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Interdiscip Toxicol
2018 Dec 01;114:275-288. doi: 10.2478/intox-2018-0027.
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Novel pentacyclic triterpene isolated from seeds of Euryale Ferox Salisb. ameliorates diabetes in streptozotocin induced diabetic rats.
Ahmed D
,
Khan MI
,
Sharma M
,
Khan MF
.
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The present research was carried out to study the effect of 2β-hydroxybetulinic acid 3β-oleiate (HBAO), a novel compound isolated from the seeds of Euryale ferox salisb. on glycemic control, antioxidant status and histopathological morphological alterations in the liver, pancreas, kidney and heart in streptozotocin induced type-2 diabetes in rats. HBAO was isolated from the seeds of Euryale ferox salisb. according to Lee. Isolation of the active principle HBAO was performed for the first time. To date there are no reports on the isolation and evaluation of 2β-hydroxybetulinic acid 3β-oleiate (HBAO) from Euryale ferox salisb. Assessment of different biochemical parameters like the effect of HBAO on glycemic control, plasma insulin, glycosylated hemoglobin, hepatic glucose-6-phosphate dehydrogenase, glucose-6-phosphatase and fructose-1-6-biphosphatase, hepatic hexokinase, lipid profile, antioxidant marker and histopathology of pancreas, liver and kidney examination was done at the end of the experimentation, i.e. on day 45. HBAO exhibited remarkable improvement in glycemic control, lipid levels, plasma insulin, glycogenic liver enzymes and antioxidant activity in diabetic rats, along with progressive enhancement of distortive histopathological morphology of liver, pancreas and kidney. The results strongly suggest that HBAO could be a potential therapeutic agent in diabetes.
Figure 1. Chemical structure of isolated compound (HBAO).
Figure 2. Effect of HBAO on Blood Glucose at different time interval of therapy: Group 1: Normal control; Group 2: Normal + HBAO (60 mg/kg p.o.); Group 3: Diabetic Control (Infused with STZ 60 mg/kg i.p); Group 4: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; Group5: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; Group6: Diabetic + HBAO (60 mg/kg p.o ) & continue till End; Group 7: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 3. Effect of HBAO on Plasma Insulin at different time interval of therapy: Group 1: Normal control; Group 2: Normal + HBAO (60 mg/kg p.o.); Group 3: Diabetic Control (Infused with STZ 60 mg/kg i.p); Group 4: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; Group5: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; Group6: Diabetic + HBAO (60 mg/kg p.o ) & continue till End; Group 7: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 4. Effect of HBAO on Gluconeogenic hepatic enzymes at different time interval of therapy: Group 1: Normal control; Group 2: Normal + HBAO (60 mg/kg p.o.); Group 3: Diabetic Control (Infused with STZ 60 mg/kg i.p); Group 4: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; Group5: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; Group6: Diabetic + HBAO (60 mg/kg p.o ) & continue till End; Group 7: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 5. Effect of HBAO on Lipid Profile at different time interval of therapy: Group 1: Normal control; Group 2: Normal + HBAO (60 mg/kg p.o.); Group 3: Diabetic Control (Infused with STZ 60 mg/kg i.p); Group 4: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; Group5: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; Group6: Diabetic + HBAO (60 mg/kg p.o ) & continue till End; Group 7: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 6. Effect of HBAO on Antioxidant marker enzymes at different time interval of therapy: Group 1: Normal control; Group 2: Normal + HBAO (60 mg/kg p.o.); Group 3: Diabetic Control (Infused with STZ 60 mg/kg i.p); Group 4: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; Group5: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; Group6: Diabetic + HBAO (60 mg/kg p.o ) & continue till End; Group 7: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 7. Effect of HBAO on Body Weight at different time interval of therapy: Group 1: Normal control; Group 2: Normal + HBAO (60 mg/kg p.o.); Group 3: Diabetic Control (Infused with STZ 60 mg/kg i.p); Group 4: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; Group5: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; Group6: Diabetic + HBAO (60 mg/kg p.o ) & continue till End; Group 7: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 8. Effect of isolate HBAO on histological profile of Pancreas in normal, STZ-induced diabetic untreated and STZ-induced diabetic treated wistar rats. (Original magnification 40x, DXIT 1200 , Nikon, Japan). NPAN: Normal Control; PHBAO-60.: Normal + HBAO (60 mg/kg p.o.); STZP: Diabetic Control (Infused with STZ 60 mg/kg i.p); SPHBAO-20: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; SPHBAO-40-: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; SPHBAO-60: Diabetic + HBAO (60 mg/kg p.o.) & continue till End; PGLIM: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 9. Effect of isolate HBAO on histological profile of Kidney in normal, STZ-induced diabetic untreated and STZ-induced diabetic treated wistar rats. (Original magnification 40x, DXIT 1200 , Nikon, Japan). NKAN: Normal Control; KHBAO-60.: Normal + HBAO (60 mg/kg p.o.); STZK: Diabetic Control (Infused with STZ 60 mg/kg i.p); SKHBAO-20: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; SKHBAO-40-: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; SKHBAO-60: Diabetic + HBAO (60 mg/kg p.o.) & continue till End; KGLIM: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
Figure 10. Effect of isolate HBAO on histological profile of Liver in normal, STZ-induced diabetic untreated and STZ-induced diabetic treated wistar rats. (Original magnification 40x, DXIT 1200 , Nikon, Japan). NLAN: Normal Control; LHBAO-60.: Normal + HBAO (60 mg/kg p.o.); STZL: Diabetic Control (Infused with STZ 60 mg/kg i.p); SLHBAO-20: Diabetic + HBAO (20 mg/kg p.o.) & continue till End; SLHBAO-40-: Diabetic + HBAO (40 mg/kg p.o.) & continue till End; SLHBAO-60: Diabetic + HBAO (60 mg/kg p.o.) & continue till End; LGLIM: Diabetic + Glimepiride (10mg/kg p.o.) & continue till End. END = 45 Days.
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,
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,
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Ahmed,
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2014,
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Arulselvan,
Beneficial effects of Murraya koenigii leaves on antioxidant defense system and ultra structural changes of pancreatic beta-cells in experimental diabetes in rats.
2007,
Pubmed
Bolkent,
Effects of chard (Beta vulgaris L. var. Cicla) extract on pancreatic B cells in streptozotocin-diabetic rats: a morphological and biochemical study.
2000,
Pubmed
Evans,
Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes.
2002,
Pubmed
Gupta,
Antihyperglycemic and hypolipidemic activity of aqueous extract of Cassia auriculata L. leaves in experimental diabetes.
2009,
Pubmed
Kaleem,
Antidiabetic and antioxidant activity of Annona squamosa extract in streptozotocin-induced diabetic rats.
2006,
Pubmed
King,
Understanding and addressing unique needs of diabetes in Asian Americans, native Hawaiians, and Pacific Islanders.
2012,
Pubmed
Lee,
Antioxidant activity of extracts from Euryale ferox seed.
2002,
Pubmed
,
Echinobase
Maritim,
Diabetes, oxidative stress, and antioxidants: a review.
2003,
Pubmed
Mithieux,
A novel function of intestinal gluconeogenesis: central signaling in glucose and energy homeostasis.
2009,
Pubmed
Mitra,
Effect of D-400, a herbomineral formulation on liver glycogen content and microscopic structure of pancreas and liver in streptozotocin induced diabetes in rats.
1996,
Pubmed
Nordlie,
Regulation of glucose production by the liver.
1999,
Pubmed
Packer,
Reactions of the carbon tetrachloride-related peroxy free radical (CC13O.2) with amino acids: pulse radiolysis evidence.
1978,
Pubmed
Rai,
Bioaccumulation of toxic metals (Cr, Cd, Pb and Cu) by seeds of Euryale ferox Salisb. (Makhana) W.
2002,
Pubmed
,
Echinobase
Rochette,
Diabetes, oxidative stress and therapeutic strategies.
2014,
Pubmed
Suraamornkul,
Insulin clamp-derived measurements of insulin sensitivity and insulin secretion in lean and obese asian type 2 diabetic patients.
2010,
Pubmed
Szkudelski,
The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas.
2001,
Pubmed
Thannickal,
Reactive oxygen species in cell signaling.
2000,
Pubmed
Wang,
Effect of Vaccinium bracteatum Thunb. leaves extract on blood glucose and plasma lipid levels in streptozotocin-induced diabetic mice.
2010,
Pubmed
Yoon,
Selective beta-cell loss and alpha-cell expansion in patients with type 2 diabetes mellitus in Korea.
2003,
Pubmed
Zhang,
Antihyperglycaemic and anti-oxidant properties of Andrographis paniculata in normal and diabetic rats.
2000,
Pubmed
