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Application of Nano-MitoPBN in preparing medicines for resisting oxidation and treating diabetes

A diabetes drug and anti-oxidation technology, applied in the fields of biology and medicine, can solve problems such as unknown effects in the body, achieve the effects of reducing peripheral blood sugar levels, promoting mitochondrial function, and reducing oxidative stress levels

Inactive Publication Date: 2019-08-23
FUDAN UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

However, the in vivo role of MitoPBN remains unknown (Murphy et al., 2003)

Method used

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  • Application of Nano-MitoPBN in preparing medicines for resisting oxidation and treating diabetes
  • Application of Nano-MitoPBN in preparing medicines for resisting oxidation and treating diabetes
  • Application of Nano-MitoPBN in preparing medicines for resisting oxidation and treating diabetes

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0033] Example 1: Nano-MitoPBN targeted removal of mitochondrial ROS improves blood sugar and abnormal glucose tolerance in diabetic mice

[0034] After 3 weeks of STZ stress mice, random blood glucose levels in diabetic mice were significantly increased, and Nano-MitoPBN intervention reduced the increase in blood glucose in diabetic mice caused by STZ. The results of intraperitoneal glucose tolerance test reflected the impaired glucose tolerance of diabetic mice, and Nano-MitoPBN intervention improved the impaired glucose tolerance of diabetic mice. See figure 1 As shown in the figure, C represents the normal control group, D represents the diabetic group (STZ+HFD), D+NM represents the diabetic Nano-MitoPBN intervention group, and D+V represents the diabetic + empty vector group.

Embodiment 2

[0035] Example 2: Nano-MitoPBN reduces the level of oxidative stress in diabetic mice

[0036] Oxidative stress in organisms is caused by the imbalance between oxidative damage and antioxidant system. Malondialdehyde (MDA) is an oxidation end product of free radicals acting on lipid peroxidation in organisms, and the level of MDA can reflect the level of oxidative damage in organisms. The results showed increased MDA content in diabetic mice (see figure 2 ), the total antioxidant capacity (TAOC) in the body was significantly reduced (see image 3 ), the expression of antioxidant enzymes in vivo weakened, indicating that there was a certain degree of oxidative damage in diabetic mice, and Nano-MitoPBN intervention significantly reduced the level of oxidative stress in diabetic mice. In the figure, C represents the normal control group, D represents the diabetic group (STZ+HFD), D+NM represents the diabetic Nano-MitoPBN intervention group, and D+V represents the diabetic + em...

Embodiment 3

[0037] Example 3: Nano-MitoPBN improves liver cell mitochondrial function in diabetic mice

[0038] Mitochondrial respiratory control rate (RCR) reflects mitochondrial function and is commonly expressed as the ratio of respiration rate, which is the ratio of state 3 respiration rate to state 4 respiration rate, and is a sensitive indicator for evaluating the integrity of mitochondrial structure and coupling degree of oxidative phosphorylation. An increase in RCR indicates that the mitochondrial function is enhanced, and a decrease in RCR, the closer to 1, the more the mitochondrial respiratory chain is uncoupled from oxidative phosphorylation, and the mitochondrial function is impaired. Through the determination of mitochondrial RCR in mouse liver tissue, we found that the mitochondrial respiratory function of diabetic mice was significantly impaired, and the mitochondrial respiratory function of diabetic mice was restored after Nano-MitoPBN intervention (see Figure 4 ). ATP...

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PUM

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Abstract

The invention belongs to the technical fields of biology and medicine, and particularly relates to application of Nano-MitoPBN in preparing medicines for resisting oxidation and treating diabetes. Dueto the micro-compartmentalization effect, Nano-MitoPBN can remove mitochondrion superoxide / hydrogen peroxide generated by single electron leakage of a liver mitochondrion electron transport chain, increase the respiration rate of a mitochondrion state 3 and the respiration control ratio, improve synthesis of ATP, and promote the function of mitochondria. In addition, by reducing ROS, Nano-MitoPBNreduces gluconeogenesis, increases glycolysis, reverses ROS-mediated liver glycometabolism reprogramming in diabetic animals, then reduces the peripheral blood glucose level of the diabetic animals and restores the glucose tolerance of the diabetic animals. Nano-MitoPBN serves as a material for preparing the medicines for treating diabetes, can be used for targeting liver prevention and relievingand treating diabetes, and can obtain a remarkable curative effect with a very small dosage.

Description

technical field [0001] The invention belongs to the technical field of biology and medicine, and in particular relates to the application of Nano-MitoPBN, a liver-targeted mitochondrial spin capture agent, in the preparation of drugs for anti-oxidation and changing abnormal metabolism of diabetes. Background technique [0002] Diabetes mellitus (DM) is a metabolic disorder attributable to insufficient insulin secretion, diminished insulin action, or insulin resistance and has become an emerging global health problem. Currently, there are only a few effective therapeutic strategies against this multifactorial disease, however, each therapy has its limitations and drawbacks. For example, although the most widely used drug, metformin, is effective in reducing hepatic glucose levels, the mechanism is complex without any clear molecular target, and the drug has side effects in the gastrointestinal tract. Other medications also have side effects, causing hyperinsulinemia or hypog...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K9/127A61K31/662A61P39/06A61P3/10
CPCA61K9/127A61K31/662A61P3/10A61P39/06
Inventor 施冬云刘珊林吴美玲
Owner FUDAN UNIV
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