scholarly journals In vivo antidiabetic activity of aqueous and ethyl acetate leaf extract of Senna singuena (Delile) in alloxan induced diabetic mice

2017 ◽  
Vol 6 (2) ◽  
pp. 84-92
Author(s):  
Njogu M. Stephen ◽  
◽  
Arika M. Wycliffe ◽  
Machocho K. Alex ◽  
Ngeranwa J.N. Joseph ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Plant Extract ◽  
Leaf Extract ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Scientific Data ◽  
Hypoglycemic Activity ◽  
Antidiabetic Activity ◽  
Type I ◽  
Diabetic Mice

The folkloric claims that Senna singuena confers antidiabetic effect to prescribed patients has received long term clinical application accompanied by limited scientific data in support of such claims. This study aimed at bioscreening for hypoglycemic activity of the aqueous and organic fractions of S. singuena in alloxan induced diabetic mice. Type I diabetes mellitus was induced in mice by intraperitoneal administration of alloxan monohydrate followed by graded doses of the aqueous and ethyl acetate leaf extract administered to the experimentally diabetic mice following an overnight fast. The composition of the various phytochemicals of the plant extract was quantitatively assessed using standard procedures. Oral and intraperitoneal administration of the aqueous and ethyl acetate leaf extract caused a significant reduction in plasma glucose level in a dose independent manner in both fractions. The hypoglycemic activity could be attributed to phytoconstituents found in the plant extract. The generated data supports the folkloric claims associating S. singuena with hypoglycemic effects. However, there is need for further studies on this plant to investigate the mechanism of its activity and determine its safety profiles in order to explore possibilities of developing a new antidiabetic drug.

scholarly journals In Vivo Hypoglycemic Effect of Kigelia africana (Lam): Studies With Alloxan-Induced Diabetic Mice

2018 ◽  
Vol 23 ◽  
pp. 2515690X1876872 ◽  
Author(s):  
Stephen M. Njogu ◽  
Wycliffe M. Arika ◽  
Alex K. Machocho ◽  
Joseph J. N. Ngeranwa ◽  
Eliud N. M. Njagi
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Ethyl Acetate ◽  
Leaf Extract ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Physiological Saline ◽  
Diabetic Control ◽  
Type I ◽  
Diabetic Mice

The claims by the traditional herbal medicine practitioners that Kigelia africana has bioactivity against several diseases, including diabetes mellitus, were investigated in this study. Type I diabetes mellitus was induced in mice by intraperitoneal administration of alloxan monohydrate followed by treatment with the therapeutic doses of the aqueous and ethyl acetate leaf extract of K africana to the experimentally diabetic mice. The treatment effects were compared with the normal control, diabetic control, and diabetic control rats treated with a standard antidiabetic drugs (insulin administered intraperitoneally at 1 IU/kg body weight in 0.1 mL physiological saline or glibenclamide administered orally at 3 mg/kg body weight in 0.1 mL physiological saline). Phytochemical composition of the leaf extract was assessed using standard procedures and mineral elements assessed using atomic absorption spectrophotometry and total reflection X-ray fluorescence system. Oral and intraperitoneal administration of the aqueous and ethyl acetate leaf extract caused a statistically significant dose-independent reduction in plasma glucose level in alloxan-induced diabetic mice. The observed hypoglycemic activity of this plant extract could be attributed to the observed phytochemicals and trace elements, which have been associated with exhibiting antidiabetic properties. Therefore, the data appear to support the hypoglycemic effects of K africana validating its folkloric usage.

scholarly journals Contribution of Trem2 Signaling to the Development of Painful Diabetic Neuropathy by Mediating Microglial Polarization in Mice

2021 ◽  
Author(s):  
Xin Chen ◽  
Yue Le ◽  
Wan-you He ◽  
Jian He ◽  
Yun-hua Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Mechanical Allodynia ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Lumbar Spinal Cord ◽  
Type I ◽  
Painful Diabetic Neuropathy ◽  
Diabetic Mice

Abstract Background Painful diabetic neuropathy (PDN) is a common and intractable complication of diabetes mellitus, with little effective treatment. PDN has been associated with spinal neuroinflammation characterized by microglial activation. Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), specifically localized on microglia, has been identified as a vital factor in modulating neuroinflammation and microglial phenotypes in neural diseases. Therefore, we hypothesized that spinal TREM2 might contribute to PDN and neuroinflammation by regulating microglial activity and phenotypes. Methods Type I diabetes mellitus was elicited by a single intraperitoneal administration of streptozotocin (STZ) in mice. The pain behaviors were reflected by paw mechanical withdrawal thresholds (PMWT) and thermal withdrawal latency (PTWL). Results We demonstrated that up-regulation of microglial TREM2 and amplification of both microglial M1 and M2 response was along with the presence of diabetes-related mechanical allodynia and thermal hypersensitivity. Moreover, we found that overexpression of TREM2 in microglia aggravated the symptom of PDN, amplified microglia M1 response, and suppressed microglia M2 polarization in the lumbar spinal cord of diabetic mice. However, inhibition of TREM2 with anti-TREM2 neutralizing antibodies attenuated mechanical allodynia and thermal hyperalgesia in diabetic mice. Besides, we identified Galectin-3 (GLT-3) as the potential ligand of the TREM2 receptor in facilitating the progression of PDN. Conclusions TREM2 could be a critical microglial membrane molecule that modulates microglial phenotypes pain hypersensitivity in PDN. GLT-3 might act as a specific ligand to trigger TREM2 signaling in PDN or other neuropathic pain.

scholarly journals Contribution of TREM2 Signaling to the Development of Painful Diabetic Neuropathy by Mediating Microglial Polarization in Mice

2021 ◽  
Author(s):  
xin chen ◽  
Yue Le ◽  
Si-qi Tang ◽  
Wan-you He ◽  
Jian He ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Mechanical Allodynia ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Lumbar Spinal Cord ◽  
Type I ◽  
Painful Diabetic Neuropathy ◽  
Diabetic Mice

Abstract Background: Painful diabetic neuropathy (PDN) is a common and intractable complication of diabetes mellitus, with little effective treatment. PDN has been associated with spinal neuroinflammation characterized by microglial activation. Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), specifically localized on microglia, has been identified as a vital factor in modulating neuroinflammation and microglial phenotypes in neural diseases. Therefore, we hypothesized that spinal TREM2 might contribute to PDN and neuroinflammation by regulating microglial activity and phenotypes.Methods：Type I diabetes mellitus was elicited by a single intraperitoneal administration of streptozotocin (STZ) in mice. The pain behaviors were reflected by paw mechanical withdrawal thresholds (PMWT) and thermal withdrawal latency (PTWL). Results：We demonstrated that up-regulation of microglial TREM2 and amplification of both microglial M1 and M2 response was along with the presence of diabetes-related mechanical allodynia and thermal hypersensitivity. Moreover, we found that overexpression of TREM2 in microglia aggravated the symptom of PDN, amplified microglia M1 response, and suppressed microglia M2 polarization in the lumbar spinal cord of diabetic mice. However, inhibition of TREM2 with anti-TREM2 neutralizing antibodies attenuated mechanical allodynia and thermal hyperalgesia in diabetic mice. Besides, we identified Galectin-3 (GLT-3) as the potential ligand of the TREM2 receptor in facilitating the progression of PDN.Conclusions: TREM2 could be a critical microglial membrane molecule that modulates microglial phenotypes pain hypersensitivity in PDN. GLT-3 might act as a specific ligand to trigger TREM2 signaling in PDN or other neuropathic pain.

scholarly journals Ingested interferon α suppresses Type I diabetes in non-obese diabetic mice

Diabetologia ◽  
1998 ◽  
Vol 41 (10) ◽  
pp. 1227-1232 ◽  
Author(s):  
S. A. Brod ◽  
M. Malone ◽  
S. Darcan ◽  
M. Papolla ◽  
L. Nelson
Keyword(s):  
Type I Diabetes ◽  
Interferon Α ◽  
Type I ◽  
Diabetic Mice

scholarly journals Specific PKC βII inhibitor: one stone two birds in the treatment of diabetic foot ulcers

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Sushant Kumar Das ◽  
Yi Feng Yuan ◽  
Mao Quan Li
Keyword(s):  
Wound Healing ◽  
Protein Kinase ◽  
Peripheral Blood ◽  
Wound Closure ◽  
Type I Diabetes ◽  
Healing Process ◽  
Wound Healing Process ◽  
Peripheral Blood Flow ◽  
Type I ◽  
Diabetic Mice

To explore whether or not inhibition of protein kinase C βII (PKC βII) stimulates angiogenesis as well as prevents excessive NETosis in diabetics thus accelerating wound healing. Streptozotocin (STZ, 60 mg/kg/day for 5 days, i.p.) was injected to induce type I diabetes in male ICR mice. Mice were treated with ruboxistaurin (30 mg/kg/day, orally) for 14 consecutive days. Wound closure was evaluated by wound area and number of CD31-stained capillaries. Peripheral blood flow cytometry was done to evaluate number of circulating endothelial progenitor cells (EPCs). NETosis assay and wound tissue immunofluorescence imaging were done to evaluate the percentage of neutrophils undergoing NETosis. Furthermore, the expression of PKC βII, protein kinase B (Akt), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), and histone citrullation (H3Cit) were determined in the wound by Western blot analysis. Ruboxistaurin accelerated wound closure and stimulated angiogenesis in diabetic mice. The number of circulating EPCs was increased significantly in ruboxistaurin-treated diabetic mice. Moreover, ruboxistaurin treatment significantly decreases the percentages of H3Cit+ cells in both peripheral blood and wound areas. This prevented excess activated neutrophils forming an extracellular trap (NETs) formation. The expressions of phospho-Akt (p-Akt), phospho-eNOS (p-eNOS), and VEGF increased significantly in diabetic mice on ruboxistaurin treatment. The expressions of PKC βII and H3Cit+, on the other hand, decreased with ruboxistaurin treatment. The results of the present study suggest that ruboxistaurin by inhibiting PKC βII activation, reverses EPCs dysfunction as well as prevents exaggerated NETs formation in a diabetic mouse model; thereby accelerating the wound healing process.

scholarly journals Hypoglycemic Activity of Aqueous Extracts fromCatharanthus roseus

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Elisa Vega-Ávila ◽  
José Luis Cano-Velasco ◽  
Francisco J. Alarcón-Aguilar ◽  
María del Carmen Fajardo Ortíz ◽  
Julio César Almanza-Pérez ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Intraperitoneal Administration ◽  
Free Fraction ◽  
Hypoglycemic Activity ◽  
Aqueous Extracts ◽  
Diabetic Mice ◽  
Aqueous Fraction ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Stem Extract

Introduction.Catharanthus roseus(L.) is used in some countries to treat diabetes. The aim of this study was to evaluate the hypoglycemic activity of extracts from the flower, leaf, stem, and root in normal and alloxan-induced diabetic mice.Methods. Roots, leaves, flowers, and stems were separated to obtain organic and aqueous extracts. The blood glucose lowering activity of these extracts was determinate in healthy and alloxan-induced (75 mg/Kg) diabetic mice, after intraperitoneal administration (250 mg/Kg body weight). Blood samples were obtained and blood glucose levels were analyzed employing a glucometer. The data were statistically compared by ANOVA. The most active extract was fractioned. Phytochemical screen and chromatographic studies were also done.Results. The aqueous extracts fromC. roseusreduced the blood glucose of both healthy and diabetic mice. The aqueous stem extract (250 mg/Kg) and its alkaloid-free fraction (300 mg/Kg) significantly () reduced blood glucose in diabetic mice by 52.90 and 51.21%. Their hypoglycemic activity was comparable to tolbutamide (58.1%, ).Conclusions. The best hypoglycemic activity was presented for the aqueous extracts and by alkaloid-free stem aqueous fraction. This fraction is formed by three polyphenols compounds.

scholarly journals Preclinical evaluation of antidiabetic activity of poly herbal plant extract in streptozotocin induced diabetic rats

2016 ◽  
Vol 5 (2) ◽  
pp. 45-49
Author(s):  
P.P. Gupta ◽  
◽  
J. Haider ◽  
R.P. Yadav ◽  
U. Pal ◽  
...  
Keyword(s):  
Body Weight ◽  
Plant Extract ◽  
Leaf Extract ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Antidiabetic Activity ◽  
Sprague Dawley ◽  
Pancreatic Cell ◽  
Partial Restoration ◽  
Herbal Plant

Objective: To study and compare the effect of Poly herbal plant extract (PHPE) with Glibenclamide (GL) on various parameters in Streptozotocin (STZ) induced diabetic rats. Methods: Diabetes was induced by combining High Fat-diet and injecting low dose Streptozotocin (35 mg/kg body wt.) to Sprague-dawley rats. Diabetic rats were treated with chloroform leaf extract of Azadirachta indica, aqueous leaf extract of Bougainvillea spectabilis and ethanolic seed extract of Trigonella foenum graecum combined in ratio of 1:2:3 respectively at dose of 600 mg/kg body weight by oral gavaging for 28 days. The results were compared with standard anti diabetic drug Glibenclamide given in dose of 500 µg/kg body weight. Results: Increase in body weight of both PHPE and GL treated diabetic rats was found to be statistically significant (p<0.05) compared to diabetic control rats. Decline in FBG levels of both PHPE and GL treated diabetic rats were found to be highly significant statistically (p<0.001) when compared to diabetic control rats at the end of study. Total Cholesterol (TC) and Triglycerides level in diabetic rats treated with PHPE were found to be highly statistically significant (p<0.001) compared to diabetic control rats. Pancreas of PHPE treated diabetic rats revealed partial restoration in size and number of islet of langerhans. Reduction in widening between acinar and islet cells noted. Glibenclamide treated diabetic rats showed much more improvement in pancreatic cell architecture by returning to its normal structure and size. Conclusion: In present study PHPE has shown to decrease elevated FBG level and improve in body weight at the end of study in diabetic rats which can be suggested due to modification in carbohydrate metabolic pathways, stimulation of insulin production by the pancreas, increased peripheral utilization of glucose in the cells and regeneration of β-cells of the pancreas.

scholarly journals Administration of Sulfatide to Ameliorate Type I Diabetes in Non-Obese Diabetic Mice

2014 ◽  
Vol 79 (4) ◽  
pp. 260-266 ◽  
Author(s):  
S. Rhost ◽  
L. Löfbom ◽  
J.-E. Månsson ◽  
A. Lehuen ◽  
M. Blomqvist ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Type I ◽  
Diabetic Mice
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