Diabetes is a systemic chronic metabolic disease caused by hyperglycemia, which can cause various physiological complications. There is no radical cure for diabetes, so the treatment of diabetes is a worldwide problem. At present, the drugs for diabetes such as insulin and other hypoglycemic agents can only treat the symptoms but not the root causes, and there are certain side effects in the process of treatment. Compared with western medicine, Chinese herbal medicine or other adjuvant therapies have similar effects, but it is regrettable that the important toxic and side effects are very small or non-toxic.
AucubinIt is extracted from traditional Chinese medicine and has many potential clinical applications. Although it has not been reported that aucubin has the function of reducing blood glucose and increasing body weight and the activity of regulating a variety of injury factors that increase blood glucose, many experiments have shown that aucubin may be a good drug for the treatment of diabetic encephalopathy. Apoptosis is common in diabetes mellitus and its complications. Apoptosis can cause many neurogenic disorders, such as Alzheimer's disease and Parkinson's disease. Recently, apoptosis has also been described in diabetic encephalopathy. The results showed that apoptosis also occurred in the hippocampus of STZ induced diabetic rats, and the apoptosis of hippocampal neurons had a selected correlation with the decline of cognitive ability. After aucubin treatment, the number of apoptotic cells in hippocampus was significantly reduced compared with that in diabetic encephalopathy group, and the activity of neuronal cells was enhanced. All results suggested that aucubin could attenuate the occurrence of cognitive impairment associated with neuronal apoptosis.
Bcl-2 family is the most important family of apoptosis regulators. Many members of Bcl-2 family have been studied. All studies have shown that the imbalance of Bcl-2 and Bax expression proteins plays an important role in cell survival. Bcl-2 inhibits cell death by protecting mitochondrial membrane, releasing cytochrome c, apoptosis inducing factor and other proteins, and activating caspase-3. Aucubin treatment inhibits the expression of Bax protein, increases the expression of Bcl-2 protein, and increases the expression of Bcl-2 protein, thus inhibiting neuronal apoptosis. These results suggest that aucubin can not only resist injury, but also inhibit apoptosis by regulating the expression of Bax and Bcl-2 proteins. Therefore, aucubin has a certain hypoglycemic effect, and more importantly, it can alleviate the damage caused by encephalopathy. It can also weaken the learning errors caused by encephalopathy and reduce the damage of hippocampal neurons.