• Title/Summary/Keyword: Streptozotocin diabetes

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Betulinic Acid Ameliorates Postprandial Hyperglycemia in Diabetic Mice (STZ에 의한 당뇨 유발 마우스에서 betulinic acid의 식후 고혈당 개선 효과)

  • Lee, Jung-Kyung;Lee, Hyun-Ah;Han, Ji-Sook
    • Journal of Life Science
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    • v.32 no.8
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    • pp.589-594
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    • 2022
  • The objective of this study was to investigate whether betulinic acid can inhibit the activities of carbohydrate-digesting enzymes and reduce postprandial hyperglycemia in mice with streptozotocin-induced diabetes. Our results revealed that betulinic acid has potent inhibitory effects on α-glucosidase and α-amylase activities. The half-maximal inhibitory concentrations (IC50) of betulinic acid were 12.83±6.81 and 18.32±3.24 μM for α-glucosidase and α-amylase, respectively. This result indicates lower IC50 values and higher inhibitory activities than those of acarbose, an oral hypoglycemic drug. The increase in postprandial blood glucose levels was significantly suppressed in the betulinic acid group than in the control group of diabetic and normal mice. Postprandial blood glucose levels were 23.22±1.1, 24.38±1.31, and 21.05±1.36 μM in the betulinic acid group compared to 24.64±1.7, 27.22±1.58, and 26.36±1.40 μM in the control group of diabetic mice at 30, 60 and 120 min, respectively. The area under the curve also significantly decreased with the administration of betulinic acid in diabetic mice, however, it did not decrease more than that after acarbose administration. Our results showed that betulinic acid may be a potent inhibitor of carbohydrate-digesting enzymes and ameliorate postprandial hyperglycemia in diabetic mice.

Expression of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 after Administration of Endotoxin in Diabetic Rats (내독소로 자극된 당뇨 쥐에서 단백분해효소와 그 억제제 발현)

  • Seo, Ki Hyun;Choi, Jae Sung;Na, Joo Ok;Uh, Soo Taek;Kim, Yong Hoon;Park, Choon Sik
    • Tuberculosis and Respiratory Diseases
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    • v.61 no.3
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    • pp.256-264
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    • 2006
  • Background: An acute lung injury(ALI) is characterized by the recruitment, activation, and apoptosis of inflammatory cells, numerous products released by inflammatory cells such as reactive oxygen species, inflammatory mediators, and a variety of proteolytic enzymes. It was reported that bacterial infections in diabetics showed impaired PMN functions such as reduced PMN respiratory burst and decreased microbicidal activity in inflamed tissue. However, the effect of the proteinase - inhibitor (MMP-9 vs TIMP-1) in ALI in diabetics is unclear. This study evaluated the differences in the expression of MMP-9 and TIMP-1 after the stimulation of endotoxin in a rat model. Methods: Six-week-old male Sprague-Dawley rats were classified into normal, DM, LPS and DM+LPS groups. The peripheral blood, BAL fluids, and lung tissues were obtained from individual rats. The MMP-9 activity was measured by gelatin zymography and the TIMP-1 level was measured by Western blotting. Results: The total BAL cells of the DM-LPS groups were significantly lower than the LPS groups (p < 0.01). The MMP-9 activities in the serum were higher in the DM+LPS groups than in the other groups. The MMP-9 activities in the BAL fluids were significantly higher in the DM+LPS group than in the normal and diabetic rats (p < 0.05). TIMP-1 expressions in the BAL fluids were significantly lower in the DM+LPS group than other groups (p < 0.05). The ratio between MMP-9 and TIMP-1 in the BAL fluids was significantly higher in the DM+LPS groups (p < 0.05). Conclusion: In ALI in diabetics the higher MMP-9 activity and lower TIMP-1 level are believed to prolonged and intensify the course of inflammation.