No abstract available.
Apoptosis*

No abstract available.
Apoptosis

No abstract available.
Apoptosis* ; Carcinogenesis*

No abstract available.
Apoptosis* ; Hyperplasia*

No abstract available.
Apoptosis* ; Lung*

Like every biological body, the cells under 4 phases: generation growth, development and end. There are 2 ways of the end of cell: necrosis death or apoptosis. The apoptosis related with some diseases that these disorders may be etiological mechanism of diseases. Today, the etiological mechenism of apoptosis has been discovered. The ways of inhibition or stimulation of this process in diseases of increased apoptosis are being studied.
Apoptosis ; cells

Mitochondrion is a multifunctional organelle in cells and responsible for energy production, cell apoptosis and various life processes. Dysfunctional mitochondria are associated with hundreds of diseases. Increasing evidences have shown that extracellular mitochondria can be endocytosed by cells, directly into cells, and then play roles in cells. Mitochondria are the organelles that are extremely sensitive to oxygen content and pH of microenvironment that induces the adverse effect based on the cellular environment: mitochondria will increase cell survival and viability when they arrive in cells of physiological environment, but mitochondria will cause cell death when they enter the hypoxic and acidic tumor tissues, because they can produce a large amounts of oxygen free radicals. The pharmacological feature of environmental responsiveness of mitochondria could make them as a potential biological drug to kill cancer cells and restore the function of damaged tissues. Currently, mitochondria are used in the treatment of central nervous system diseases (Parkinson's disease, depression, schizophrenia, etc.), peripheral system diseases (ischemic myocardial injury, fatty liver, emphysema, etc.) and tumor. In this review, we summarize the research progress, medical application and challenges of mitochondrial therapy.
Apoptosis ; Mitochondria

No abstract available.
Apoptosis* ; Diphosphonates*

No abstract available.
Apoptosis* ; Osteoarthritis*

OBJECTIVE: To investigate the effects of quercetin on the apoptosis of platelets and to analyze the intrinsic mechanism. METHODS: Firstly, the effects of quecetin on the apoptosis of platelets was detected by flow cytometry. Secondly, Western blot was used to detect the expression of apoptosis-related proteins in the platelets treated with quercetin for 2 and 4 day. RESULTS: By flow cytometry, it was found that the apoptosis of platelets in the quercetin-treated group (2, 4 and 8 μmol/L) was inhibited, the apoptosis rate of platelets in 2, 4 and 8 μmol/L quercetin group was 3.12%±0.32%, 2.89%±0.15% and 2.31%±0.28%, respectively, which were signigicantly lover than that in control group (P＜0.01). With the increase of quecetin concentration, the proportion ratio of platelets significantly decreased in a concentration-dependent manner（r=-0.9985）. Similar results were observed on the 4th day. Western blot showed that the treatment with quercetin (2, 4 and 8 μmol/L) promoted the expression of anti-apoptotic protein BCL-2, inhibited the expression of pro-apoptotic protein BAX, resulting in a significant increase in the ratio of BCL-2/BAX (P＜0.01), thereby inhibiting the apoptosis of platelets. Similar results were observed on the 4th day. CONCLUSION Quercetin can inhibit platelet apoptosis by increasing the ratio of apoptosis-related protein BCL-2/BAX in a concentration-dependent manner.
Apoptosis ; Apoptosis Regulatory Proteins ; Blood Platelets ; Quercetin