106 results about "Nuclear translocation" patented technology

The invention belongs to the technical field of cytotoxicity intervention, and particularly relates to application of an inhibitor JSH-23 in preparation of a medicine for preventing and / or treating ovarian toxicity caused by environmental toxin combined exposure. Aiming at the condition that MC-LR and NaNON combined exposure can activate NF-kappa B to induce KK-1 cell nitrification stress and cause mouse ovarian dysfunction, JSH-23 is selected as an intervention agent, and it is found that after KK-1 cells are pretreated by JSH-23, NF-kappa B nuclear translocation induced by the KK-1 cells due to MC-LR and NaNON combined exposure is remarkably inhibited, iNOS protein rising induced by toxin combined exposure is remarkably reduced, and NF-kappa B nuclear translocation induced by the KK-1 cells due to NF-kappa B combined exposure is remarkably inhibited. The increase of the levels of ONOO and 3-NT of nitration stress markers is effectively relieved, which indicates that JSH-23 can participate in the nitration stress of KK-1 cells caused by combined exposure of MC-LR and NaNO2 by inhibiting NF-kappa B activation, and a foundation is laid for screening antidotes after exposure of environmental toxins.

The invention belongs to the technical field of biological medicine, discloses a novel venom polypeptide composite dendrimer as well as a preparation method and application thereof, and particularly discloses scorpion venom polypeptide, and the amino acid sequence of the scorpion venom polypeptide is FLGGSLSSIF. According to the invention, a novel scorpion venom polypeptide (marked as C9) is separated and identified, and a novel polypeptide-polyamidoamine dendritic compound G5C9 (i.e., nanoparticles) with a glioblastoma (GBM) targeting effect is constructed. Compared with the polypeptide C9, the cell uptake efficiency of the G5C9 is obviously improved. G5C9 can enter cells through endocytosis and target lysosome to destroy functions of the lysosome and mTORC1, so that nuclear translocation of TFEB is promoted, and autophagic death of the cells is induced. Therefore, the G5C9 provides a novel mode for targeting the anti-GBM in vitro and in vivo.

The invention belongs to the technical field of biological medicine, and particularly relates to application of cynarin as a cGAS-STING signal channel inhibitor in preparation of anti-inflammatory drugs. It is found for the first time that cynarin can inhibit phosphorylation of STING and translocation of STING by influencing the stability of STING spatial conformation, so that channel downstream protein activation is inhibited, nuclear translocation of IRF3 is hindered, expression of a series of interferon-induced related genes such as IFN-beta, CXCL10 and ISG15 is inhibited, finally secretion of IFN-beta can be hindered, cGAS-STING inflammatory response can be inhibited by targeting STING, and the application of cynarin in inhibiting cGAS-STING inflammatory response is achieved. A new thought and a new means are provided for developing an auxiliary treatment method aiming at STING related inflammations.

Amino acid sequences capable of enhancing nuclear translocation are provided. Also referred to a nuclear localization signals (NLS) the sequences can be linked to or grafted into antibodies or fragments or fusion proteins thereof to enhance nuclear translocation of the antibody. Compositions and antibodies including an NLS conjugated or otherwise linked directly or indirectly to an active agent cargo are also provided. Exemplary cargo includes proteins, peptides, carbohydrates, polysaccharides, nucleic acid molecules, inorganic molecules, organic molecules, and diagnostic agents. Pharmaceutical compositions further including a pharmaceutically acceptable carrier are also provided. Methods of delivering the composition or antibody alone or with a cargo linked thereto to the nucleus of cell, methods of selecting or screening for compositions having a desired cellular activity, and methods of treating diseases and disorders are also provided.

The invention relates to the technical field of hepatic failure treatment, and particularly discloses application of tsRNA-20 or a simulant thereof in preparation of drugs for treating chronic plus acute hepatic failure and / or promoting liver cell proliferation. Through tsRNA sequencing and qRT-PCR verification, down-regulated expression of the tsRNA-20 in a plasma sample and liver tissue in chronic and acute hepatic failure is determined, and cell experiments find that the tsRNA-20 regulates an ACPH / GRHL1 axis to promote liver cell proliferation. Specifically, it is found that tsRNA-20 is combined with an amidyl peptide hydrolase (ACPH), so that a Ras-ERK pathway is activated, nuclear translocation of a granulocyte-like transcription factor 1 (GRHL1) is promoted, and finally liver cell proliferation is enhanced. Therefore, when the tsRNA-20, the precursor tRNA-GIy-CCC thereof and the regulated objects ACPH and GRHL1 thereof are applied to treatment of the chronic and acute liver failure, the tsRNA-20, the precursor tRNA-GIy-CCC thereof and the regulated objects ACPH and GRHL1 thereof can be used as targets to be regulated to promote liver cell proliferation, so that liver regeneration is promoted, the treatment effect of the chronic and acute liver failure is improved, the lifetime of patients with liver diseases is prolonged, and the tsRNA-20, the precursor tRNA-GIy-CCC and the regulated objects ACPH and GRHL1 possibly become new targets for precise treatment. The clinical application value is relatively high.

The invention provides novel application of gastrodin, and belongs to the technical field of biological medicine. By constructing an MCAO model of cerebral arterial thrombosis and detecting the influence of GAS on MCAO mouse and OGD-induced microglial cell ferroptosis, it is found that GAS alleviates the ferroptosis of cerebral arterial thrombosis, it is found through molecular docking and cell thermal displacement experiments that GAS is specifically bound with Alkbh5, the stability of protein is improved, nuclear translocation of Alkbh5 is promoted, and the GAS can be used for treating cerebral arterial thrombosis. Therefore, the methylation level of N6-methyladenosine (m6A) of a glutamic acid-cysteine ligase modified subunit (Gclm) is reduced, the expression of the Gclm is increased, the synthesis of glutathione is enhanced, and finally ferroptosis of microglial cells is inhibited. Therefore, the gastrodin can be used for preparing the medicine for treating the ferroptosis of the cerebral arterial thrombosis, and a new natural medicine source is provided for preventing and treating the ferroptosis of the cerebral arterial thrombosis.

This invention discloses the application and method of a STAT1-targeting inhibitor in the treatment of immune thrombocytopenic purpura (ITP). It employs ivermectin, a STAT1 nuclear translocation inhibitor, and fludarabine, a STAT1 activation inhibitor. By injecting either the activation inhibitor or the nuclear translocation inhibitor, the platelet count in a mouse model of ITP is increased. Fludarabine, a fluorinated nucleotide analog of vidarabine, is non-radioactive and a small-molecule phosphorylation inhibitor. Ivermectin is a small-molecule inhibitor of nuclear translocation mediated by α / β1 introgression protein. Both have high bioavailability and are widely used to treat various hematological diseases with good safety profiles. Their application in treating ITP is safe, effective, and shows high compliance.

The invention relates to application of NMRK2 in regulating and improving myocardial ischemia reperfusion injury, and belongs to the technical field of biological medicine. Based on the lack of medicines for effectively preventing and treating myocardial ischemia-reperfusion injury at present, the invention develops a protection method based on NMRK2 signal regulation and control, specifically, a preparation for enhancing NMRK2 expression or activity is adopted to prepare the medicines for preventing or treating myocardial ischemia-reperfusion injury, and the medicines can systematically enhance the anti-oxidation defense capability of myocardial cells, so that the anti-oxidation defense capability of myocardial cells is enhanced. The tissue injury caused by reperfusion is improved, so that the myocardial ischemia reperfusion injury is effectively prevented and treated. Furthermore, it is found that the NMRK2 can inhibit excessive activation of MST1 / p-MST1 in a Hippo pathway and promote YAP nuclear translocation, so that NADK expression is up-regulated, a Trx1 antioxidant system is enhanced, and a new 'NMRK2-YAP-NADK-Trx1 antioxidant signal pathway' is formed.

The invention belongs to the technical field of traditional Chinese medicine, and particularly relates to a parent structure of a PKM2 agonist and application of the PKM2 agonist, the PKM2 agonist is hypaconitine screened from a monkshood alkaloid part, the chemical formula of the PKM2 agonist is C33H45NO10, and the structural formula of the PKM2 agonist is shown in the description. The hypaconitine has the functions of inhibiting phosphorylation of tumor cell PKM2 protein, inhibiting conversion from tetramer to dimer, enhancing PKM2 activity and inhibiting PKM2 nuclear translocation; the parent structure of the hypaconitine is composed of diterpenoid skeleton atoms, and the parent nucleus of the hypaconitine is C19 diterpenoid alkaloid; according to the invention, a PKM2 activating component in monkshood alkaloid is screened by using computer-aided drug design, and it is reported for the first time that hypaconitine has a PKM2 activating effect; a certain foundation is laid for the research on the anti-tumor mechanism of the radix aconiti carmichaeli, a basis is provided for the clinical application of the anti-tumor of the radix aconiti carmichaeli, and a new parent structure is provided for the research and development of a PKM2 agonist.

The present invention discloses a plasmid vector and cell line that can induce targeted genomic DNA double-strand breaks. The present invention constructs a nuclease AscI expression plasmid based on a lentiviral vector backbone by integrating the Tet-on chemically inducible transcription control system and the ERT2 ligand-dependent nuclear localization control system. The vector regulates the transcription of AscI through the Tet-on system and uses the 4-hydroxytamoxifen-induced ERT2 system to achieve spatiotemporal specific nuclear translocation of the endonuclease AscI. The present invention also constructs and screens a cell line that stably expresses AscI. With the help of small chemical molecules, the spatiotemporal expression of the AscI endonuclease in cells can be precisely regulated, thereby inducing DNA double-strand breaks at specific sites in the genome. The present invention provides an efficient and accurate research tool for the field of DNA damage repair, which can be widely used in studying DNA damage repair mechanisms and high-throughput screening of related drugs.

The invention belongs to the technical field of medicine preparation, and particularly relates to application of DHGC in preparation of a medicine for treating acute kidney injury ferroptosis mediated by an SIRT3 / NRF2 axis. Experiments prove that DHGC can activate SIRT3 in a targeted manner, up-regulate the expression level of SIRT3, promote NRF2 deacetylation and drive NRF2 nuclear translocation, and further up-regulate the expression level of GPX4, so that the effect of resisting ferroptosis caused by acute kidney injury is achieved.

This invention belongs to the field of biopharmaceutical technology, and specifically relates to the application of D724-0491 in the preparation of products for the prevention and treatment of breast cancer. D724-0491 inhibits the binding of HBXIP and KEAP1, reduces the level of NRF2 nuclear translocation, thereby inducing oxidative stress in tumor cells and promoting cancer cell death. It is a novel targeted therapy drug for breast cancer, improving the prognostic survival rate of breast cancer patients.

This invention proposes the application of psoralen as an Nrf2 agonist in drug preparation. This invention is the first to discover that psoralen is a specific Nrf2 agonist. Psoralen can directly target and bind to the Nrf2 protein, improving its stability, promoting its phosphorylation and nuclear translocation, thereby activating the Nrf2 signaling pathway, upregulating the expression of downstream antioxidant, anti-inflammatory, and anti-ferroptosis-related proteins, and achieving cell protection and tissue repair functions.

The application relates to the technical field of biological medicine, and provides an anti-GPC3 full humanization single-domain antibody and application thereof. The application uses phage display technology to obtain one anti-human GPC3 specificity full humanization monoclonal single-domain antibody through antibody screening by targeting human GPC3 protein. The obtained single-domain antibody can be specifically combined with human GPC3, and can effectively inhibit the nuclear translocation of YAP, provides an effective alternative antibody drug for GPC3-targeted HCC treatment, and has a potential clinical application prospect.

The invention relates to application of lentinan in preparation of a medicine for enhancing Kukuzhou cell immune function, and belongs to the technical field of immunopharmacology. The invention discloses a mechanism and application of lentinan LNT (Lentinan) based on a TLR2 (Toll-Liver Receptor 2) signal channel for enhancing the immune function of liver cumness cells and promoting lysosome maturation. By constructing an LNT fluorescence labeling system, a Kuptake cell in-vivo tracing model and a TLR2 function intervention model, it is proved that LNT can be directly combined with TLR2 and activate a TLR2 / MyD88 / NF-kappa B signal axis, and therefore the phagocytosis and immune response capacity of Kuptake cells is enhanced. Meanwhile, TLR2 signal-induced reactive oxygen species (ROS) up-regulation can promote TFEB dephosphorylation and nuclear translocation, lysosome maturation is driven, and degradation metabolism of LNT is accelerated. The invention provides a TLR2-based immune enhancement mechanism of the LNT, and provides a theoretical basis and an application basis for developing immunomodulatory targeted drugs.

The invention discloses an application of a P4HA1 inhibitor in preparation of a medicine for treating congenital megacolon-related enterocolitis, deeply clarifies an immune metabolic axis of 'P4HA1-hydroxyproline-eIF5A-IRF4-IL17', and discloses a new mechanism that metabolite hydroxyproline regulates the activity of eIF5A and promotes nuclear translocation of IRF4 so as to enhance TH17 cell mediated inflammatory response. Therefore, a brand new perspective is provided for understanding metabolic immune regulation of intestinal inflammation. By using the P4HA1 inhibitor (such as 1, 4-DPCA), secretion of IL-17 can be effectively inhibited, intestinal inflammation injury of HAEC model mice can be remarkably relieved, and a clear pharmacodynamic basis is achieved.

T lymphocytes play a key role in the immune response and their functions are intimately linked to metabolic programs. During immune responses, T cells undergo a metabolic reprogramming notably characterized by an increased aerobic glycolysis. Using a quantitative phosphoproteomic approach, the inventors have identified a new transcription factor called Foxk1 as being highly phosphorylated in T cells upon T Cell Receptor (TCR) engagement. The results also indicate that Foxk1 phosphorylation and nuclear translocation is dependent of the AKT-mTOR kinase activities. Using T-cell specific Foxk1 deficient mice (Foxk1- / -), we demonstrated that Foxk1 is required for full T cell activation. Foxk1-deficient T cells exhibited reduced proliferation and cytokine secretion following TCR stimulation. Furthermore, T cells from Foxk1- / - mice were less prone to acquire an effector like phenotype than wild-type cells when challenged in vivo. Conversely, Foxk1 overexpression in T cells enhanced their effector functions in a TCR-dependent manner. In CD8+ T cells, this effect also results into enhanced cancer cell killing capacity in vitro, and improved tumor rejection in vivo. Altogether, these results indicated that Foxk1 is a major regulator of T cell metabolism and thus, of T cell effector functions. Thus, the present invention relates to host immune cells engineered to overexpress a Foxk1 polypeptide and their use of the treatment of cancer.

The invention discloses application of carnosic acid in resisting vascular aging for a long time and inhibiting the ubiquitination level of TP53, the carnosic acid acts on TP53 protein to inhibit the ubiquitination level and nuclear translocation of K63 of the TP53 protein, so that the proliferation time of vascular endothelial cells in the replication and aging process is prolonged, the damage repair capacity of the vascular endothelial cells is improved, and the application of the carnosic acid in resisting vascular aging for a long time and inhibiting the ubiquitination level of the TP53 protein is realized. The damage repair capability comprises proliferation activity, migration capability and angiogenesis capability. According to the application disclosed by the invention, the direct action target TP53 of CA for resisting vascular senescence is defined for the first time, and the application has profound significance on research on vascular senescence and TP53 protein and provides a new scheme for treatment of vascular senescence.

The invention discloses a method and a device for monitoring dynamic response of cell nucleus to perceive extracellular mechanical stimulation. The device mainly comprises a single cell compression mechanical control system, a constant-temperature liquid-phase mechanical control experimental platform and a fluorescent microscopic imaging system. According to the invention, a single living cell can be compressed at the mechanical scale of nano-Newton (nN), the morphological change of the cell and the nuclear translocation dynamic process of YAP protein are monitored in real time, and the mechanism that the cell senses extracellular mechanical stimulation and responds to mechanical stimulation can be disclosed by representing the dynamic process of YAP nuclear translocation (the ratio of the fluorescence intensity of the YAP protein in the cell nucleus and the cytoplasm). The main method adopted by the invention comprises the following steps: firstly, artificially modifying a functionalized probe which can be used for realizing nano-cattle precision and is mechanically controlled by a single cell; a 3KPa PAA hydrogel substrate coated with type I Collagen is prepared, and a constant-temperature liquid-phase mechanical control experiment platform simulating human physiological conditions is constructed; a fluorescence microscopic imaging system is integrated below the experiment platform.

The invention relates to a PKM2-based nano glycopeptide activator and application thereof.The nano glycopeptide activator comprises three functional units, namely a PKM2 targeted activation unit R3, a self-assembly unit R2 and a response unit R1, and the chemical structure of the nano glycopeptide activator is shown in the formula (I). After administration, the nano glycopeptide activator can be enriched to a tumor site through targeting of sugar receptor transporter protein or an EPR effect; after entering tumor cells, the polypeptide is subjected to in-situ fibrosis deformation under the hydrolysis action of glycohydrolase, so that specific targeting and retention are realized; the nano-fiber with the PKM2 targeting activation unit can promote conversion of dimer PKM2 into tetramer PKM2, inhibit nucleation of PKM2, and prevent the DNA damage repair process of tumor cells.

The invention belongs to the technical field of biological medicines, and particularly relates to application of benzethonium chloride as an STAT3 inhibitor in preparation of a medicine for treating head and neck tumors. The invention proves that BZN is directly combined with STAT3 protein to reduce tyrosine phosphorylation and nuclear translocation of the STAT3 protein, so that expression of downstream MCL-1 is reduced, and head and neck tumor cells are subjected to apoptosis. According to the application disclosed by the invention, the STAT3 is determined to be a potential target of the BZN, and the BZN is proved to be combined with STAT3 protein in head and neck tumor cells FaDu and CAL-27, so that the CAL-27 and FaDu cells are subjected to apoptosis, and an anti-tumor effect is achieved. BZN is expected to become a new action target of STAT3.

The invention discloses a compound containing a general formula I as well as a preparation method, a pharmaceutical composition and application thereof. Specifically, the invention provides a compound with a structure as shown in a general formula I, and a racemate, an R-isomer, an S-isomer, a pharmaceutically acceptable salt or a mixture of the racemate, the R-isomer, the S-isomer and the pharmaceutically acceptable salt. The compound has a good effect on promoting transcription factor EB (TFEB) nuclear translocation and promoting lysosome generation, and can be used for preventing, treating or adjunctively treating various diseases related to lysosome dysfunction and insufficient biosynthesis. The compound can be used for treating neurodegenerative diseases, especially neurodegenerative diseases caused by accumulation of pathological proteins (such as beta-amyloid protein and alpha-synuclein) in the brain, such as Alzheimer's disease (AD), Parkinson's disease (PD) and the like. # imgabs0 #

The invention discloses application of Keratin5 low expression and PADI3 nuclear translocation in serving as a predictive marker for invasion and metastasis of head and neck squamous cell carcinoma, belongs to the technical field of biological medicine, verifies clinical applicability of KRT5 low expression and / PADI3 nuclear translocation (namely KRT5low / PADI3nucle) serving as a predictive index so as to fill the blank of the prior art, and provides a novel predictive marker for invasion and metastasis of head and neck squamous cell carcinoma. A novel molecular marker and an intervention target spot are provided for precise diagnosis and treatment of the head and neck squamous cell carcinoma; the KRT5 and PADI3 co-expression region forms a specific micro-domain difference and a specific mode in tumor tissues, can be used as an effective head and neck squamous cell carcinoma metastasis prediction marker, and has important scientific significance and application value for optimizing clinical diagnosis and treatment strategies.

The present invention provides the use of liriope muscari saponin C in the preparation of anti-respiratory virus drugs, belonging to the field of antiviral drug preparation. The liriope muscari saponin C of the present invention shows different degrees of inhibitory effects on influenza virus (H1N1) and novel coronavirus (SARS-CoV-2), showing good antiviral application prospects. Liriope muscari saponin C effectively inhibits the replication of influenza virus and the infection of SARS-CoV-2 to host by inhibiting the nuclear translocation of influenza virus vRNP complex and the binding of SARS-CoV-2 S protein and ACE2.

The application belongs to the technical field of biological medicine and molecular biology, and particularly relates to application of umbilical cord blood plasma-derived extracellular vesicles and related bioactive molecules thereof in treatment of Alzheimer's disease. Specifically, the application isolates extracellular vesicles (UCBP-sEVs) from umbilical cord blood plasma, which has the effect of improving Alzheimer's disease. Further research finds that high enrichment of miR-16-2-3p therein is a key molecule for mediating treatment of Alzheimer's disease. miR-16-2-3p targets and inhibits expression of ROCK2, reduces phosphorylation level of TFEB and promotes nuclear translocation of the same, activates microglial autophagy-lysosome pathway, and thus promotes phagocytosis and degradation of intracerebral beta amyloid, and therefore has good practical application value.

The invention relates to an application of a zinc finger protein Zfp260 phosphorylation site for regulating osteogenesis, and particularly discloses an application of a biomarker in preparation of a medicine for regulating bone regeneration and repair, and the biomarker comprises one or a combination of more of Y173 phosphorylation, S182 phosphorylation and S197 phosphorylation of the zinc finger protein Zfp260. The invention finds that any phosphorylation defect mutation of the three sites Y173, S182 and S197 can obviously change the binding force and nuclear translocation signal with kinase PKC alpha, and each mutant cannot save the cell mineralization defect caused by Zfp260 knockout, and prompts that the newly found Zfp260 phosphorylation sites Y173, S182 and S197 play important roles in Zfp260 related diseases and the regulation process of promoting bone regeneration and repair.

The invention relates to the technical field of biological medicines, and particularly discloses a nanocapsule SMCPM and application thereof in medicines for treating or preventing osteosarcoma and pulmonary metastasis. The SMCPM is composed of a photosensitizer Ce6 carried by mesoporous silicon oxide-manganese oxide particles, an NRF2 inhibitor ML385 and an OS targeting peptide PT-7. Experiments prove that the SMCPM is high in penetrating power and strong in cell killing effect; by down-regulating NRF2 expression and reversing nuclear translocation, a biochemical inhibitory microenvironment can be effectively repaired, the tolerance of cells to active oxygen and epithelial-mesenchymal transition activated and induced by a NOTCH1 signal axis are remarkably reduced, the oxidative stress level of the cells is enhanced, and PIT-induced immunogenic cell death is promoted; the released Mn < 2 + > and double-stranded DNA can regulate and control an immunosuppressive microenvironment by activating an STING pathway in cells, thereby inhibiting the growth of osteosarcoma and preventing lung metastasis.

The invention discloses application of a targeted Nup85 inhibitor in preparation of a medicine for preventing or treating hepatocellular carcinoma, and relates to the technical field of biological medicine and tumor immunotherapy. The invention provides an application of a targeted Nup85 inhibitor in preparation of a medicine for preventing or treating hepatocellular carcinoma. The inhibitor prevents and / or treats hepatocellular carcinoma by enhancing CD8 + T cell functions, enhancement of the CD8 + T cell functions is realized by regulating STAT1 / CCL5 / CXCL10 pathways, and Nup85 reduces expression of CCL5 and CXCL10 by inhibiting nuclear translocation of phosphorylated STAT1, so that infiltration and activation of CD8 + T cells are inhibited. The invention discloses an immune escape mechanism that Nup85 inhibits CD8 + T cell infiltration by inhibiting p-STAT1 nuclear translocation and down-regulating CCL5 / CXCL10 expression in liver cancer for the first time, provides a new liver cancer immunotherapy target, and broadens the application of nucleopore protein in tumor immunotherapy; the target Nup85 inhibitor can be obtained through a conventional means, a new clinical application direction of the target Nup85 inhibitor is defined, and the target Nup85 inhibitor has good clinical transformation and development prospects.

The present invention discloses a method for constructing a transgenic mouse with systemic overexpression of human α-Syn-NLS. First, the human α-Syn coding sequence and the SV40 nuclear translocation signal sequence are obtained by PCR. Then, an entry clone vector containing the target sequence is constructed through a BP reaction. After digestion with enzymes, the entry clone vector is constructed into a recombinant expression vector containing the target sequence through an LR reaction. After digestion with enzymes again, using the lentiviral LV overexpression vector pLV-EGFP:T2A:Puro-EF1A as the backbone vector, the recombinant expression vector pDown-hSNCA / SV40NLS containing the target sequence is constructed into the lentiviral vector, and virus packaging and purification are carried out to obtain the pLV virus overexpressing nuclear import α-Syn. The virus is injected by the method of pronuclear injection of fertilized eggs to obtain a transgenic mouse with systemic overexpression of nuclear import human α-Syn protein, which can stably overexpress α-Syn for a long time and solve the problem of nuclear import at the same time. This model has important value for studying the comprehensive functions and mechanisms of α-Syn nuclear import.

The invention discloses a composition for improving skin inflammation as well as application and a production method of the composition. The composition is prepared from the following components in parts by weight: 2 to 6 parts of curcumin monocarbonyl analogue cyclodextrin inclusion compound and 0.3 to 0.5 part of allantoin. The curcumin monocarbonyl analogue cyclodextrin inclusion compound is prepared from the following components in parts by weight: 0.5 to 1.5 parts of curcumin monocarbonyl analogue and 98.5 to 99.5 parts of beta-cyclodextrin, and the composition is applied as a skin care product. Aiming at skin inflammation caused by chronic symptoms, NF-kappa B nuclear translocation is blocked, multi-target anti-inflammation is achieved, and the effect is better directly aiming at core pathogenic genes. The allantoin increases the dissolution and absorption of the curcumin monocarbonyl analogue cyclodextrin inclusion compound, promotes the hydration of cuticle and reduces the irritation to the skin; the use effect is milder, and the composition is more suitable for non-invasive dermatitis.