Protective Effect of Astragaloside IV against Pancreatic Injury Induced by Cadmium Combined with High Fat and High Sugar in Diabetic Mice
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Abstract:
The protective effect of astragaloside IV against pancreatic injury induced by cadmium combined with high fat and high sugar diet in diabetic mice was studied. Diabetic model was established through high fat and high sugar combined with cadmium damage. Mice were randomly divided into a normal group, model group and protective group. After 8 weeks of modeling, the protective group were given different concentrations of astragaloside IV (As-IV) for 4 weeks. The blood glucose content, malondialdehyde (MDA) content，superoxide dismutase (SOD) content and glutathione (GSH) content were determined. Ultrathin sections of the pancreatic tissue were made and examined under transmission electron microscopy to investigate changes in subcellular structure. The results showed that the MDA content of the model group increased significantly, which was 1.90 times that of normal group (p<0.01). The contents of SOD and GSH decreased, which were 48.10% (p<0.01) and 44.40% of those of the normal group (p<0.05); Compared with the model group, the low, medium, and high dose protective groups had lower blood glucose level, with their MDA contents being 82.10% (p<0.05), 68.40% (p<0.01) and 58.90% (p<0.01) of those of the model group. The SOD contents of the medium and high dose groups increased 1.52 times (p<0.05) and 1.72 times (p<0.01), respectively. The GSH content of the high-dose protective group increased most significantly, which was twice that of the model group (p<0.01). The results of transmission electron microscopy showed that the density of secreted granules and mitochondria in the subcellular structure of the pancreas increased significantly, indicating that the high glucose environment can aggravate the oxidative stress in the pancreas causing damage; the intake of AS-IV decreased significantly the contents of various indicators and weakened the damage. Astragaloside IV may reduce the oxidative damage of the pancreas and preserve its normal function by scavenging free radicals.
