Vitexin is a flavonoid compound with high content in hawthorn, which has clear pharmacological activities such as anti-inflammatory and inhibition of lipoxygenase. Its chemical formula is C21H20O10, with a molecular weight of 432.3775, and it appears as a yellow powder.
Yuan et al. found that vitexin protects against ethanol induced liver injury through the Sirt1/p53 signaling pathway. Chen et al. reported that vitexin can inhibit colitis related mouse carcinogenesis by regulating macrophage polarization; Studies abroad have also found that vitiligo is related to oxidative stress. Vitexin can activate the MAPK-Nrf2/ARE pathway, thereby protecting melanocytes from oxidative stress and improving vitiligo symptoms. Wang et al. found that vitexin can alleviate lipopolysaccharide induced pancreatic cell damage by inhibiting the release of HMGB1. There are also studies showing that vitexin can inhibit alpha glucosidase in the small intestinal brush border, thereby reducing the breakdown and absorption of carbohydrates. The research and development of vitexin is of great significance.
Diabetes (DM) is a metabolic disease characterized by hyperglycemia. Its prevalence rate is increasing year by year in the world, and it has become the fourth disease that needs priority. Excessive blood sugar concentration can cause metabolic disorders in the body, leading to tissue damage and functional impairment. Diabetes can be divided into type 1 and type 2 according to the insulin level in the body. Among them, type 1 diabetes is caused by the destruction of pancreatic islet beta cells, which leads to a serious shortage of insulin secretion, so that liver glycogen cannot be decomposed and utilized as a direct energy material. When the energy supply required for maintaining life activities in the body is insufficient, neutral fats in the body decompose, and the decomposition products are mainly free fatty acids. Excessive content of free fatty acids can increase the generation of reactive oxygen species (ROS). In type 1 diabetes patients, excessive ROS content in the body leads to oxidative stress reaction. Oxidative stress response refers to the state in which the antioxidant system in the body is insufficient to balance and promote oxidation. It is a negative effect of free radicals produced in the body, which has a serious impact on the life activities of all organisms, and can even lead to cell apoptosis, organ tissue degeneration, and the occurrence of cancer. Due to the low content of antioxidant enzymes in islet β cells, they are more sensitive to ROS, and being attacked by ROS will lead to functional damage of islet β cells, increased apoptosis of islet β cells, further causing functional failure of islet β cells, and ultimately leading to the formation of diabetes. Type 2 diabetes patients have the ability to produce insulin in their bodies, and even the insulin content is higher than that of normal individuals.
In this study, different doses of vitexin were continuously administered to type 1 diabetes mice for four weeks. The activities of SOD, GSH-PX, T-AOC and MDA enzymes in the serum and liver of the mice were detected. The relative expression of mRNA of antioxidant genes copper zinc superoxide dismutase (SOD 1), manganese superoxide dismutase (SOD 2), glutathione peroxidase 1 (GPX-1) and glutathione peroxidase 4 (GPX-4) in the liver tissue of the mice was detected by qRT PCR method. The effects of these genes on the activities of antioxidant enzymes and the expression of antioxidant genes in mice were studied from the enzymology and gene levels.

This study found that vitexin can reduce the blood glucose concentration of type 1 diabetes mice, significantly enhance the total antioxidant capacity T-AOC, significantly increase the enzyme activities of SOD, GSH-PX and the expression of related genes, and extremely significantly reduce the content of MDA.
Blood sugar is an important source of energy for the body’s cells, tissues, and organs. Ayeh et al. found that quercetin has a hypoglycemic effect. Other studies have shown that total flavonoids of Houttuynia cordata Thunb can reduce blood sugar in type 1 diabetes mice. The above studies all indicate that flavonoids have hypoglycemic effects. The results of this experiment show that vitexin can reduce the blood sugar concentration of type 1 diabetes mice, which is consistent with the above research results. Insulin is the only hypoglycemic hormone in the body, and its content can be used to judge the degree of pathological changes in diabetes. The content of free radicals in diabetes patients is more than that in normal individuals. Too much free radicals attack pancreatic islet beta cells, resulting in a serious shortage of insulin content, which leads to the inability of glucose to be used, and makes the blood sugar concentration in diabetes patients increase. The reason why vitexin can reduce the blood sugar concentration of type 1 diabetes mice may be that vitexin can clear free radicals in the body, inhibit the attack of free radicals on pancreatic islet β cells, thereby reducing the decline of insulin content, increasing the utilization rate of glucose, so as to achieve the hypoglycemic effect and reduce the glucose content in the body.
High sugar levels can increase oxidative stress in the body, increase free radical content, and downregulate antioxidant capacity. Because the cardiac metabolic activity is high and the antioxidant capacity is low, it is more likely to cause oxidative damage. The content of nitric oxide synthase (NOS) and NO in diabetes patients is significantly increased or one of the reasons for diabetes cardiomyopathy. Oxidative stress can alter hemodynamics through various pathways, causing damage to the kidneys and resulting in renal dysfunction. Excessive free radicals can attack pancreatic beta cells, causing pancreatic damage. As the content of free radicals in the body increases, pancreatic beta cells gradually decrease and insulin levels decrease, leading to a decrease in the body’s ability to inhibit liver glycogen breakdown and a decrease in liver glycogen content, resulting in liver damage. In addition, excessive free radicals can also increase the content of inflammatory factors, reduce the body’s immune system, and cause spleen damage as well as lung damage. The reason why vitexin has a protective effect on various organs may be that vitexin can inhibit the production of free radicals in the body, reduce the content of NOS and NO, thereby protecting the heart. The reduction of free radicals can also weaken the attack on pancreatic beta cells, protect the pancreas and increase insulin content, improve glucose utilization efficiency, inhibit hepatic gluconeogenesis, effectively increase hepatic glycogen content, and thus protect the liver. Due to the decrease in the content of free radicals in the body, the content of inflammatory factors in the body gradually decreases, reducing the attack of inflammatory factors on the lungs. As the body’s immune system gradually recovers, the spleen, which participates in immune regulation, is also greatly improved. The antioxidant capacity is effectively enhanced, oxidative stress is reduced, and hemodynamics are improved, thereby reducing kidney damage.
The current research shows that the pathogenesis of diabetes is complex, and its important pathogenesis is that the accumulation of reactive oxygen free radicals reduces the antioxidant capacity of the body. Luo et al. found that vitexin can inhibit the generation of free radicals. The results of this experiment showed that vitexin can significantly increase the activities of SOD, GSH-PX, and T-AOC enzymes in serum and liver, and reduce the content of MDA. The reasons for this may be due to several factors. Firstly, free radicals can react with the phenolic hydroxyl groups in vitexin to generate semi Kun free radicals. Due to its stable properties, the chain reaction of free radicals is terminated, and the antioxidant capacity of the body is improved. Secondly, excessive free radicals can cause lipid peroxidation, leading to an increase in MDA content. Vitexin can inhibit lipid peroxidation, thereby reducing MDA levels in serum and liver and enhancing the body’s antioxidant function. The third is the existence of Fenton reaction (Fe2++H2O2 → Fe3++· OH+· OH -) in cells. Vitexin can undergo complexation reaction with Fe2+, and the complexation site is between 4-carbonyl and 5-hydroxy groups. Complexation with Fe2+can effectively reduce the generation of · OH, form complex precipitation, reduce free radicals, and improve the body’s antioxidant capacity. Vitexin can increase the enzyme activities of SOD, GSH-PX and T-AOC in the liver and serum of type 1 diabetes mice, reduce the content of MDA, and effectively improve the antioxidant capacity of the body. The antioxidant activity of antioxidant enzymes is closely related to their gene expression.
The degree of oxidation in the body exceeds its ability to clear oxides, and the stability of the oxidation and antioxidant systems is disrupted, resulting in oxidative damage. Under low-level oxidative stress, the body’s antioxidant proteins are activated through the cis acting elements of antioxidant response elements (ARE) or electrophilic response elements (EpRE). ARE can regulate the response of antioxidant enzymes to oxidative stress in the body at the transcriptional level. Under normal physiological conditions, nuclear factor E2 related factor 2 (Nrf2) binds to Kelch like ECH associated protein-1 (Keap1) in the cytoplasm, and its activity is inhibited. It is degraded under the action of ubiquitin protease to maintain the low transcriptional activity of Nrf2 under physiological conditions. When the cell is in an oxidative stress state, the originally bound Nrf2 is uncoupled from Keap1, and the activated Nrf2 enters the nucleus and forms a dimer with small Maf proteins, thereby recognizing and binding to ARE elements and activating downstream gene transcription. As a result, the transcriptional activity of antioxidant enzymes in the body is reduced. Improve, thus balancing oxidative damage to the body.
In this experiment, the expression of four antioxidant genes SOD-1, SOD-2, GPX-1 and GPX-4 in the liver of type 1 diabetes mice after four weeks of intragastric administration of vitexin significantly increased, which may be due to two reasons. On the one hand, the severe oxidative stress in the body of type 1 diabetes mice may make the antioxidant system of the body insufficient to balance the attack of free radicals, leading to serious oxidative damage to cells. The endogenous antioxidant system of the body is not enough to eliminate free radicals. Vitexin can not only eliminate free radicals in the body, but also complexe with metal ions, reduce the oxidative damage of free radicals and metal ions to cells, promote the nuclear translocation of Nrf2, and increase Nrf2 and then increase the expression of SOD-1, SOD-2, GPX-1 and GPX-4 genes in the liver of type 1 diabetes mice. On the other hand, the decrease of SOD, GSH-PX and T-AOC enzyme activities in type 1 diabetes mice may lead to the increase of free radicals in the body, resulting in oxidative damage to cells, insufficient energy supply of the mitochondrial system and blocked DNA and RNA transcription, which significantly reduces the expression of antioxidant genes in the liver of diseased mice. As vitexin has the function of scavenging free radicals in vivo, after intragastric administration, DNA and RNA transcription in mouse cells were improved, and the expression levels of SOD-1, SOD-2, GPX-1 and GPX-4 genes in the liver of type 1 diabetes mice were increased. Deng et al. found that quercetin can activate the nuclear translocation expression of Nrf2 in human primary liver cells incubated with ethanol. Ganesan et al. found that vitexin improves insulin secretion by activating key proteins involved in regulating apoptosis in beta cells, including NF κ B and Nrf2. The above research results are consistent with the results of this experiment.
The results showed that vitexin could significantly increase the activities of SOD, GSH-PX and T-AOC enzymes in serum and liver of type 1 diabetes mice, and reduce the content of MDA; The expression of SOD-1, SOD-2, GPX-1 and GPX-4 genes in the liver of type 1 diabetes mice was significantly up-regulated. In conclusion, vitexin can improve oxidative damage in type 1 diabetes and has a good antioxidant effect.