand,Diabetes Res ClinPract.,2011,92, 303-311. [3] HMohan.Textbook of pathology.5th Edition, New Delhi,Jaypee Brothers Medical Publishers,2005, 850. [4] SGenuth; KGAlberti;PBennett; JBuse; RDefronzo; RKahn,Diab Care.,2003,2, 3160-3167. [5] IDF, 2012, Diabetes Atlas, 5th Edition, http://www.idf.org/diabetesatlas/5e/the-global-burden (accessed 08.11.12). [6] JHDoughari;AMEl-Mahmood; ITyoyina,Afr J Pharm Pharmacol.,2008,2, 7-13. [7] AV Khan; QU Ahmed; IShukla; AA Khan,Asian Pacific journal of tropical biomedicine.,2012,2, 189-194. [8] DArcanjo; A Albuquerque;BMelo-Neto;LSantana; M Medeiros; ACitó,Braz J Biol.,2012,72, 505-509. [9] MV Vijayakumar;SSingh; RRChhipa; MKBhat,Brit J pharmacol.,2005,146, 41-48. [10] M Eddouks; HJouad;M Maghrani; A Lemhadri; R Burcelin,Phytomedicine.,2003,10, 594-599. [11] LLi; CZheng; Y Fu; D Wu;XYang; HShen;Biol Trace Elem Res.,2012,145, 101-108. [12] RDARibeiro; F de Barros; F de Melo; C Muniz; SChieia; MWanderley; G Trolin,J.Ethnopharmacol.,1988,24, 19-29. [13] KV Prasad; KBharathi;KKSrinivasan,Indian JPharmacol.,1993,37, 337-341. [14] DJ Newman; GM Cragg; KM Snader,J Nat Prod.,2003,66, 1022-1037. [15] CMarie-Magdeleine;LUdino; LPhilibert; BBocage; HArchimede;Res Vet Sci.,2014,96,127-132. [16] GETrease; WCEvans;Trease and Evan’s Textbook of Pharmacognosy.13th Edition, Cambridge University Press, London, 1989,546. [17] NRakieten; MRakieten; MNadkarni,Cancer ChemotherRep.,1962,29, 91–98. [18] MEddouks; DChattopadhyay;NAZeggwagh, Evidence-Based Complementary and Alternative Medicine.,2012. [19] PTrinder,Ann ClinBiochem.,1969,6, 24-27. [20] DLDrabkin; JHAustin,J Biol Chem.,1932,98, 719–733. [21] SSNayak; TNPattabiraman,ClinChimActa.,1981,109, 267–274. [22] JKing. The transaminases: alanine and aspartate transaminases. In: Practical clinical enzymology, 1st Edition, Van NostrandReinhold, London, 1965a,363–395. [23] JKing. The hydorlases-acid and alkaline phosphatases. In: Practical clinical enzymology, 1st Edition, VanNostrand Reinhold, London, 1965b, 199–208. [24] OH Lowry; NJ Rosebrough; AL Farr; RJRandall,J Biol Chem.,1951,193,265–275. [25] J Brod; JHSirota,J Clin Invest.,1948,27, 645. [26] SNatelson; MLScott; CABeffa,Amer J Clin Pat.,1951,21, 275-76. [27] WTCaraway. Uric acid. D. Seligson 1st Edition, Standard Methods of Clinical Chemistry, Vol. 4, Academic Press, New York,1963, 239–247. [28] WT Friedewald; RI Levy; DSFredrickson,Clin Chem.,1972,18, 499–502. [29] P Bradbury; KCGordon. Theory and practice of histological techniques. Connective tissue and stains. 3rd Edition, Edinburgh London Melbourne and New York, Churchill Livingstone Inc, 1990, 119-142. [30] MRao; SSubramanian, Med Chem Res.,2009,18, 443-446. [31] JAOjewole,Phytomedicine.,2003,10, 675-681. [32] RJKoeing; CMPeterson; CKilo;Diabete.,1976,25, 230–240. [33] GC Sheela; KT Augusti,IndianJ Exp Biol.,1992,30, 523–526. [34] EHHarris,ClinDiab.,2005,23,115-119. [35]AScott.2012 The management of hypersmolar hypoglycemic state in adults withdiabetes.iLondon:iDiabetesiUK;i[online]iAvailableifrom: https://www.diabetes.org.UK/Aboutus/What-we-say.What-we say/ Improving-diabetes-health-care/Management-ofthe-hypersmolar-hypoglycemicstate-HHS-inadults-with-diabetes/ [accesed on 16th April, 2014). [36] MKaleem; PMedha; QUAhmed; MAsif; BBano,Singapore Med J.,2008,49(10), 800. [37] SS Lal; YSukla; ASingh; EAAndriyas; AMLall,Asian J Med Sci.,2009,1, 33-34. [38] JYu; PJCui; WLZeng; XLXie; WJLiang; GBLin; LZeng,Food Chem.,2009,117, 42–47. [39] RP Agrawal; P Sharma; M Pal; A Kochar; DKKochar,Diabetes Res ClinPract.,2006,73, 211–214. [40] MNWoo; SHBok; MKLee; HJKim; SMJeon; GMDo; SKShin; TYHa; MSChoi,J Med Food.,2008,11, 169– 178. [41] DJHausenloy;DMYellon,CurrOpinCardiol.,2009,24, 473–482. [42] JJ Badimon; BIbanez,RevEspCardiol.,2010, 63, 323–333. [43] MAMironova; RLKlein; GTVirella; MFLopes-Virella,Diabetes.,2000,49, 1033-1049.
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| spellingShingle |
Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice
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| summary |
The use of medicinal plants as source of remedies for the treatment of many diseases dated back to prehistory and people of all continents have this old tradition. I the present study, methanolic tepal extract (MTE) of Musa paradisiaca was evaluated for phytochemical screening, andin vivo antidiabetic therapeutic efficacy in streptozotocin (STZ)-induced diabetic mice. Diabetic mice were administered 500 mg/kg per day of MTE orally for one month. The mice were sacrificed and blood collected for key biochemical parameters such as, blood glucose, insulin, hemoglobin and glycosylated hemaoglin (HbA 1c), creatinine, urea, uric acid, total protein, lipid profile, aminotransferases and alkaline phosphatase. The histopathological studies of pancreas, liver and kidney was also performed. Preliminary phytochemical screening reveals the presence of phenolics, flavonoids, glycosides, terpenoids, tannins and alkaloids. Elevated blood glucose, HbA1c creatinine, urea and uric acid and decreased level s of plasma insulin and hemoglobin were significantly (p<0.05) reverted back to near normal in STZ-induced diabetic mice after oral administration of MTE. Plasma protein, lipid profile, transaminases and alkaline phosphatase were also significantly normalized (p<0.05) after the treatment. Histopathological analysis indicated tissue damages in the diabetic untreated mice. MTE treated groups shows the tissue protection (of pancreas and liver) against peroxidation damage, thus signifying tissue integrity maintenance of MTE. It can be inferred that thein vivo antidiabetic therapeutic efficacy of tepals of Musa paradisiaca may be attributed to the presence of phytochemicals such as phenolics, flavonoids, alkaloids etc.
|
| title |
Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice
|
| title_full |
Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice
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| title_fullStr |
Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice
|
| title_full_unstemmed |
Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice
|
| title_short |
Biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of Musa paradisiaca studied in STZ-induced diabetic mice
|
| title_sort |
biochemical evaluation of antihyperglycemic and hypolipidemic effects of methanolic tepal extract of musa paradisiaca studied in stz-induced diabetic mice
|