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Application of miR-221 and inhibitor thereof to preparation of medicine for regulating and controlling liver fat deposition, liver fibrosis or hepatocellular carcinoma

A technology of mir-221, 1.mir-221, applied in the field of biomedicine, can solve the problems of target gene translation inhibition and/or messenger stability degradation

Active Publication Date: 2022-01-11
RUIJIN HOSPITAL AFFILIATED TO SHANGHAI JIAO TONG UNIV SCHOOL OF MEDICINE +1
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0002] MicroRNAs (microRNA, miRNA) are small non-coding RNAs (usually 21–23 nucleotides in length) that cause translational repression of target genes and / or decrease messenger stability by binding to the 3′ untranslated region of specific genes

Method used

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  • Application of miR-221 and inhibitor thereof to preparation of medicine for regulating and controlling liver fat deposition, liver fibrosis or hepatocellular carcinoma
  • Application of miR-221 and inhibitor thereof to preparation of medicine for regulating and controlling liver fat deposition, liver fibrosis or hepatocellular carcinoma
  • Application of miR-221 and inhibitor thereof to preparation of medicine for regulating and controlling liver fat deposition, liver fibrosis or hepatocellular carcinoma

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0247] Example 1: Expression of microRNA in liver tissue

[0248] To identify microRNAs involved in hepatic lipid metabolism, inflammatory infiltration, and fibrosis formation, liver tissues were screened for microRNA expression. Analyzes were performed to identify dysregulated microRNAs in the livers of MCD-diet mice, CCl4-treated mice, and high-fat diet-induced obese C57Bl6 / J mice, all three of which are animal models of steatohepatitis. Discovered a pair of conserved and widely expressed microRNAs miR-221 and miR-222 (see figure 1 ) was upregulated in the livers of these models. q-PCR results showed that miR-221 and miR-222 were up-regulated by 2-3 times in the liver of MCD-diet mice, and miR-221 and miR-222 were up-regulated by 1 in the liver of high-fat diet-induced obese mice. -2 times (see Table 4).

[0249] Table 4: miR-221 and miR-222 are upregulated in the liver of MCD-diet mice and high-fat diet-induced obese mice.

[0250] control diet MCD diet ...

Embodiment 2

[0254] Example 2: Knockout of miR-221 and miR-222 alleviates liver fat accumulation, inflammatory infiltration and collagen deposition, and fibrosis formation in animals

[0255] MCD diet mice are commonly used as a model of steatohepatitis. Therefore, an MCD diet model was established in control mice and miR-221 / 222 knockout mice to evaluate the effect of miR-221 / 222 on steatohepatitis. Evaluation of the knockout effect of miR-221 / 222 in the liver of KO mice (see Table 6).

[0256] Table 6: Expression levels of miR-221 and miR-222 in the liver of control mice and miR-221 / 222-LKO mice

[0257] Control mice miR-221 / 222-LKO mice Relative expression value of miR-221 1 0.15 Relative expression value of miR-222 1 0.11

[0258] Knockout of miR-221 and miR-222 reduces liver fat deposition in MCD-fed mice ( image 3 ). miR-221 / 222-LKO mice were given MCD diet for 6 weeks, and oil red staining oil red area of ​​liver sections was statistically found th...

Embodiment 3

[0278] Example 3: Overexpression of miR-221 / 222 worsens steatohepatitis caused by MCD diet, aggravates liver fat accumulation, inflammatory infiltration and collagen deposition, and fibrosis formation

[0279] Adenovirus AD-miR-221 / 222 infected the liver of miR-221 / 222LKO mice to re-express miR-221 / 222 in the liver. Using adenovirus AD-miR-221 / 222 overexpressing miR-221 / 222 and control adenovirus AD-GFP (titer 1*10 11 ) tail vein injection (200 μl / only) of miR-221 / 222LKO mice aged 8 weeks, while fed with MCD diet for 6 weeks. After 6 weeks, the expression of miR-221 / 222 in the mouse liver tissue was detected, and it was found that AD-miR-221 / 222 could increase the expression of miR-221 / 222 in the knockout mouse liver (Table 15).

[0280] Table 15: miR-221 / 222 LKO mice tail vein injection of AD-miR-221 / 222 and AD-GFP, fed with MCD diet for 6 weeks, the expression of miR-221 / 222 in liver tissue

[0281]

[0282] Infection of miR-221 / 222LKO mice with adenovirus AD-miR-221 / 22...

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Abstract

The invention discloses a medicine of miR-221 and an inhibitor thereof for preparing a medicine for regulating and controlling liver fat deposition, liver fibrosis or hepatocellular carcinoma. The miR-221 and the inhibitor thereof can be used as a detection target; and the liver fat infiltration level, liver collagen fiber deposition, plasma cholesterol level and serum transaminase are reduced by inhibiting the activity of the miR-221, insulin resistance is improved or malignant proliferation of liver cells is inhibited, and a new medication approach is provided for treating, preventing or delaying the liver diseases caused by metabolic disorders.

Description

technical field [0001] The invention belongs to the technical field of biomedicine, and in particular relates to miR-221 and its inhibitors used in the preparation of drugs for regulating hepatic fat deposition, liver fibrosis or hepatocellular carcinoma. It should be noted that the present invention is a divisional proposal based on the patent application with application number 201810952098.9. Background technique [0002] MicroRNAs (microRNA, miRNA) are small non-coding RNAs (usually 21–23 nucleotides in length) that cause translational repression of target genes and / or decrease messenger stability by binding to the 3′ untranslated region of specific genes. The number of microRNAs discovered so far exceeds 2500, and new candidate microRNA genes are still being discovered, and their expression patterns are often developmental and / or tissue-specific, although some microRNAs are stably expressed throughout the organism. miRNA is an important gene regulator, involved in the ...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K45/00A61K31/7115A61K31/712A61K31/7125A61P1/16A61P35/00A61P3/10A61P3/00A61P3/04A61P3/06C12N15/113C12Q1/6886C12Q1/6883
CPCA61P1/16A61P35/00A61K31/7115A61K31/712A61K31/7125C12N15/113C12Q1/6883C12Q1/6886C12N2310/141A61K45/00A61P3/10A61P3/00A61P3/04A61P3/06
Inventor 宁光曹亚南姜秀丽山爱景
Owner RUIJIN HOSPITAL AFFILIATED TO SHANGHAI JIAO TONG UNIV SCHOOL OF MEDICINE
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