[A diabetic model for liver oxidant damage in mice].
Jiao, B Wang, Huang Cy, Shan Yu, Yin Wy
Abstract
Jiao, B Wang, Huang Cy, Shan Yu, Yin Wy
Abstract
OBJECTIVE: To observe the liver oxidant damage for diabetic model in mice. METHODS: Male kunming mice were feed with high fat dietary for a week and then were randomly divided into two groups by weight, with 10 mice in each group. One group was induced by small dose streptozotocin (STZ) and obtained STZ-induced diabetic mice, and the other group was regarded as the control. Both of the two groups were feed with high fat dietary. After 6 weeks, the activities of enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. Glutathione (GSH), maleic dialdehyde (MDA), nitric oxide (NO) levels in the liver and the liver viscera quotient were also measured. Liver histological manifestations were observed. RESULTS: In diabetes group, there was a significant decrease in body weight, and the activities of GSH, CAT, and NOS decreased significantly (t value were 5.370, 10.639, 5.235, 3.089, respectively, P < 0.01). While, the liver viscera quotient, the levels of MDA, GSH-PX and NO increased remarkably (t value were -6.246, -2.728, -2.660, -4.924, respectively, P < 0.01 or P < 0.05). The significant difference was not observed in SOD between the two groups (t value was -0.405, P > 0.05). The liver histological damages were observed in diabetes group, light microscope observation showed hepatocytes swelling, ballooned changing and fatty droplets clustering. CONCLUSION: The oxidant damage might exist in the liver diabetic model in mice.
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OBJECTIVE: To observe the liver oxidant damage for diabetic model in mice. METHODS: Male kunming mice were feed with high fat dietary for a week and then were randomly divided into two groups by weight, with 10 mice in each group. One group was induced by small dose streptozotocin (STZ) and obtained STZ-induced diabetic mice, and the other group was regarded as the control. Both of the two groups were feed with high fat dietary. After 6 weeks, the activities of enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. Glutathione (GSH), maleic dialdehyde (MDA), nitric oxide (NO) levels in the liver and the liver viscera quotient were also measured. Liver histological manifestations were observed. RESULTS: In diabetes group, there was a significant decrease in body weight, and the activities of GSH, CAT, and NOS decreased significantly (t value were 5.370, 10.639, 5.235, 3.089, respectively, P < 0.01). While, the liver viscera quotient, the levels of MDA, GSH-PX and NO increased remarkably (t value were -6.246, -2.728, -2.660, -4.924, respectively, P < 0.01 or P < 0.05). The significant difference was not observed in SOD between the two groups (t value was -0.405, P > 0.05). The liver histological damages were observed in diabetes group, light microscope observation showed hepatocytes swelling, ballooned changing and fatty droplets clustering. CONCLUSION: The oxidant damage might exist in the liver diabetic model in mice.
Key concepts: Streptozotocin, Glutathione peroxidase, Superoxide dismutase, Internal medicine, Glutathione, Endocrinology, Diabetes mellitus, Nitric oxide