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Cellular oncosis is an important non-apoptosis mode of cell death characterized by cell swelling and karyolysis. Studies have indicated that cellular oncosis is involved in the progress of tumor and cardiovascular diseases as well as other diseases. The selection of appropriate detection method is the key to the study of cellular oncosis. However, there is still no unified standard of detection methods for cellular oncosis. Therefore, this paper summarizes the concept and characteristics of cellular oncosis, as well as principle, the advantages and disadvantages of existing detection methods, so as to provide reference for the selection of detection methods and promote the research on cellular oncosis.
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Objective To investigate the oncosis of skeletal muscle cells during heatstroke, and the mechanism severe heatstroke associated with rhabdomyolysis. Methods The human skeletal muscle cells (HSKMC) were divided into control group and heat shock group. The control group was incubated at 37 ℃, 5% CO2 cell incubator, while the heat shock group was exposed at 43 ℃, 5% CO2 cell incubator for 2 hours, followed by incubating at 37 ℃, 5% CO2 cell incubator. At incubation point of 0, 6, 12, and 24 hours, the CCK-8 method was used to detect cell viability; the LDH method was used to detect cytotoxicity; the transmission electron microscope was used to detect cell ultrastructure changes; Annexin -FITC/PI double staining method was used to detect double-positive cell rate; Western blotting method was used to detect porimin and caspase-3 protein expression. Results Compared with the control group, HSKMC cell viability decreased with cytotoxicity increased at 0 h after rewarming in a time-dependent manner (P0.05). Conclusion Heat stroke-induced oncosis rather than apoptosis of skeletal muscle cells.
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Objective To observe the expression of glial fibrillary acidic protein ( GFAP), and the pathological and ultrastructnral changes of astrocytes in the CA1 subfield of the hippocampus following global cerebral ischemia and reperfusion, and to explore the neuroprotective mechanism of mild hypothermia. Methods Global cerebral ischemia was established in rats by a modified version of Pulsinelli's method. Ninety-six rats were divided into three groups including a sham-operated group, a normothermic ischemic reperfusion (IR) group and a hypothermic ischemic reperfusion (HIR) group. Each group had four subgroups which were sacrificed for 6, 12 or 24 hours, or 4 days after reperfusion (for each subgroup n = 8 ). Hematoxylin-eosin (HE) staining was used to observe morphological changes in neurons in the CA1 subfield of the hippocampus. TUNEL methods were used to detect apoptosis among those neurons. Immunohistochemical staining was used to detect the expression of GFAP in the CA1 subfield and the mechanism of astrocyte pathology. GFAP TUNEL double-labeled immunohistochemistry was used with both the shamoperated and experimental groups. Electron microscopy was also used to evaluate morphological changes in astrocytes 24 hours and 4 days after ischemia and reperfusion. Results Compared with the sham-operated group, expression of GFAP immunoreactive positive cells increased gradually in the CA1 subfield of the IR group rats. Compared with the IR group, expression of GFAP immunoreactive positive cells was significantly lower in the HIR group at all time points. Microscopic observation at the 4th day showed that some astrocytes in the CA1 subfield had died through oncosis. Conclusions Mild hypothermia can significantly decrease the expression of GFAP immunoreactive positive cells and the number of apoptotic neurons in the CA1 subfield of the hippocampus, minimize cell oedema and provide protection for neurons. Oncosis kills astrocytes following global cerebral ischemia and reperfusion.
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Objective To study the relationship between the oncosis of pancreatic acinar cells and activa-tion of macrophage in rat model of acute pancreatitis (AP). Methods The pancreatic acinar cells were isolated by two-step enzyme digestion, and then they were divided into control group, AP group and test group. Pancreatic acinar cells were cultured with caerulein in AP group, with caerulein and endothelin in test group, and with culture medium in control group. The oncesis rate of the pancreatic acinar cells was detected after acridine orange and ethidium bromide fluorescent staining. The supernatant was collected to detect the release of amylase and lactate dehydrogenase (LDH). The macrophages were cultured with 1 ml of supematant for 6 hours, and then the protein level of tumor necrosis factor-α (TNF-α) was measured by ELISA. Results Few oncotic pancreatic acinar cells were observed in the control group, and the levels of amylase and LDH secreted by pancreatic acinar cells and TNF-α secreted by macrophage were (1175±165)kU/L, (846±118)U/L and (36±5)μg/L, respectively. Oncotic pancreatic acinar cells were observed in AP group, and the levels of amylase, LDH and TNF-α were (7130±680) kU/L, (4262±626) U/L and (155±18) μg/L, respectively, which were significantly higher than those in control group (t = 5.184, 4.277, 3.665, P < 0.05). The levels of amylase, LDH and TNF-α were even higher in test group, and they were (9240±1177) kU/L, (6937±893)U/L and (268±35)μg/L, respectively, which were significantly higher than those in AP group (t = 2.251, 2.825, 2.843, P < 0.05). Conclusions The release of amylase was changed as the oncosis of pancreatic acinar cells occurred. The secretion of TNF-α was along with the degree of oncosis of pancreatic acinar cells. The results of the study indicate that a relationship exists among the inflammatory response of macrophage, the release of contents of pancreatic acinar cells and the oncosis of the pancreatic acinar cells.
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Oncosis is a special kind of non-apoptotic cell death mode. It is characterized by cellular swelling, organelle swelling, blebbingand increased membrane permeability. More and more attentions pay to the research of this field in recent years. The review discuss the recent advances of oncosis on pathological change, molecular mechanisms and detection approaches.
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We elucidated the effects of various components of ischemic medium on the outcome of simulated ischemia-reperfusion injury. Hypoxia for up to 12 hours induced neither apoptotic bodies nor LDH release. However, reoxygenation after 6 or 12 hours of hypoxia resulted in a marked LDH release along with morphological changes compatible with oncotic cell death. H9c2 cells were then subjected to 6 hours of simulated ischemia by exposing them to modified hypoxic glucose-free Krebs-Henseleit buffer. Lowered pH (pH 6.4) of simulated-ischemic buffer resulted in the generation of apoptotic bodies during ischemia, with no concomitant LDH release. The degree of reperfusion-induced LDH release was not affected by the pH of ischemic buffer. Removal of sodium bicarbonate from the simulated ischemic buffer markedly increased cellular damages during both the simulated ischemia and reperfusion. Addition of lactate to the simulated ischemic buffer increased apoptotic cell death during the simulated ischemia. Most importantly, concomitant acidosis and high lactate concentration in ischemic buffer augmented the reperfusion-induced oncotic cell death. These results confirmed the influences of acidosis, bicarbonate deprivation and lactate on the progression and outcome of the simulated ischemia-reperfusion, and also demonstrated that concomitant acidosis and high lactate concentration in simulated ischemic buffer contribute to the development of reperfusion injury.
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Acidosis , Hypoxia , Apoptosis , Cell Death , Hydrogen-Ion Concentration , Ischemia , Lactic Acid , Myocytes, Cardiac , Reperfusion , Reperfusion Injury , Sodium BicarbonateABSTRACT
Objective:To investigate the effect of artesunate(ART) on human leukemia cell line K562. Methods:Inhibition of proliferation was measured by a colorimetric MTT assay. The morphological changes of K562 were observed under a light microscope and an electron microscope. Flow cytometry assay detected the ratio of apoptosis and oncosis of K562 cell lines which were induced at three different times by three different concentrations of ART. Results:ART extract clearly inhibited the proliferation of K562. The 50% effective dose evaluated on 24h,48h,and 72h of ordinal exposure to the extract,were 65.17?g/ml,31.63?g/ml,and 10.51?g/ml,respectively,ART extract-treated cells exhibited morphological changes typical of oncosis and apoptosis. Futheremore,the ratio of apoptosis was not different from to that of oncosis. Conclusion:Artesunate can control proliferation of the K562 human leukemia cell line in two forms:oncosis and apoptosis. The ratio of oncosis and apoptosis present typical dose-dependence and time-dependence.
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Objective To discuss the impact of zedoary turmerie oil(ZTO) injection over oncosis index and Bcl-2 expression of human ovarian cancer SKOV3 cell.Methods After ZTO injection acted on human ovarian cancer SKOV3 cells,the changes in the nucleus were observed by fluorescence microscope,oncosis index was counted by projection electron microscope,the situation of cell DNA breakage was observed by agarose gel electrophoresis,and cell Bcl-2 gene expression was observed by immunohistochemical method.Results After treated by ZTO injection for 48 hours,human ovarian cancer SKOV3 cells shows that oncosis cell was swelling in fluorescence microscope,the volume increased,the membrane area narrowed,the nuclear chromatin expansed.The oncosis index increased with dose-effect relationship,DNA electrophoresis showed diffuse type and Bcl-2 gene expression was down-regulated.Conclusion ZTO injection can increase oncosis index of human ovarian cancer SKOV3 cell with the concentration,and lower Bcl-2 gene expression,which may be one of the mechanisms of ZTO injection caused oncosis of SKOV3 cell.
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Objective To investigate the correlation of oncosis and TNF-? in D-galactosamine (D-GalN) induced acute hepatic injury. Methods Acute hepatic injury model was induced by D-GalN in 24 SD rats, and 12 rats served as control. At 4, 8, 12, 16, 20, 24 h after intraperitoneal injection of D-GalN, the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, and the tumor necrosis factor-? (TNF-?) in liver tissue were measured. The pathological changes of liver and the oncosis of hepatocytes were observed by TEM. Results In acute hepatic injury, the levels of ALT, AST, TNF-? mRNA, OI were higher than that of control group (P
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Objective To explore the roles and clinical significance of glutamine(GLN) in carbon tetrachloride(CCl_(4)) induced acute hepatic injury.Methods The SD rats were divided into model group,GLN pretreated group and control group.The animal model was established by CCl_(4) intraperitoneal injection.GLN at dose of 1 g/kg was intragastrically administrated for 7 d before intraperitoneal injection of CCl_(4) in the rats of GLN pretreated group.The rats were executed 4,8,12,16,24 h after injure.To evaluate the hepatic injury,the serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were detected by automatic biochemistry analysator.The liver tissue was observed by light microscope and transmission electron microscope(TEM).The expression of nuclear factor-?B(NF-?B) was detected by immunohistochemistry and the tumor necrosis factor?(TNF-?) was detected by reverse transcription polymerase chain reaction(RT-PCR).The apoptosis of hepatocyte was detected by TUNEL.The oncosis index was detected by TEM.Results The levels of ALT,AST,NF-?B,TNF-? mRNA in model group were apparently elevated as compared to control group(P
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Oncosis is another form of cell death, which is different from apoptosis. The review will discuss the recent advances of oncosis on pathological morphology, nuclear biochemical changes and molecular mechanisms. [
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50?mol/L induced markedly oncotic cell death,but no apoptosis was observed.TEM examination indicated that a form of cell death accompanied by cellular swelling,organelle swelling and vacuolization,mitochondrial swelling and cristae membrane loss,and nucleus swelling, chromatin scattering or karyolysis,which characterized as oncosis.When treated with 50,200?mol/L of ART for 5 h, the intracellular ROS level of Panc-1 cells markedly increased to 1.60 and 4.49 fold compared with that of untreated cells,respectively.Pretreatment with TCEP effectively attenuated ART-induced intracellular ROS level and decrease the oncosis in Panc-1 cells.Conclusions:ART exerts profound cytotoxic effects on Panc-1 cells and induces an oncosis- like cell death,which is quite different from apoptosis.The cellular generation of ROS and its peroxidation damage may be one of the mechanisms for its anti-tumor effect on pancreatic cancer.
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Objective To evaluate the relationship of oncosis and the expression of microvessel density (MVD) in colorectal carcinoma and its clinical significance Methods The expression of MVD and oncosis were detected by immunohistochemical method and transmission electron microscope in 64 cases of colorectal carcinoma Results Oncosis existed in colorectal carcinoma Oncosis index (OI) in tissues of colorectal carcinoma decreased with the decrease of differentiation grades ( F=8 590?2, P
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Objective:To observe oncosis in human peripheral blood T lymphocytes.Methods:Peripheral blood T lymphocytes of healthy adult was separated with Percoll(1.073 g/ml)and harvested by using nylon column.The cultured cells were divided into control and dexamethasone(DXM)group,and cell morphology was observed through light microscope,electron microscope and fluorescent microscope.And incidence rate of oncosis was analyzed by flow cytometry.Results:①Oncosis could be observed in cultured T lymphocyte after 96h.②In different concentrations of DXM group(1?10-6,1?10-5,1?10-4,1?10-3mol/L),The incidence of oncosis T lymphocytes was(3.49?0.42)%,(5.17?0.48)%,(8.44?0.72)%,(17.93?1.50)%.③During different cultured period(48,72,96,120h),The oncositic rate of T lymphocytes in DXM group was(0.53?0.10)%,(6.36?0.80)%,(20.60?1.59)%,(25.56?1.76)%.Conclusion:Oncosis can be seen in human peripheral blood T lymphocytes,and DXM could induce oncosis.