Application of microRNA-326 inhibitor to the preparation of medicament for treating cataract

Abstract

The present invention relates to application of a microRNA-326 inhibitor to the preparation of medicaments for treating cataract. By experiments, the present invention proves that microRNA-326 can inhibit the expression of FGF1 to further achieve down-regulation of expression of betaB2 crystal protein; and the content change if betaB2 crystal protein is a key factor in cataract, and the down-regulation of expression of betaB2 crystal protein causes cataract. The invention suggests that inhibition of microRNA-326 can be used for the treatment of cataract, and microRNA-326 can be used as marker for cataract diagnosis.

Description

technical field [0001] The invention relates to the technical field of molecular biology, in particular to the application of an inhibitor of microRNA-326 in the preparation of a medicine for treating cataract. Background technique [0002] All kinds of reasons, such as aging, genetics, local nutritional disorders, immune and metabolic abnormalities, trauma, poisoning, radiation, etc., can cause lens metabolic disorders, resulting in lens protein denaturation and opacity, which is called cataract. Obstruction cannot be projected on the retina, resulting in blurred vision. It is more common in people over 40 years old, and the incidence rate increases with age. [0003] microRNAs (miRNAs) are a class of endogenous non-coding RNAs with regulatory functions found in eukaryotes. Mature miRNAs are produced from longer primary transcripts through a series of nuclease cleavage processes, and then assembled into RNA-induced silencing complex (RNA-induced silencing complex, RISC), ...

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Problems solved by technology

[0005] BetaB2 crystallin protein (CRYBB2) is closely related to the occurrence of cataracts. Studies have shown that its expression decreases in the lens of cataract patients (Huang CH, Wang YT, Tsai CF, Chen YJ, Lee JS, Chiou SH. Phosphoproteomics characterization of novel phosphorylated sites of lens proteins from normal and cataractous human eye lenses. Molecular Vision 2011; 17:186-198.), CRYBB2 gene mutations often occur on exon 6, resulting in abnormal amino acid folding, resulting in abnormal lens structure, weakening the water-soluble Stability in the state, causing changes in the transparency of the lens, eventually leading to the occurrence of congenital cataracts (Chen W, Chen X, Hu Z, Lin H, Zhou F, Luo L, Zhang X, Zhong X, Yang Y, Wu C ,Lin Z,Ye S,Liu Y.A Missense Mutation in CRYBB2Leads to Progressive Congenital Membranous Cataract by Impacting the Solubility and Function of bB2-Crystallin.PLoS One.2013;8(11):e81290.)

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