CN118813580A - IKKα protein truncations and their application in preventing UVB-induced skin photodamage - Google Patents

Abstract

The invention provides an IKK alpha protein truncated body and application thereof in preventing UVB-induced skin photodamage reaction, and provides a nucleic acid molecule for encoding the truncated body, a vector containing the nucleic acid molecule, a recombinant host cell containing the vector and a primer for amplifying the nucleic acid molecule. The invention discloses an IKK alpha protein truncated body capable of removing the N end, which can antagonize the activation and pro-apoptosis effect of a PERK-p53-PERP pathway induced by UVB, and the mutant and the derivative thereof have application values in preventing the photo-damage reaction of the skin induced by UVB and preparing a product for preventing the photo-damage of the skin induced by UVB.

Description

IKKα protein truncations and their application in preventing UVB-induced skin photodamage reactions

Technical Field

The invention relates to the field of genetic engineering, and in particular to a truncated form of IKKα protein and application thereof in preventing UVB-induced skin photodamage reaction.

Background Art

Ultraviolet (UV) is one of the main risk factors for skin damage and photoaging. According to the wavelength, UV rays can be divided into three types: long-wave ultraviolet (Ultraviolet A, UVA, 320-400 nm), medium-wave ultraviolet (Ultraviolet B, UVB, 280-320 nm) and short-wave ultraviolet (Ultraviolet C, UVC, 100-280 nm). Although UVC is harmful to organisms, it is difficult to reach the earth's surface through the atmosphere due to its short wavelength. Compared with UVA, UVB has a shorter wavelength and stronger biological effects, so the skin damage caused by UVB is more serious. UVB radiation stimulates the production of reactive oxygen species (ROS), which causes oxidative stress and inflammatory reactions in the skin, leading to tissue damage. Studies have shown that UVB can destroy the structure and function of proteins, lipids and nucleic acids, thereby causing pathological damage reactions such as skin burns, blistering, dermatitis and even skin cancer. Therefore, the prevention and control strategies, technologies and drug research of UVB-induced photodamage effects have always attracted much attention.

In order to prevent and control the skin photodamage reaction caused by UVB radiation, the use of photochemical protective agents to interfere with skin photodamage has become a research hotspot. However, in the prior art, most drugs for preventing UVB-induced skin photodamage have insignificant anti-photodamage effects, and their effects need to be further improved. Therefore, it is of great significance to conduct in-depth research on the mechanism of skin photodamage and develop more effective anti-photodamage products, such as producing therapeutic drugs or cosmetics with beneficial properties for preventing UVB-induced skin photodamage, protecting the skin from UVB-induced skin photodamage, and having low antigenicity and good biocompatibility.

Previous studies have screened p53 binding proteins and upstream protein kinases, and found that the catalytic subunit IKKα of IKK (inhibitor of kappa B kinase) binds to and induces PERK activation under UVB stimulation, further activating the PERK-p53-PERP signaling pathway, and ultimately mediating the apoptosis effect of skin keratinocytes and stromal cells (Lun Song et al., 2021). However, due to the large size of the IKKα protein molecule, it is not suitable for drug preparation, so its truncated form is urgently needed to study the subsequent functions. Truncated forms are of great significance for studying the pathogenesis, diagnosis and treatment of diseases.

Summary of the invention

In order to make up for the deficiencies of the prior art, the object of the present invention is to provide a truncated form of IKKα protein and application thereof.

In order to achieve the above object, the present invention adopts the following technical solution:

In a first aspect, the present invention provides a truncated form of IKKα protein, the amino acid sequence of the truncated form is shown in SEQ ID NO: 1 in the sequence listing.

A second aspect of the present invention provides a biomaterial comprising:

(i) a nucleic acid molecule encoding the truncated form described in the first aspect of the present invention;

(ii) a vector comprising the nucleic acid molecule described in (i); or

(iii) a recombinant host cell comprising the nucleic acid molecule described in (i) and/or the vector described in (ii).

Furthermore, the base sequence of the nucleic acid molecule is shown in SEQ ID NO: 2 in the sequence listing.

Furthermore, the vector includes a eukaryotic expression vector, a prokaryotic expression vector, an artificial chromosome and/or a phage vector.

Furthermore, the recombinant host cell is prokaryotic or eukaryotic.

Furthermore, the recombinant host cells include yeast cells, CHO cells, 293 cells, plant cells, and Escherichia coli cells.

In the present invention, the term "nucleic acid molecule" refers to a polymer molecule of any length composed of a single nucleotide: adenine (A), cytosine (C), guanine (G), thymine (T) (or uracil (U) in RNA), such as DNA, RNA or its modification. The nucleic acid molecule can be a natural nucleic acid molecule; a synthetic nucleic acid molecule; a combination of one or more natural nucleic acid molecules and one or more synthetic nucleic acid molecules. In the context of the present invention, it refers to a DNA sequence that is transcribed and translated into a polypeptide in a host cell when placed under the control of an appropriate regulatory sequence. The sequence may include, but is not limited to, a prokaryotic sequence, a cDNA from eukaryotic mRNA, a genomic DNA sequence from eukaryotic (e.g., mammalian) DNA, and even a recombinant DNA sequence. In a specific embodiment of the present invention, a "nucleic acid molecule" refers to a nucleic acid molecule capable of encoding a truncated form of the IKKα protein described in the first aspect of the present invention. Once the sequence of the truncated form of the present invention is isolated, the truncated form IKKα-C can be mass-produced using genetic engineering technology.

In the present invention, the nucleotide sequence of the modified nucleic acid molecule also belongs to the protection scope of the present invention. The term "modification" refers to any form of modification of the nucleotide sequence, such as substitution, deletion, insertion and/or addition of nucleotides. The term "substitution" refers to replacing one or more nucleotides in the original nucleotide sequence with different nucleotides. The term "deletion" refers to the reduction of one or more nucleotides in the original nucleotide sequence. The term "insertion" or "addition" refers to a change in a nucleotide sequence that results in the addition of one or more nucleotides compared to the original nucleotide sequence.

In the present invention, the term "vector" refers to an artificial construct that can deliver and preferably express one or more target genes or sequences in a host cell. The vector of the present invention can be an expression vector, which contains sufficient cis-acting elements for expression, and other elements for expression can be provided by a recombinant host cell or in an in vitro expression system. The expression vector includes all expression vectors known in the art, including eukaryotic expression vectors, prokaryotic expression vectors, artificial chromosomes, phage vectors, etc.

In the present invention, the term "recombinant host cell" includes "transformants" and "transformed cells", and can be used to produce any type of cell system described in the first aspect of the present invention, including eukaryotic cells, for example, mammalian cells (such as CHO cells, 293 cells), insect cells, yeast cells, plant cells; and prokaryotic cells, for example, Escherichia coli cells.

The third aspect of the present invention provides a primer comprising a forward primer and a reverse primer, wherein the primer can amplify the nucleic acid molecule described in the second aspect of the present invention.

The base sequence of the forward primer is shown in SEQ ID NO: 3 in the sequence listing; the base sequence of the reverse primer is shown in SEQ ID NO: 4 in the sequence listing.

In the present invention, the term "primer" refers to a macromolecule with a specific nucleotide sequence that is stimulated to synthesize at the start of nucleotide polymerization and is connected to the reactant in the form of hydrogen bonds. Primers include DNA replication primers (RNA primers) of organisms in nature and primers (usually DNA primers) synthesized artificially in polymerase chain reaction (PCR). In the context of the present invention, primers usually refer to two artificially synthesized oligonucleotide sequences, one primer is complementary to a DNA template strand at one end of the target region, and the other primer is complementary to another DNA template strand at the other end of the target region. Its function is to serve as the starting point of nucleotide polymerization, and nucleic acid polymerase can start synthesizing new nucleic acid chains from its 3' end. Primers artificially designed in vitro are widely used in polymerase chain reaction, sequencing, and probe synthesis.

The fourth aspect of the present invention provides a derivative of the truncated body described in the first aspect of the present invention or the biomaterial described in the second aspect of the present invention, wherein the derivative is formed by the truncated body or nucleic acid molecule and other substances in a modified, encapsulated and/or covalently bound form.

Furthermore, the modification includes one or more of phosphorylation, acetylation, methylation, ubiquitination, glycosylation, hydroxylation, sulfation, and fatty acylation.

Furthermore, the encapsulation includes liposome encapsulation, exosome encapsulation, metal nanoparticle encapsulation, silica encapsulation, polysaccharide nanocarrier encapsulation, synthetic polymer nanocarrier encapsulation, cell penetrating peptide encapsulation, protein cage encapsulation, and virus-like particle encapsulation.

Furthermore, the other substances include one or more components selected from the group consisting of free adjuvants, stabilizers, buffers, surfactants, salts and preservatives.

In the present invention, the term "derivative" refers to a substance formed by a modification, encapsulation and/or covalent binding of a truncated protein or a nucleic acid molecule encoding a truncated protein according to the present invention with other substances, which maintains the desired activity or characteristics of the protein or nucleic acid molecule. In one embodiment of the present invention, the protein has co-translational and/or post-translational modifications, such as one or more of phosphorylation, acetylation, methylation, ubiquitination, glycosylation, hydroxylation, sulfation, and fatty acylation. These modifications can be obtained by production in mammalian cells or by in vitro site-directed modification of synthetic peptides. When the protein of the present invention has an amino acid substitution relative to a related reference sequence, the substitution is preferably a conservative amino acid substitution. The protein of the present invention may also include modified amino acids. Amino acid modifications may include, for example, phosphorylation, acetylation, methylation, amidation, or any other amino acid modification known in the art, as long as the protein maintains the desired characteristics.

The fifth aspect of the present invention provides a pharmaceutical composition for preventing UVB-induced skin photodamage, characterized in that it comprises the truncation described in the first aspect of the present invention, the biomaterial described in the second aspect of the present invention and/or the derivative described in the fourth aspect of the present invention.

In the present invention, the term "UVB" refers to ultraviolet B, with a wavelength of 280-320 nm, which is the main cause of skin redness and sunburn, and tends to damage the more superficial layers of the skin. It plays a key role in the development of skin cancer and plays an important role in tanning and photoaging. Studies have shown that UVB can destroy the structure and function of proteins, lipids and nucleic acids, thereby causing pathological damage reactions such as skin burns, blistering, dermatitis and even skin cancer.

Furthermore, the pharmaceutical composition also includes a second therapeutic substance and/or a pharmaceutical excipient.

In the present invention, the term "pharmaceutical excipients" refers to excipients and additives used in the production of drugs and the preparation of prescriptions; they are substances other than active ingredients that have been reasonably evaluated in terms of safety and are included in pharmaceutical preparations. In addition to excipients, carriers, and stability enhancement, pharmaceutical excipients also have important functions such as solubilization, dissolution assistance, and sustained and controlled release. They are important ingredients that may affect the quality, safety, and effectiveness of drugs.

Furthermore, the second therapeutic substance includes cytokines, chemotherapeutic substances and small molecule drugs.

Furthermore, the pharmaceutical composition also includes a pharmaceutically acceptable carrier.

In the present invention, the term "pharmaceutically acceptable carrier" refers to a substance for animals (particularly for humans) listed in a pharmacopoeia approved by a government regulatory agency or otherwise recognized. In addition, a "pharmaceutically acceptable carrier" is generally any type of non-toxic solid, semisolid or liquid filler, diluent, encapsulating material or formulation adjuvant. The term "carrier" refers to any drug carrier used with an active ingredient that does not itself induce the production of antibodies harmful to the individual receiving the composition and can be applied without excessive toxicity, and can be a diluent, adjuvant, excipient or carrier for treatment. Such carriers can be sterile liquids, such as water, oil, saline, glycerol and ethanol. Auxiliary substances, such as wetting agents or emulsifiers, pH buffer substances, etc., can also be present in such vehicles.

The pharmaceutical composition of the present invention can also be used in combination with other drugs that resist UVB-induced light damage. Other compounds that resist UVB-induced light damage can be administered simultaneously with the main active ingredient (e.g., IKKα-C, a truncated form of the IKKα protein), or even administered simultaneously in the same composition. Other therapeutic compounds can also be administered separately in a separate composition or in a dosage form different from that of the main active ingredient. Partial doses of the main ingredient (e.g., IKKα-C, a truncated form of the IKKα protein) can be administered simultaneously with other compounds that resist UVB-induced light damage, while other doses can be administered separately.

The sixth aspect of the present invention provides the use of the truncate described in the first aspect of the present invention, the biomaterial described in the second aspect of the present invention, the derivative described in the fourth aspect of the present invention and/or the pharmaceutical composition described in the fifth aspect of the present invention in the preparation of a product for preventing UVB-induced skin photodamage.

The seventh aspect of the present invention provides a method for preparing the truncated body described in the first aspect of the present invention, which method includes artificial synthesis and genetic engineering technology.

Furthermore, the genetic engineering technology includes transforming or transfecting the recombinant host cell described in the second aspect of the present invention with the nucleic acid molecule described in (i) and/or the vector described in (ii) to obtain the recombinant host cell described in (iii).

In the present invention, the term "genetic engineering technology" is also called "gene splicing technology" and "DNA recombination technology". It is a genetic technology that uses molecular genetics as a theoretical basis and modern methods of molecular biology and microbiology as a means to construct hybrid DNA molecules in vitro with genes from different sources according to a pre-designed blueprint, and then introduce them into living cells to change the original genetic characteristics of organisms, obtain new varieties, and produce new products. Genetic engineering technology provides a powerful means for the study of gene structure and function.

The term "transformation" refers to the phenomenon that a cell of a certain genotype absorbs DNA from a cell of another genotype from the surrounding medium, causing its genotype and phenotype to change accordingly. In genetic engineering, it is an important means of introducing plasmids or viral vectors into recombinant host cells. The term "transfection" refers to the process in which a cell acquires a new phenotype by actively or passively introducing exogenous DNA fragments under certain conditions. Whether it is transfection or transformation, the key factor is to treat bacteria or cultured cells with calcium chloride to increase the permeability of the cell membrane, so that exogenous DNA or RNA can easily enter the cell.

Advantages and beneficial effects of the present invention:

The present invention first discovered that the IKK kinase catalytic subunit IKKα can mediate the induced activation of PERK and further activate the p53-PERP signaling pathway. The IKKα truncated IKKα-C provided by the present invention can antagonize UVB-induced PERK-p53-PERP pathway activation and cell apoptosis-promoting effects, and compared with the full-length IKKα protein, the truncated IKKα-C molecule is smaller and easier to make into medicine, and has potential application value in the prevention and control of UVB-induced skin photodamage reactions.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG1 is a diagram showing the activation of the PERK-p53-PERP pathway induced by UVB in HaCaT cells mediated by IKKα;

FIG2 is a structural analysis diagram of IKKα binding to PERK, FIG2A is a diagram of the construction scheme of wild-type IKKα and its truncated mutants, and FIG2B is a diagram of the difference in binding ability between wild-type IKKα and its truncated mutants and PERK;

FIG3 is an analysis diagram of the ability of IKKα-C to regulate the activation of the PERK-p53-PERP pathway;

FIG. 4 is an analysis of the ability of IKKα-C to regulate UVB-induced pro-apoptotic responses.

DETAILED DESCRIPTION

The present invention is further described in detail below in conjunction with specific embodiments, and the examples provided are only for illustrating the present invention, rather than for limiting the scope of the present invention. The examples provided below can be used as a guide for further improvement by those of ordinary skill in the art, and do not constitute a limitation of the present invention in any way.

The experimental methods in the following examples are conventional methods unless otherwise specified, and the materials and reagents used in the following examples are commercially available unless otherwise specified.

In the present invention, IKKα includes wild type, also known as CHUK, BPS2, IKK1, IKKA, IKBKA, IKK-1, TCF16, NFKBIKA. The term covers full-length, unprocessed IKKα. The term covers, for example, IKKα genes, human IKKα, and IKKα from any other vertebrate source, including mammals, such as primates and rodents (e.g., mice and rats). As a preferred embodiment, in the present invention, IKKα is a human gene with a gene ID of 1147.

IKKα truncations include mutants and fragments of IKKα, and the term encompasses any form of IKKα derived from processing in cells. The term encompasses naturally occurring variants of IKKα (e.g., splice variants or allelic variants). The term encompasses, for example, mutants and fragments of human IKKα, as well as mutants and fragments of IKKα from any other vertebrate source, including mammals, such as primates and rodents (e.g., mice and rats). As a preferred embodiment, in the present invention, IKKα truncations are mutants constructed by the construction scheme in Example 2, including truncated mutants IKKα-N of 1-320 amino acids; truncated mutants IKKα-C of 321-745 amino acids.

In the present invention, the term "cytokine" refers to a class of small molecule proteins with a wide range of biological activities that are synthesized and secreted by immune cells (such as monocytes, macrophages, T cells, B cells, NK cells, etc.) and non-immune cells (such as endothelial cells, epidermal cells, fibroblasts, etc.) after stimulation. Cytokines generally regulate cell growth, differentiation and effects by binding to corresponding receptors, and regulate immune responses. Cytokines can be divided into interleukins, interferons, tumor necrosis factor superfamily, colony stimulating factors, chemokines, growth factors, etc.

In the present invention, the term "chemotherapeutic substances" refers to chemical agents that can specifically work on certain microorganisms and have selective toxicity. Compared with non-specific chemical agents, they have little or very little toxicity to the human body and can be used to treat diseases caused by microorganisms. Chemotherapeutic substances are suitable for both applying to the surface of the body and being absorbed into the body through oral administration or injection. Chemotherapeutic substances are divided into two categories according to their sources. One category is artificially synthesized, mainly some growth factor analogs, which are called synthetic drugs; the other category is produced by microorganisms and is called antibiotics.

In the present invention, the term "small molecule drug" mainly refers to chemically synthesized drugs, which are usually organic compounds with a molecular weight of less than 1000. Small molecule drug structures have good spatial dispersibility, can be taken orally, can enter cells and act on intracellular targets, and have good drugability and pharmacokinetic properties.

In the present invention, "HaCaT cells" refer to human immortalized keratinocytes. The cells are derived from the skin tissue of normal adults and spontaneously transform into immortalized human keratinocytes after in vitro culture. They are widely used in skin biology and differentiation research. Under the high calcium content culture conditions of standard culture medium and fetal serum, HaCaT cells have a partially to fully differentiated phenotype. HaCaT cells are adherent cells, which appear typical epithelial cell-like under a microscope, and are positive for keratin, keratinocyte cross-linked outer membrane protein, and intermediate filament-related protein.

In the present invention, the term "immunoprecipitation" (IP) refers to a method of small-scale affinity purification of antigens using specific antibodies fixed on solid supports such as magnetic beads or agarose resins. It is a classic method for studying protein interactions based on the specific interaction between antibodies and antigens. When cells are lysed under non-denaturing conditions, many protein-protein interactions existing in intact cells are retained, which is an effective method for determining the physiological interaction between two proteins in intact cells.

In the present invention, the term "WESTERN-BLOT" refers to immunoblotting, also known as protein blotting, which is a method for detecting a certain protein in a complex sample based on the specific binding of antigen and antibody. This method is a new immunobiochemical technique developed on the basis of gel electrophoresis and solid phase immunoassay technology. Since immunoblotting has the high resolution of SDS-PAGE and the high specificity and sensitivity of solid phase immunoassay, it has become a conventional technique for protein analysis. Immunoblotting is often used to identify a certain protein and can perform qualitative and semi-quantitative analysis of the protein. Combined with chemiluminescence detection, the expression differences of the same protein in multiple samples can be compared at the same time.

In the present invention, the term "phthalocyanine blue rejection test" refers to a method of staining cells with phthalocyanine blue to quickly distinguish live cells from dead cells. Phthalocyanine blue, also known as trypan blue, is a biological staining reagent used to detect cell membrane integrity. The cell membrane structure of normal living cells is intact and can exclude phthalocyanine blue, preventing it from entering the cell; while cells that have lost their activity or have incomplete cell membranes have increased cell membrane permeability and can be stained blue by phthalocyanine blue. It is generally believed that the loss of cell membrane integrity means that the cell is dead.

The present invention will be further described in detail below in conjunction with the accompanying drawings and examples. The following examples are only used to illustrate the present invention and are not intended to limit the scope of the present invention. Simple improvements to the present invention made according to the essence of the present invention all fall within the scope of protection claimed in the present invention.

Example 1 IKKα regulates PERK-p53-PERP pathway activation

1. UVB irradiation treatment of HaCaT cells to establish a skin photodamage model

Previous studies have confirmed that treating cells with UVB at a dose of 0.5 kJ/ ^m2 for 12 hours can induce apoptosis in human keratinocytes (HaCaT), thereby establishing a UVB-induced skin photodamage model.

2. Knockdown of IKKα protein verifies its effect on activation of PERK-p53-PERP pathway

IKKα siRNA was transfected into HaCaT cells. When the expression level of IKKα was knocked down, the wild-type IKKα and its kinase activity-deficient mutant IKKα-KM were complemented, and the changes in the phosphorylation modification levels of PERK and p53 and the expression level of PERP were detected by the Western-BLOT method.

The results are shown in Figure 1. Knocking down the expression level of IKKα in HaCaT cells can significantly inhibit the induced activation of PERK and p53 and the induced expression of PERP. Under the above conditions, complementation of wild-type IKKα can completely restore the activation of the PERK-p53-PERP pathway, but complementation of the IKKα kinase activity-deficient mutant IKKα-KM has no such effect, indicating that IKKα is the key upstream protein kinase that mediates UVB-induced activation of the PERK-p53-PERP pathway.

Example 2 Construction of IKKα mutants and analysis of their PERK binding ability

1. Construction of IKKα truncation mutants

According to the structural and functional domain characteristics of IKKα, a series of IKKα truncated mutants were constructed, including full-length IKKα (WT-IKKα) with 1-745 amino acids, N-terminal truncated mutant IKKα-N with 1-320 amino acids, and C-terminal truncated mutant IKKα-C with 321-745 amino acids, as shown in A in Figure 2.

The primers for constructing the full-length and various IKKα mutants are shown in Table 1:

Table 1. Primer sequences for full-length and truncated mutants of IKKα

The above primer pairs were used to amplify IKKα and its mutant cDNAs, and inserted into the pcDNA3.1-FLAG empty vector to construct expression plasmids.

2. Screening for IKKα truncations that lose PERK binding ability

The wild-type IKKα and its truncated mutant expression plasmids were transfected into HaCaT cells respectively, and the whole cell lysate was taken and immunoprecipitated with anti-FLAG antibody. The immunoprecipitate was identified with anti-PERK antibody; IKKα mutants that lost PERK binding ability were screened.

The results are shown in Figure 2B , showing that the N terminus of IKKα mediates its binding reaction with PERK, and thus the C-terminal mutant of IKKα (IKKα-C) completely loses PERK binding reactivity.

Example 3 IKKα-C mutant regulates PERK-p53-PERP pathway induction and activation and mediates cell apoptosis

1. In HaCaT cells with knocked-down IKKα expression levels, full-length IKKα and IKKα mutants that lost the ability to bind to PERK were complemented, and the WESTERN-BLOT method was used to detect the difference in the ability of wild-type and mutant IKKα in mediating UVB-induced PERK-p53-PERP pathway activation before and after UVB irradiation. The results are shown in Figure 3. Compared with wild-type IKKα, the IKKα-C truncation lost the ability to activate PERK and p53 and induce PERP expression.

2. The phthalocyanine blue exclusion test was used to detect the difference in the ability of wild-type and mutant IKKα in mediating UVB-induced cell apoptosis before and after UVB irradiation. The statistical results are shown in Figure 4. IKKα-C truncation can also antagonize UVB-induced apoptosis in human skin keratinocytes.

The above results indicate that the C-terminal IKKα truncated mutant IKKα-C has the function of targeting PERK and antagonizing UVB-induced apoptosis of skin keratinocytes.

The amino acid sequence, nucleotide sequence and the sequences of the amplification primers of the full length and mutants of IKKα in the present invention are shown in Table 2:

Table 2. IKKα related sequences

The present invention has been described in detail above. For those skilled in the art, without departing from the purpose and scope of the present invention, and without the need to carry out unnecessary experimental conditions, the present invention can be implemented in a wide range under equivalent parameters, concentrations and conditions. Although the present invention provides embodiments, it should be understood that the present invention can be further improved. In a word, according to the principles of the present invention, the application is intended to include any changes, uses or improvements to the present invention, including departure from the disclosed scope in the application, and changes made with conventional techniques known in the art.

Claims (10)

1. A truncated form of IKKα protein, characterized in that the amino acid sequence of the truncated form is as shown in SEQ ID NO: 1 in the sequence listing. 2. A biomaterial comprising: (i) a nucleic acid molecule encoding the truncated form of claim 1; (ii) a vector comprising the nucleic acid molecule described in (i); or (iii) a recombinant host cell comprising the nucleic acid molecule described in (i) and/or the vector described in (ii). 3. The biomaterial according to claim 2, characterized in that The base sequence of the nucleic acid molecule is shown in SEQ ID NO: 2 in the sequence listing; The vectors include eukaryotic expression vectors, prokaryotic expression vectors, artificial chromosomes and/or phage vectors; The recombinant host cell is prokaryotic or eukaryotic; The recombinant host cells include yeast cells, CHO cells, 293 cells, plant cells, and Escherichia coli cells. 4. A primer comprising a forward primer and a reverse primer, wherein the primer can amplify the nucleic acid molecule described in (i) in the biological material according to claim 2; The base sequence of the forward primer is shown in SEQ ID NO: 3 in the sequence listing; The base sequence of the reverse primer is shown in SEQ ID NO: 4 in the sequence listing. 5. A truncated form of claim 1 or a derivative of the biomaterial of claim 2, characterized in that: The derivatives are truncated bodies or nucleic acid molecules formed by modification, inclusion and/or covalent binding of other substances. 6. The derivative according to claim 5, characterized in that The modification includes one or more of phosphorylation, acetylation, methylation, ubiquitination, glycosylation, hydroxylation, sulfation, and fatty acylation; The encapsulation includes liposome encapsulation, exosome encapsulation, metal nanoparticle encapsulation, silica encapsulation, polysaccharide nanocarrier encapsulation, synthetic polymer nanocarrier encapsulation, cell penetrating peptide encapsulation, protein cage encapsulation, and virus-like particle encapsulation; The other substances include one or more components selected from the group consisting of free adjuvants, stabilizers, buffers, surfactants, salts and preservatives. 7. A pharmaceutical composition for preventing UVB-induced skin photodamage, characterized in that it comprises the truncation according to claim 1, the biomaterial according to any one of claims 2-3 and/or the derivative according to any one of claims 5-6. 8. The pharmaceutical composition according to claim 7, characterized in that the pharmaceutical composition further comprises a second therapeutic substance and/or a pharmaceutical excipient; The second therapeutic substance includes cytokines, chemotherapeutic substances and small molecule drugs; The pharmaceutical composition also includes a pharmaceutically acceptable carrier. 9. Use of the truncate according to claim 1, the biomaterial according to any one of claims 2-3, the derivative according to any one of claims 5-6 and/or the pharmaceutical composition according to any one of claims 7-8 in the preparation of a product for preventing UVB-induced skin photodamage. 10. A method for preparing the truncated form of claim 1, the method comprising artificial synthesis and genetic engineering techniques; The genetic engineering technology includes transforming or transfecting the recombinant host cell described in claim 2 with the nucleic acid molecule described in (i) and/or the vector described in (ii) to obtain the recombinant host cell described in (iii).