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The invention discloses application of USP15 in preparation of a bladder cancer radiotherapy sensitizer, and belongs to the technical field of biological medicine. The objective of the invention is to improve the radiotherapy sensitivity of bladder cancer. The invention relates to an application of USP15 in preparation of a bladder cancer radiotherapy sensitizer. The USP15 is used for preparing the bladder cancer radiotherapy sensitizer. The radiotherapy sensitivity of the bladder cancer is improved by overexpressing the USP15. The USP15 can regulate and control the stability of FIS1 protein through ubiquitination modification so as to inhibit the mitochondrial function, and the activation of the regulation and control pathway is the core mechanism of the USP15 for exerting the radiotherapy sensitization effect. In conclusion, the invention not only provides a new thought for molecular mechanism research of bladder cancer radiotherapy sensitization, but also provides a potential strategy for treatment of clinical radiotherapy resistant bladder cancer patients, and has important drug development value and clinical application prospect.

This invention belongs to the field of plant tissue culture technology, specifically disclosing a method for producing Polygonatum polysaccharides using Polygonatum yunnanense tissue culture, comprising the following steps: explant disinfection, callus induction, callus proliferation and induction culture: selecting vigorous callus tissue, transferring it to a culture medium: White medium + 2,4-D 1.5 mg / L + VC 20 mg / L + sucrose 40 g / L + 30 mg / L inducer + agar 6 g / L, pH 5.8, after culture, collecting the callus, drying it, and then extracting Polygonatum yunnanense polysaccharides; the inducer is Polygonatum yunnanense endophytic basidiomycetes (… Talaromyces sp. The fermentation broth extract of HJF23; the HJF23 preservation number is CCTCC NO: M2021344. This invention not only realizes the efficient biosynthesis of Polygonatum yunnanense polysaccharide, but also significantly enhances its functional activity.

The invention discloses an active peptide capable of directionally inducing IPSCS cracking, a preparation method of the active peptide and application of the active peptide in a preparation for repairing liver injury. Experiments prove that the active peptide provided by the invention has a remarkable protective effect on a liver injury model induced by cyclophosphamide and shows a definite anti-oxidative stress effect. The result shows that a key path of chemotherapy injury can be intervened from the source by simulating or enhancing an endogenous protection mechanism of the liver. Compared with the existing exogenous synthetic drugs or single-component natural products, the product provided by the invention has the potential advantages of more comprehensive action mechanism and better biogenic property. Meanwhile, the extract is derived from directionally differentiated functional cells, and a brand new thought and material basis are provided for developing a novel chemotherapy liver protective agent which does not affect the chemotherapy curative effect and has good biocompatibility.

The invention belongs to the field of drugs for inflammatory dermatosis, and discloses an application of myrcene in preparation of drugs for inflammatory dermatosis, which comprises the following steps: combining a mouse AD model (DNCB) with human epidermal keratinocytes (NHEK) and mouse macrophages (RAW264.7); the improvement effect of the MYR is evaluated by adopting histology and immunofluorescence technologies; by integrating transcriptomics and proteomics analysis, the molecular mechanism of MYR for relieving AD symptoms is clarified, and the causal relationship is verified by using a pharmacological inhibitor. The conclusion of the invention is as follows: Myrcene alleviates AD sample inflammation by inhibiting FAK / Src-YAP / TAZ axis. A repeatable mechanism framework is established by the data, and the natural monoterpenoids are associated with biomechanical-nuclear signal transduction and innate immune regulation in AD.