44results about How to "Inhibit autophagy" patented technology

A method for inhibiting the autophagy of motor neurons in a subject is provided. The method comprises administrating to the subject an effective amount of an active ingredient selected from the group consisting of a compound of formula (I), a pharmaceutically acceptable salt of the compound, a pharmaceutically acceptable ester of the compound and combinations thereof:

wherein A is a C1-C5 alkyl optionally having one or more unsaturated bonds and optionally being substituted by one or more substituents selected from a group consisting of —OH, ═O and C1-C3 alkyl; X is H, —OH,

Y is O or S and can optionally combine with A to form a five-membered ring; and R₁ is H or a substituted or unsubstituted C1-C20 alkyl, wherein one or more —CH₂— of the C1-C20 alkyl are optionally being replaced by —NH— or —O—.

Belonging to the field of medicine preparation, the invention in particular relates to application of berberine in preparation of drugs inhibiting subcutaneous adipose and visceral adipose cell autophagy. The invention takes high fat fed mice as experimental objects to test whether berberine inhibits autophagy of subcutaneous adipose and visceral adipose cells of the mice. Specifically, the process includes: feeding C57BL/6 mice with high fat for 12 weeks, then dividing the mice into a high fat group and a berberine group, continuing the high fat diet and berberine gavage once a day for 4 weeks, using Western Blot to detect the change of autophagy related protein, and using Real-time PCR to detect the change of the corresponding mRNA level. Results show that: under high fat feeding, subcutaneous and visceral adipose tissue autophagy increases, and berberine could effectively inhibit subcutaneous adipose and visceral adipose autophagy of the high fat fed mice, thus providing the experimental data and theoretical basis for more reasonable application of berberine in treatment of obesity clinically.

The invention provides a nano-medicine, a preparation method thereof and an application of the nano-medicine. The nano-medicine comprises a calcium phosphate substrate, a chemotherapy medicine, a photo-thermal agent and an autophagy inhibitor, the chemotherapy medicine is sealed in the calcium phosphate substrate, the surface of the calcium phosphate substrate is modified by the photo-thermal agent, and the autophagy inhibitor is loaded into a pore of the photo-thermal agent. According to the nano-medicine, chemotherapy and thermotherapy are combined, calcium phosphate serves as a rigid substrate, the chemotherapy medicine and the photo-thermal agent are sealed in the rigid substrate of the calcium phosphate, the autophagy inhibitor of a cell is loaded on the rigid substrate, so that chemotherapy and thermotherapy effects can be improved by inhibiting autophagy, and tumor treatment effects are improved.

The invention discloses new use of a 3, 4-broken cycloartane type triterpenoid compound. The compound is nigranoic acid or kadsuric acid, and is used in preparation of autophagy inhibitors and preparation of drugs for increasing the treatmnet sensitivity of anti-tumor drugs. The compound can be used for inhibiting ubiquitination modification of an autophagy receptor p62 and prevent activation of ap62 autophagy receptor function, and can inhibit the protective autophagy of tumor cells induced by anti-tumor drugs. The invention also provides an anti-tumor pharmaceutical composition, which comprises the 3, 4-broken cycloartane triterpenoid compound and an anti-tumor drug capable of easily causing tumor cell protective autophagy, can inhibit tumor cell growth and promote tumor cell death, andcan be used for treating cancers such as breast cancer and the like.

Methods of treating autophagy related diseases, e.g. cancer and malaria, using novel autophagy inhibiting agents are described.

The invention belongs to the technical field of medicinal preparations with organic and effective components, and discloses a detection method for influences of micro RNA-138-5p on human pancreatic cancer cell apoptosis under hypoxia. After up-regulation of miR-138-5p mimics, autophagy-associated protein of western blot detection experimental groups is inhibited; pancreas tumor cell autophagic vacuoles of confocal microscopy examination experimental groups are increased. The apoptotic cell percentage plus the necrotic cell percentage and differences between the groups have remarkable significance, and expression of apoptosis-associated protein of the western blot detection experimental groups is regulated up. MiR-138-5p and SIRT1 3'UTR regions are complementarily combined to inhibit reduction of SIRT1 expression. The miR-138-5p plays an important role in autophagy fluxes under hypoxia of pancreatic cancer cells, expression of SIRT1 is regulated through direct targeting to inhibit hypoxia-induced autophagy, and apoptosis of the panc-1 pancreatic cancer cells is promoted at the same time.

The invention discloses application of tanshinone I in preparation of tumor cell autophagy inducer drugs. Compared with the prior art, the invention for the first time finds that tanshinone I can induce autophagy of tumor cells and has a remarkable treatment effect on cervical cancer, breast cancer or liver cancer, especially cervical cancer. Research proves that tanshinone I can inhibit cancer cell growth, inhibit cancer cell mitochondrial injury and autophagy, and induce the expression of tumor cell autophagy molecules and cutting of autophagy molecule LC3.

The invention discloses an application of an SGLT2 inhibitor to preparation of a product for improving sensitivity of an antitumor drug. The inventor finds that the SGLT2 inhibitor Canagliflozin can inhibit the autophagy phenomenon of stress protection generated by tumor cells during chemotherapeutic drug treatment by inhibiting the expression and functions of P-glycoprotein in the tumor cells, sothat the sensitivity of the tumor cells to chemotherapeutic drugs is improved, and the treatment effect of the drug is enhanced. The inhibitor of the type can exist in the form of liquid, dry powderor extract, can be made into capsules, tablets, injections, pills, granules, powder and other various dosage forms with health-care or medicinal effects together with various conventional auxiliary materials, and can be combined with other chemotherapeutic drugs to be used for treating malignant tumors.

The invention discloses an application of ICTF (trifluoro-icaritin) to preparation of a drug for activating Akt signals and inhibiting autophagy. When ICTF is applied to a drug for treating cardiovascular diseases, it is proved that ICTF can relieve ischemia reperfusion-induced EGG damage, reduce myocardial oxidative stress of ischemia reperfusion injury, inhibit autophagy and apoptosis of myocardial cells, improve activation of the Akt signals and reduce levels of autophagy markers Beclin-1 and LC3-II. The drug for treating the cardiovascular diseases has development prospect and is especially used for treating myocardial ischemia (myocardial infarction) reperfusion injury.

The invention discloses novel medical application of tizoxanide and/or nitazoxanide and a pharmaceutically acceptable salt thereof, namely application of tizoxanide and/or nitazoxanide in the preparation of an autophagy inducer and application of drugs for treating and inhibiting diseases related to mTOR expression. According to the application, the tizoxanide and/or nitazoxanide and the pharmaceutically acceptable salt thereof can achieve related medicine effects by reducing PI3K and AKT protein phosphorylation and reducing ERK protein phosphorylation, the autophagy inhibition function in cells is reduced accordingly, and the cells are induced to achieve autophagy.

The invention discloses a medicine for treating erectile dysfunction and application thereof. The medicine for treating the erectile dysfunction comprises an inhibitor of a Wnt signal channel. The invention finds that the Wnt signal channel is a key channel activated by the fibroblast for the first time, and proves that the inhibitor using the Wnt signal channel can obviously inhibit the expression of collagen in the fibroblast derived from the cavernosum so as to inhibit the fibrosis of the penis cavernosum; therefore, the inhibitor of the Wnt signal channel has the potential of serving as the medicine for treating the erectile dysfunction, and a new thought is provided for developing the medicine for treating the erectile dysfunction.

The invention discloses an application of seneciphylline in preparation of antitumor medicines. The seneciphylline can inhibit HeLa cell proliferation and induce HeLa cell autophagy in a dose dependent and a time dependent manner. In addition, the seneciphylline inducing the HeLa cell autophagy is depended on activation of MEK/ERK1/2 pathway. The invention provides a novel treatment medicine of treating human cervical cancer.

The invention relates to application of a curcumin analogue CD35 to preparation of a medicine for treating breast cancer. A chemical formula of the curcumin analogue CD35 is 1-(4-hydroxy-3-methoxyphenyl)-5-(2-nitrophenyl)-1,4-pentadiene-3-one, and a structural formula is shown in the description; the curcumin analogue CD35 is used for down-regulating the expression of YAP proteins in a Hippo path to inhibit the autophagy of breast cancer cells, so as to inhibit the energy metabolism of the breast cancer cells. The curcumin analogue CD35 provided by the invention has remarkable advantages of improving the targeting ability of the medicine for treating the breast cancer and reducing the toxic and side effects of the medicine.

The invention discloses an application of Abemaciclib in preparation of a medicine for treating NAFLD. After the Abemaciclib is administered to a C57BL/6 mouse by intragastric administration for 2 weeks, histopathology and serum biochemical results show that the Abemaciclib can improve the liver lipidemia of the mouse and reduce the contents of serum ALT, AST and liver triglyceride. In-vitro experiment results show that the Abemaciclib can resist oxidative stress damage of cells through SESN2 and other mediated anti-oxidative stress pathways. In addition, our studies found that Abemaciclib caninduce HepG2 cells to form intracytoplasmic vacuoles similar to autophagy, presuming that Abemaciclib may improve NASH by inducing autophagy and inhibiting liver fibrosis.

The invention discloses a pharmaceutical composition capable of inhibiting acetylation of PINK1 of vascular endothelial cells, which is characterized in that astaxanthin is contained and also discloses the use of the pharmaceutical composition in the preparation of medicaments for preventing and/or treating cardiovascular diseases including, but not limited to, atherosclerosis, coronary heart disease, angina pectoris, cerebral thrombosis, hypertension, hyperglycemia, hyperlipidemia, myocardial infarction, ischemic cor pulmonale and the like.

The invention relates to a platinum-copper alloy/chloride ion transporter composite tumor treatment preparation and a preparation method and application thereof. The preparation method comprises the step that a chloride ion transporter is loaded to the surfaces of platinum-copper alloy nanoparticles through the electrostatic interaction. The preparation has the advantages of being good in controllability, small in side effect and the like, and the efficient tumor treatment effect can be achieved.