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Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/13408
Title: Therapeutic role of Rauwolfia serpentina in minimizing the risk of glycosylation and associated biomarkers in experimentally induced type 1 diabetic mice
Authors: Azmi, Muhammad Bilal
Qureshi, Shamim Akhtar
Ahmed, Syed Danish Haseen
Khan, Auwais Ahmed
Ahsan, Muhammad
Mudassir, Hina Akram
Imtiaz, Fauzia
Rais, Sumera
Keywords: Alloxan
anaemia
catalase
glycosylation
Rauwolfia serpentina
superoxide dismutase
Issue Date: 16-Jan-2021
Publisher: Karachi: Faculty of Pharmacy & Pharmaceutical Sciecnes, University of Karachi
Abstract: Present work investigates the effects of hydro-methanolic roots extract (HyMREt) of Rauwolfia serpentina in type 1 diabetic mice. Mice were divided into normal, diabetic, negative and positive controls (I-IV) and three test (HyMREt doses) groups (V-VII - 50, 100, &150mg/kg). Allocated treatment of each group was given orally for 14 days in overnight fasted state. Percent change in fasting blood glucose (FBG), body weights, body tissue weights, hepatic glycogen, total lipids, glycosylated hemoglobin (HbA1c), complete blood profile and antioxidant enzymes including catalase (CAT) and superoxide dismutase (SOD) were estimated. HyMREt doses produced meaningful (p<0.0001) reduction (-39 to -53%) in FBG. Hemoglobin (Hb) levels were raised, HbA1c were considerably decreased (4.5-3.77%) and glycosylation (HbA1c to Hb) ratio was expressively (p<0.0001) improved in test groups. Dose-wise improvement (p< 0.05) in total glycogen and decrement (p<0.05) in lipids were observed in livers of test groups. HyMREt significantly decreased (p<0.05) percent inhibition of SOD and CAT. HyMREt doses progressively (p<0.05) improved RBC and other hematological parameters while decrement was only noticed in leucocyte counts. Administration of test doses of HyMREt were significantly reduced the glycosylation, oxidative stress and anemia caused by alloxan intoxication in mice.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/13408
ISSN: 1011-601X
Appears in Collections:Issue 01

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