70 results about "Apoptosis pathway" patented technology

The invention discloses an application of ansamitocin P-3 (Ansamitocin P-3) in preparation of a medicine for treating gastric cancer. The invention proves that the ansamitocin P-3 enables gastric cancer cells to die by influencing the apoptosis pathway of the cells through cytological research. Meanwhile, a stomach cancer abdominal cavity planting model of a nude mouse is constructed, and it is also observed that the ansamitocin P-3 has a killing effect on stomach cancer in the model. The invention provides a new application of ansamitocin P-3 in treatment of gastric cancer, and the ansamitocin P-3 has good clinical transformation value. The invention provides a new treatment means for gastric cancer patients with drug resistance.

The invention discloses a fish circRNA and application thereof, the fish is pelteobagrus fulvidraco, the circRNA is named circArid4b, and the nucleotide sequence of the circRNA is shown as SEQ ID NO.1. The invention further discloses a preparation method of the circRNA. The fish circRNA provided by the invention can regulate and control Arid4b expression of a source gene of the fish circRNA under hypoxia and bacterial infection conditions, influence apoptosis pathways and inflammatory reactions, and finally regulate and control antibacterial reactions. The invention further provides an interferent of the circRNA, the circRNA interferent can be used as a fish immunomodulator, infection of Aeromonas veronii on pelteobagrus fulvidraco under the low-oxygen condition is remarkably inhibited, and a new mode is provided for efficiently improving the antibacterial immunity of fish under the low-oxygen environment.

The invention discloses a tumor treatment molecule with a curative effect self-amplification function. Belongs to the technical field of biotechnology and new medicine, and comprises a peptide sequence Ac-Asp-Glu-Val-Asp-Cys (StBu)-Lys combined to a CBT part and a paclitaxel chemotherapy molecule connected to a lysine side chain. After the probe enters a tumor cell, the probe is specifically recognized by reducing glutathione highly expressed in the tumor cell, and an Ac-DEVDCK (PTX)-CBT structure is generated; then, a weak cell apoptosis phenomenon is initiated through a molecular grafted paclitaxel structure; the Ac-DEVD fragment is used as a high-specificity polypeptide substrate of cysteine-aspartic acid specific protease 3 which is necessary in a cell apoptosis pathway, and can be specifically cut by the cysteine-aspartic acid specific protease 3, so that the Ac-DEVDCK (PTX)-CBT is converted into CK (PTX)-CBT; then, CK (PTX)-CBT molecules are subjected to a CBT-Cys click reaction to form a cyclic dimer, and the cyclic dimer is self-assembled to form particles. According to the method, the affinity of the paclitaxel to the tubulin in the cytoskeleton is utilized, so that the tubulin in the cell is aggregated, the self-amplification effect of the curative effect of the cell is realized, and the cell is triggered to generate a pan-apoptosis effect.

The invention belongs to the technical field of gene engineering and cell transformation, and discloses a gene engineering construction method and application of anti-apoptosis human mesenchymal stem cells. Through HDAC1 K412 site specific lactic acid mutation, breakthrough improvements are realized: for example, CRISPR-Cas9-mediated accurate gene editing is utilized, only a single amino acid site is changed, that is, K412R mutation simulates persistent lactic acid, and whole genome apparent modification disturbance can be avoided; the modification does not depend on an exogenous metabolic substrate, and the negative feedback effect of traditional metabolic intervention is overcome; the mutant continuously inhibits a P53 apoptosis pathway, so that the oxidative stress mediated apoptosis resistance of the MSC is remarkably improved. According to the design concept of one target spot and one regulation, the core contradiction that long-term effectiveness and specificity cannot be considered in the prior art is fundamentally solved, and a brand new normal form is provided for stem cell treatment.

The invention belongs to the technical field of biological medicines, and relates to application of mannatide in preparation of a medicine for treating alcoholic gastric ulcer. The mannatide disclosed by the invention can be used for remarkably relieving gastric tissue hemorrhagic lesion and ulcer conditions of alcoholic gastric ulcer for the first time, and the mechanism comprises the following steps: reducing active oxygen generated by alcohol toxicity, and improving oxidative stress of a body by improving antioxidant enzyme activity of the gastric tissue; the inflammatory response of the organism is regulated by regulating and controlling an Akt / NF-kB pathway; a Bax-related apoptosis pathway is inhibited to protect gastric mucosa cells from alcohol-induced apoptosis, so that the integrity of gastric tissue mucosa is protected; the intestinal flora disorder caused by alcohol intake is regulated and controlled, and the acute alcoholic gastric ulcer is prevented by improving the intestinal flora composition of the alcoholic gastric ulcer. The application range of the mannatide is widened, and more solutions are provided for prevention or treatment of acute alcoholic gastric ulcer.

The invention relates to the technical field of biological medicine, in particular to application of selenium element in relieving hyperglycemia cerebral ischemia reperfusion injury, provides application of selenium element in relieving hyperglycemia cerebral ischemia reperfusion injury, and provides application of selenium element in relieving hyperglycemia cerebral ischemia reperfusion injury in relieving hyperglycemia cerebral ischemia reperfusion injury in relieving hyperglycemia cerebral ischemia reperfusion injury in relieving hyperglycemia cerebral ischemia reperfusion injury in relieving hyperglycemia cerebral ischemia reperfusion injury. According to the application of the cerebral ischemia-reperfusion injury relieving medicine for treating the cerebral ischemia-reperfusion injury, the mitochondrial division and fusion process is kept relatively balanced, and the activation of a mitochondrial apoptosis pathway is inhibited, so that the cerebral ischemia-reperfusion injury of a patient in the hyperglycemia state is relieved. Therefore, the cerebral ischemia reperfusion injury is aggravated; the selenium element can regulate and control a mitochondrial regeneration signal channel to improve the functions of mitochondria, so that the mitochondrial division and fusion processes are kept relatively balanced, and the activation of a mitochondrial apoptosis channel is inhibited, so that the cerebral ischemia reperfusion injury of a patient in a hyperglycemia state is relieved.

The invention relates to application of MEIS1 in preparation of an endometriosis therapeutic agent and the therapeutic agent prepared by the MEIS1. According to the invention, the influence of MEIS1 on an endometrial stromal cell apoptosis pathway is studied, endometrial stromal cell apoptosis is induced by overexpression of MEIS1 in endometrial stromal cells, and an MEIS1 lentivirus overexpression vector is used for administration to an endometriosis mouse model, so that the size and weight of a mouse endometriosis focus are remarkably reduced, and the application of MEIS1 in the endometriosis mouse model is realized. Liver and kidney biochemical indexes show that the LV-MEIS1 does not damage main organ functions and brings a new potential hope for treatment of endometriosis.

The invention discloses a probe BBM for anchoring OPA1 protein and application of the probe BBM, and belongs to the technical field of biological analysis. Based on the characteristic that the OPA1 protein is rich in hydrophobic amino acid residues and polar amino acids, the probe BBM capable of generating multiple interaction forces with the OPA1 protein is designed by reasonably introducing hydrophobic groups and polar groups. Theoretical calculation and experimental results (including OPA1 knock-down and overexpression) show that the probe realizes efficient enrichment in a mitochondrial inner membrane region. By using the unique probe, the hydrogen peroxide induced mitochondrial inner membrane viscosity change is systematically researched, and the myocardial cell oxidative damage is further confirmed to be realized by a p53 protein mediated apoptosis pathway. The method provides a reliable means for accurately evaluating the oxidative stress of the mitochondrial inner membrane, and has important promotion significance for the development of the cardiovascular research field.

The invention discloses a novel application of total glucosides of paeony in preparation of a medicine for treating triple negative breast cancer. In-vitro and in-vivo experiments prove that the total glucosides of paeony can remarkably inhibit proliferation, migration and invasion of triple negative breast cancer cells (MDA-MB-231 and MDA-MB-468), reverse an epithelial-mesenchymal transition process and induce cell apoptosis by inducing mitochondrial injury, inhibiting oxidative phosphorylation and activating a mitochondrial apoptosis pathway. In an MDA-MB-231 cell xenotransplantation tumor nude mouse model, the total glucosides of paeony can effectively inhibit tumor growth. Therefore, the total glucosides of paeony can be used for preparing the medicine for treating the triple negative breast cancer, and a new treatment choice is provided for clinic.

The invention discloses application of pyruvic acid in regulation and control of follicular development of mammals. According to the invention, pyruvic acid is taken as a research object, and the influence of pyruvic acid on oestrus day age, follicle development and granular cell proliferation and apoptosis of mammals is researched by adopting molecular and cell biology methods: HE staining and Tunel staining find that the pyruvic acid significantly increases the number of corpus luteum and luteum follicles and reduces the apoptosis of granular cells; qRT-PCR and WB results show that the mRNA and protein levels of the key genes of the proliferation pathway are up-regulated after pyruvic acid treatment and the mRNA and protein levels of the key genes of the apoptosis pathway are down-regulated after pyruvic acid treatment. In conclusion, pyruvic acid can promote the development of ovarian follicles by promoting granular cell proliferation and inhibiting granular cell apoptosis, so as to promote mouse oestrus.

The invention belongs to the technical field of medicines, and particularly discloses an oral squamous cell carcinoma inhibitor and application thereof. The inhibitor takes rutin as an active component. In-vitro experiments prove that rutin can significantly inhibit proliferation, clone formation, migration and invasion ability of OSCC cells in a dose-dependent manner, and effectively induce cell apoptosis. The action mechanism of the rutin is as follows: the rutin can directly target STAT3 protein and inhibit phosphorylation of the STAT3 protein so as to regulate and control a downstream BCL2 / CASP3 apoptosis pathway, thereby playing a role in treating OSCC. Molecular docking results further show that rutin and STAT3 have strong binding capacity. The invention discloses a new application of rutin as an STAT3 inhibitor in treating oral squamous cell carcinoma, and provides a new strategy and a candidate compound for developing high-efficiency and low-toxicity OSCC treatment medicines.

The invention discloses an application of Lumacaftor in the treatment of Parkinson's disease. The treatment effect of Lumacaftor on PD is verified through in-vitro cell experiments and in-vivo animal experiments respectively, and it is found that after Lumacaftor is used in a microglial cell-neuron co-culture PD cell model, apoptosis pathway related protein in neurons is remarkably reduced compared with a model group; after Lumacaftor treatment is performed on a PD mouse in an MPTP mouse PD model, dopaminergic neurons of the PD mouse are remarkably increased, and the motor function is improved. The application provides a new thought for effective treatment of PD, and the application prospect is wide.

The invention discloses a construction method of a nano composite material based on a zinc-based cystine coordination polymer and application of the nano composite material in anti-tumor treatment, and belongs to the technical field of composite medical materials. The preparation method comprises the following steps: preparing polydopamine coated curcumin-gelatin drug nanocrystals (Cur-coated PDA DNCs) so as to enhance the stability and modifiability of the polydopamine coated curcumin-gelatin drug nanocrystals; furthermore, the Cur (at) PDA DNCs, glucose oxidase (GOx) and a metal amino acid coordination polymer (Zn-Cys) are mixed, and the Cur (at) PDA (at) GOx / Zn-Cys composite nanomaterial (CPGZC NPs) is prepared through an in-situ growth method. The design of the whole composite material treatment system gives full play to the synergistic effect of all parts of the material, and effective compounding of multiple components is achieved. The nano composite material disclosed by the invention has the advantages that the cancer cell killing effect is obviously improved by activating cancer cell disulfide death and cell apoptosis pathways in vitro; furthermore, the compound also has an excellent anti-tumor effect in a mouse body, and has relatively high biological safety.

The invention discloses application of an NLRP3 inhibitor in preparation of a medicine for treating biliary atresia. The NLRP3 inhibitor can selectively inhibit inflammasome NLRP3 generated due to activation of an abnormal universal apoptosis pathway, further inhibits a proinflammatory factor product IL-1beta, effectively relieves formation of biliary duct atresia of BA mice, reduces the jaundice rate, and improves the body weight and the survival rate.

The invention discloses an application of pelteobagrus fulvidraco lncRNA (long non-coding RNA) in regulation and control of miR-21-y and / or a gene DAPK2, the pelteobagrus fulvidraco lncRNA is lnc432, and the Gene ID (Identity) of the pelteobagrus fulvidraco lncRNA is 125146191. The lnc432 disclosed by the invention can be used as ceRNA to be combined with miR-21-y in a targeted manner so as to regulate and control the expression of DAPK2. Under the low-oxygen condition, when the expression quantity of lnc432 is increased, bacterial infection of pelteobagrus fulvidraco can be remarkably inhibited, the immunity of fish is improved by regulating and controlling the mitochondrial apoptosis pathway and inflammatory response, and finally the antibacterial effect under the low-oxygen condition is affected.

The present invention relates to a butylphthalide dimer and a preparation method and application thereof, and the structural formula thereof is as follows: The present invention isolates butylphthalide dimer enantiomers from Lycopodiella vulgaris. The neuroprotective effect of the compound of the present invention is evaluated in a glutamate-induced neuronal cell HT-22 injury model. In particular, (-)-(6S,7R,6'R,7'S)-lycocasuarolide B(-)-2 exhibits significant neuroprotective activity in the model. At concentrations of 5μM, 10μM, 15μM, and 20μM, the cell survival rates are increased by 29.3%, 25.45%, 21.96%, and 21.57%, respectively, which is equivalent to the activity of the positive control drug 3-n-Butylphthalide. Compound (-)-2 can alleviate glutamate-induced neuronal cell death by inhibiting the apoptosis pathway.

The application discloses application of NDUFB4 as a target point in preparation of a drug for treating bladder cancer. Single cell analysis results show that NDUFB4 is highly enriched in bladder cancer epithelial cells, and can be used as a key coordinator to participate in the regulation of multiple carcinogenic signal pathways. Through shRNA-mediated gene silencing and CRISPR / Cas9-mediated gene knockout experiments, it is found that NDUFB4 deletion can significantly inhibit the proliferation, migration and invasion ability of bladder cancer cells, and cause a serious bioenergy crisis, and activate the endogenous apoptosis pathway. In a subcutaneous xenotransplant tumor model, it is further verified that NDUFB4 silencing can significantly inhibit tumor growth. The application discloses that NDUFB4 is a key coordinator between mitochondrial high-functionality and carcinogenic signal pathways, and it is suggested that NDUFB4 can become a potential target for bladder cancer treatment.

Provided are biomarkers for predicting the efficacy of an MDM2 inhibitor or a Bcl-2 / Bcl-xL dual inhibitor or a Bcl-2 inhibitor or a Bcl-xL inhibitor in treating a cancer patient. Also provided are compositions, e.g., kits, for assessing gene levels of the biomarkers, and methods of using such gene levels to predict the response of a cancer patient to an MDM2 inhibitor or a Bcl-2 / Bcl-xL dual inhibitor or a Bcl-2 inhibitor or a Bcl-xL inhibitor. Such information can be used to determine the prognosis and treatment selection of a cancer patient.

The present invention includes methods for treating a proliferative disorder comprising administering a therapeutically effective amount of crenolanib or a salt thereof in combination with pharmaceutical agent targeting apoptosis pathway proteins wherein the crenolanib and other agent are provided at least one of sequentially or concomitantly in a subject for use in the treatment of the proliferative disease, wherein the subject is a human subject.

The invention provides nanoparticles for tumor photodynamic therapy and a preparation method, a pharmaceutical composition and application thereof, and belongs to the technical field of nano biomedicine. The nanoparticle for tumor photodynamic therapy comprises: an up-conversion nanoparticle; the phospholipid layer is used for coating the up-conversion nano-particles; the nucleic acid aptamer and the endoplasmic reticulum targeting peptide are modified on the surface of the phospholipid layer; and a photosensitizer supported on the surface of the nanoparticle. The nucleic acid aptamer and the endoplasmic reticulum targeting peptide are further co-modified on the basis of the surface of the upconversion nano-particle subjected to phospholipidation treatment, so that the nano-particle can actively recognize tumor cells and deliver the tumor cells to the endoplasmic reticulum, and dual targeting on the tumor cells is realized. The loaded photosensitizer can generate reactive oxygen species (ROS) under excitation of near-infrared light, endoplasmic reticulum stress is specifically induced, then a cell apoptosis pathway is activated, and tumor cells are killed.

The invention provides application of a preparation for activating RIPKs / MLKL mediated necroptosis signal transduction in preparation of a medicine for reversing taxol drug resistance of ovarian cancer, and belongs to the technical field of biological medicine. It is found for the first time that disulfiram (DSF) can reverse ovarian cancer paclitaxel drug resistance and enhance sensitivity of ovarian cancer paclitaxel drug-resistant cells to paclitaxel. A further research discovers that the DSF is used for enhancing RIPKs / MLKL mediated necroptosis signal transduction by combining an apoptosis-inducing factor (AIF), and finally, the chemosensitivity of the paclitaxel drug-resistant ovarian cancer cells is enhanced through a caspase-dependent apoptosis pathway. The invention deeply studies an ovarian cancer paclitaxel drug resistance mechanism, discovers a new application of DSF in reversing ovarian cancer paclitaxel drug resistance, and provides a new choice for treating paclitaxel drug-resistant ovarian cancer.

The invention discloses application of salvianolic acid C in preparation of a medicine for preventing and / or treating retinal ischemia hypoxic nerve injury diseases, and relates to the technical field of biological medicines. The invention proposes and verifies for the first time that salvianolic acid C can significantly promote the formation of stress particles in photoreceptor cells under retinal ischemia and hypoxia conditions, and drives the salvianolic acid C to be assembled into a stress particle-mitochondrial micro-region in a mitochondrial adjacent region. The microcell is enriched in DDX3X, LARP1 and other key RNA binding proteins and multiple mitochondrial related proteins to cooperatively maintain mitochondrial membrane potential, inhibit mPTP opening and reduce ROS generation, so that an endogenous apoptosis pathway is inhibited, and the neuroprotective effect on a photoreceptor is achieved. On the basis, the salvianolic acid C is used for preparing the medicine for preventing and / or treating the retinal ischemia hypoxia nerve injury disease, can be used as a nerve protection supplement for existing anti-VEGF treatment, and has innovativeness and application value.

The invention discloses a screening method and application of activity and effective components of Duliang soft capsules for treating Parkinson's disease, and relates to the technical field of medicines. The method comprises the following steps: firstly, measuring the contents of nine chemical components of the Duliang soft capsule by using a high performance liquid chromatography; the method comprises the following steps: constructing an in-vitro Parkinson's disease model by utilizing MPTP to induce SH-SY5Y cell injury, determining proper modeling and administration concentrations, and screening out components with neuroprotective effects such as SENA and ISO; the research on pharmacokinetics and tissue distribution of the six chemical components in the Duliang soft capsule finds that the components are low in metabolism and distribution speed in a rat body, can penetrate through a blood brain barrier and are widely distributed in various tissues; six components contained in DL are proved to have a remarkable curative effect on PD, and the action mechanism of the six components is related to regulation and control of mitochondrial Bcl-2 and Bax cell apoptosis pathways. The screening method is comprehensive and systematic, provides an active ingredient basis for treatment of Parkinson's disease by the Duliang soft capsule, is beneficial to deep research on the treatment mechanism of the Duliang soft capsule, and promotes research and development of novel anti-Parkinson's disease drugs.

The invention belongs to the technical field of pharmaceutical compositions for removing senescent cells, and discloses a pharmaceutical composition for removing senescent cells and a preparation method and application thereof, and the pharmaceutical composition for removing senescent cells contains NK cells and fisetin. According to the pharmaceutical composition for removing senescent cells, the fisetin and the NK cells are combined for use, on one hand, the fisetin can enable the NK cells to easily recognize senescent cells; on the other hand, fisetin can relieve inhibition of SASP factors on NK cell activity, enough amount of cytotoxic particles such as perforin and granzyme are synthesized and released in NK cells, the killing efficiency on senescent cells is high, fisetin can directly trigger an apoptosis pathway of the senescent cells, and the effect of killing the senescent cells is achieved. The NK cells release cytotoxic particles to further accelerate death of the senescent cells, and fisetin and the NK cells have a synergistic effect, so that the senescent cell clearing efficiency is high.

The invention relates to the technical field of medical biology, in particular to application of Skepinone-L in killing neuroblastoma cells, and finds that the Skepinone-L can specifically kill the neuroblastoma cells and significantly inhibit proliferation, migration and clone formation capabilities of the neuroblastoma cells for the first time. An action mechanism research shows that the Skepinone-L accurately targets ubiquitin specific protease 7, and is combined with a key residue through a hydrogen bond to down-regulate USP7 expression and activate a downstream apoptosis pathway. Molecular dynamics simulation proves that the compound is high in stability. The invention provides a new candidate drug with high efficiency and low toxicity for neuroblastoma, and has remarkable clinical transformation potential.

The invention discloses application of TAB2 in diagnosis and treatment of Parkinson's disease. According to the present invention, the PD patient midbrain single cell data set analysis results show that the microglial cells are significantly increased, and the Bulk transcriptome data is combined to screen the microglial cell differential gene TAB2; after TAB2 is knocked down in PD animal and cell models, apoptosis pathway related proteins in neurons are significantly reduced compared with a model group, and the motor function of PD mice is improved. Therefore, the TAB2 has a good effect of blocking the progress of the PD, and a new direction is provided for effective diagnosis and timely treatment of the Parkinson's disease.

The application provides a semi-florin chemotherapy drug and a synthesis method thereof, relates to the technical field of drug synthesis, and the semi-florin derivative exhibits significant selective anti-tumor activity, and the mechanism of action is that after entering tumor cells, the semi-florin derivative can induce the increase of the level of reactive oxygen species (ROS) in the cells, causes the collapse of the mitochondrial membrane potential, and finally triggers the late apoptosis pathway of the cells.

This invention relates to the application of FUNDC1 inhibitors in the preparation of drugs for preventing and treating photodamage to the skin. Specifically, FUNDC1 inhibitors alleviate, reduce, or prevent photodamage by inhibiting or reducing FUNDC1 expression. This invention establishes a photodamage model using mouse skin and HaCaT cells irradiated with UVB. UVB treatment showed downregulation of FUNDC1 expression. Given that FUNDC1 overexpression exacerbates UVB-induced photodamage, this invention explores whether knocking down FUNDC1 can protect HaCaT cells and the mouse model from UVB-induced photodamage. After FUNDC1 knockdown, cell viability increased to 80%, and compared to the UVB group, ROS levels, apoptosis, and γH2Ax expression were reduced. Following UVB irradiation, FUNDC1 knockdown also alleviated mitochondrial damage, manifested as uniform mitochondrial distribution along the cell nucleus, mitochondrial membrane potential repolarization, and reduced mtROS accumulation. This invention proposes that intervening in FUNDC1-mediated mitophagy, by regulating the mitochondrial apoptosis pathway, can protect against UVB-induced mitochondrial and photodamage, providing a potential target for future mitigation of photodamage to the skin.

Compositions and methods are provided for isolating, manipulating and using for therapeutic and other purposes, mammalian, MHC Class I restricted, antigen-specific regulatory T cells. The regulatory T cells can be characterized as CD8+ cells that specifically suppress the responses of self-reactive and / or pathogenic CD4+ T cells by cytotoxic mechanisms including, without limitation, perforin, other components of the perforin / granzyme apoptosis pathway, etc. The regulatory T cells are antigen-specific, but are not activated by the same antigen as the self-reactive and / or pathogenic CD4+ T cells. In humans the regulatory T cells express inhibitory KIR proteins, e.g. one or more of KIR2DL2, KIR2DL3, and KIR3DL1.

The invention discloses application of phascolosoma esculenta-sourced oligopeptide and 5-FU in preparation of a medicine for resisting colorectal cancer, and belongs to the technical field of biological medicine. The oligopeptide is separated from a phascolosoma esculenta body, and tests prove that when the small-molecule oligopeptide and 5-FU are jointly applied at high concentration, colon cancer cell proliferation can be remarkably inhibited, and a dose-dependent synergistic effect is achieved. Oligopeptide 659 and 5-FU synergistically activate a mitochondrial apoptosis pathway, and combined medication can enhance gamma-H2AX focus formation and aggravate DNA double-chain breakage, so that CRC cell proliferation is synergistically inhibited. DLD-1 cells are inoculated to NOD-SCID female mice for modeling, then in-vivo analysis is carried out on the anti-tumor effect of the peptide 659, and the effect of the oligopeptide 659 on resisting colorectal tumors is proved again. An analysis result after mouse dissection shows that compared with a control group, the oligopeptide 659 inhibits growth of mouse tumors.