208 results about "Autophagic death" patented technology

This invention relates to: a novel use of GST-π and GST-π suppressing agents; an apoptosis-inducing agent containing as active components a drug that suppresses GST-π and a drug that suppresses autophagy; a medical composition containing said agent; and a method using said medical composition for treating diseases associated with abnormal apoptosis.

Provided are assays useful for detecting and monitoring autophagy and phospholipidosis, including the progression of lysosomal storage diseases. Drugs and treatments for lysosomal storage diseases can be monitored for effectiveness in lysosomal storage disease conditions. Drug candidates and suspected toxic agents can also be screened for toxicity to cells, tissues and organs. Also provided are methods for distinguishing between phospholipidosis activators and autophagy pathway perturbation agents.

The invention belongs to the field of medicine and biotechnology, and relates to a synergistic drug compound for treating tumors and a preparation method thereof. The drug compound is composed of one or more cell autophagy inhibitors and arginase, especially human recombinant Arginase is made into a synergistic drug compound for treating tumors, and the synergistic drug compound can inhibit autophagy by inhibiting autophagy through autophagy inhibitors to increase tumor cells' ability to arginase. sensitivity, and enhance the therapeutic effect of arginase, especially human recombinant arginase, on tumors, especially triple-negative breast cancer cells. The drug compound of the present invention can be used for clinical treatment of breast cancer, melanoma, lung cancer, brain tumor, lymphoma, leukemia and myeloma.

The invention relates to a nano-silver combined autophagy inhibitor capable of killing and damaging tumor, and particularly relates to applications of a nano-silver combined autophagy inhibitor and/or a reagent for knocking down/knocking out autophagy related gene expression on preparation of an anti-tumor medicament, and applications of the autophagy inhibitor and/or the reagent for knocking down/knocking out autophagy related gene expression on promotion of nano silver to kill and damage tumor cells.

The invention belongs to the biomedicine field, and aims at providing an expression vector for stably indicating cell autophagy activities, an establishing method and an application method thereof. By constructing a slow-virus expression plasmid containing an EGFP-LC3 autophagy reporter gene and adopting a four-plasmid system, the invention establishes a slow-virus expression vector capable of enabling cells to stably express an EGFP-LC3 gene. By using the expression vector to infect a host cell, the EGFP-LC3 gene can be stably integrated in a genome of the host cell, and the host cell can stably and efficiently express the EGFP-LC3 and indicate cell autophagy changes. A stable autophagy indicating cell can be established by using the expression vector, and the cell autophagy changes are quickly and quantitatively analyzed by an image analysis method based on Top-hat operators and morphological filtration. The invention has the characteristics of stable and reliable autophagy indication, real-time sensitivity, quick and accurate autophagy quantification, simply and convenient operation and the like, greatly facilitates autophagy observation and analysis, and can be widely used for autophagy-correlated researches.

The invention relates to the novel usage of an antimalarial medicine, in particular to the novel usage of hydroxychloroquine having sensitivity enhancing effect on various chemical anti-multiple myeloma medicaments. The novel usage is characterized in the application of hydroxychloroquine in treatment of multiple myeloma through chemotherapeutic medicaments. The hydroxychloroquine can obviously enhance the killing activity of chemotherapeutic medicines such as doxorubicine, epidoxorubicin, cis-platinum and mitoxantrone to multiple myeloma cells, and the killing activity thereof is realized by inhibiting the myeloma cell autophagy signals by hydroxychloroquine. Hydroxychloroquine can induce the quantity of the autophagy lysosomes of the multiple myeloma cells to be increased and the expression of the autophagy-associated albumen LC3-II to be increased.

The invention relates to application of GMFB (glia maturation factor beta) as a biomarker for early diagnosis of diabetic retinopathy and for diabetes progression, application of GMFB as a therapeutic target of diabetic retinopathy, a GMFB disrupter and application of the GMFB disrupter. Compared with the prior art, the invention proves that the GMFB content in vitreous body is significantly improved in early period of diabetes in rats of STZ-induced I type diabetes (TIDM). The invention is the first to prove that GMFB content gradually drops with the development of DR (diabetic retinopathy), therefore the GMFB is applicable to dynamic detection of DR progress; the invention is the first to prove that by interfering GMFB expression in rats of DR, visual function can be protected; and the invention is the first to prove that GMFB mediates retinopathy mechanism, including causing decrease of glutamine synthetase of Muller cell, death of ganglion cells and inducing autophagy of photoreceptor cells.

The invention discloses an expression method of Beclin1 and MAP1-LC3 (microtubule-associated protein 1-light chain 3) in steroid-induced avascular necrosis of femoral head of a rabbit, detection of a bone cell apoptosis index of a femoral head tissue of a rabbit SANFH (steroid-induced avascular necrosis of femoral head) model and the MAP1-LC3 expression shows that autophagy-related gene Beclin1 can regulate autophagy activity and also can selectively combine with family members of Bcl-2 (B-cell lymphoma-2) to regulate the cell apoptosis activity. By detection of the expression of the Beclin1 in the SANFH model, the expression method provides a new molecular target for treatment of SANFH. The expression method is simple and convenient in operation, better solves the problem that no study on cell apoptosis and autophagy expression and mutual relation thereof in the SANFH model is found at home and abroad, and fills the blank of the study on cell apoptosis and autophagy expression and the mutual relation thereof in an ANFH (avascular necrosis of femoral head) model.

The invention relates to a preparation method of an autophagy-imitated immune cell supported antitumor therapeutic agent. The preparation method comprises steps as follows: an antitumor therapeutic agent, cell membranes and immune cells are taken as raw materials, immune cell membranes are extracted to encapsulate the antitumor therapeutic agent, nano-particles containing apoptosis groups are co-cultured with the immune cells after being formed, the nano-particles are phagocytized by the immune cells, the antitumor therapeutic agent is enabled to be indirectly encapsulated into the immune cells, and the autophagy-imitated immune cell supported antitumor therapeutic agent is prepared. Compared with the prior art, the antitumor therapeutic agent is encapsulated with the cell membranes containing the apoptosis groups, the phagocytosis quantity of the antitumor therapeutic agent by the immune cells is increased, cell carriers meeting various demands are prepared, the problems of irregularrelease and low phagocytosis quantity of the therapeutic agent due to adoption of a traditional supporting method are solved, and meanwhile, toxicity of drugs for the cell carriers is reduced.

The invention discloses application of timosaponin AIII in anemarrhena to preparation of antitumor drugs, which belongs to the field of pharmacology. Pharmacological experiments prove that timosaponin AIII has broad-spectrum strong antineoplastic activity, especially strong and stable cytotoxicity on T475-S2 cells; timosaponin AIII has stronger capacity in killing T475-S2 cells compared with 5-Fu and paclitaxel; the IC50 value of timosaponin AIII is 6.97 +- 0.72 mu M after 24 h, the concentration of used timosaponin AIII is 6 mu M, timosaponin AIII can induce apoptosis and autophagy of T475-S2 cells, the effect of apoptosis is dominating, so timosaponin AIII can be used for preparing drugs for preventing and treating tumors.

The invention discloses application of 4-benzothiopheneaminoquinazoline derivative and salt thereof in preparing tumor treatment medicine. The in vitro and in vivo activities of the 4-benzothiopheneaminoquinazoline derivative are evaluated; and the derivative kills tumor cells by means of inducing tumor cell apoptosis and autophagy to inhibit the growth of tumor cells and provide the application in preparing medicaments for treating cancers, especially pancreatic cancer, prostate cancer, lung cancer or breast cancer. In the invention, the action mechanism and the action target of the 4-benzothiopheneaminoquinazoline derivative are studied, and the derivative has stronger inhibitory activity to a plurality of receptortyrosinekinases and provides the application of acting as an inhibitor of receptortyrosinekinase, especially polyreceptortyrosinekinase.

Provided are methods and pharmaceutical combinations utilizing a phospholipase A2 inhibitor for the inhibition of treatment-induced autophagy.

The invention provides application of sinomenine to preparation of a medicament for treating human brain glioma. As proved by experiments, the sinomenine has a function of restraining human-derived glioma U87MG and SF767 cell strains, and the function is improved along with the increase of dose and time. Moreover, the sinomenine can induce the increase of autophagosomes, increase the quantity of autophagic vesicles, prompt the expression increase of human glioma cells LC3B-II, induce autophagic death of human glioma cells, and restrain the growth of U87MG cell xenograft tumors. The sinomenine is a novel and effective glioma-resisting medicament with a great potential, and can be used for preparing a human brain glioma medicament; by adopting the sinomenine, a new way is created for medical treatment of human brain glioma, and the medical application of the sinomenine is expanded.