Реферат
PURPOSE: This study aimed to elucidate the molecular mechanisms of the anti-pancreatic fibrosis effects of matrine in rats. MATERIALS AND METHODS: Trinitrobenzene sulfonic acid was administrated to rats to establish a pancreatic fibrosis model. Rats were divided into four groups: Control, Sham, Model, and Matrine (n=8). Hematoxylin-eosin staining, Masson staining, and Azan staining were performed to evaluate pancreatic fibrosis. Expression of transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), and collagen I in pancreatic tissues was evaluated by immunohistochemical staining. mRNA and protein levels of TGF-β receptor 1 (TβR1), TβR2, and Smad2 in pancreatic tissues were determined by RT-PCR and Western blot, respectively. RESULTS: In the model group, hyperplasia of glandules around the glandular ducts, mitochondrial swelling of acinous cells, and severe fibrosis were found. Interestingly, in the Matrine group, mitochondrial swelling was only found in a small number of acinous cells, and the fundamental structures of pancreatic tissues were intact. Moreover, pancreatic fibrosis was markedly alleviated. Comparing to the Sham group, expression of α-SMA, TGF-β1, and collagen I was sharply elevated in the Model group (p < 0.05); however, their expressions were much lower in the Matrine group, compared to the Model group (p < 0.05). Compared with the Sham group, mRNA and protein levels of Smad2, TβR1, and TβR2 in the Model group were notably raised (p < 0.05). However, their high expression was significantly downregulated in the Matrine group (p < 0.05). CONCLUSION: Matrine suppressed pancreatic fibrosis by regulating TGF-β/Smad signaling in rats.
Тема - темы
Animals , Rats , Acinar Cells , Actins , Blotting, Western , Collagen , Fibrosis , Hyperplasia , Mitochondrial Swelling , RNA, Messenger , Signal TransductionРеферат
Abstract Purpose: To analyze the effect of methylene blue (MB) therapy during the liver ischemia-reperfusion injury (I/R) process. Methods: Thirty-five male Wistar rats were used, (70%) submitted to partial ischemia (IR) or not (NIR) (30%) were obtained from the same animal. These animals were divided into six groups: 1) Sham (SH), 2) Sham with MB (SH-MB); 3) I/R, submitted to 60 minutes of partial ischemia and 15 minutes of reperfusion; 4) NI/R, without I/R obtained from the same animal of group I/R; 5) I/R-MB submitted to I/R and MB and 6) NI/R-MB, without I/R. Mitochondrial function was evaluated. Osmotic swelling of mitochondria as well as the determination of malondialdehyde (MDA) was evaluated. Serum (ALT/AST) dosages were also performed. MB was used at the concentration of 15mg/kg, 15 minutes before hepatic reperfusion. Statistical analysis was done by the Mann Whitney test at 5%. Results: State 3 shows inhibition in all ischemic groups. State 4 was increased in all groups, except the I/R-MB and NI/R-MB groups. RCR showed a decrease in all I/R and NI/R groups. Mitochondrial osmotic swelling showed an increase in all I/R NI/R groups in the presence or absence of MB. About MDA, there was a decrease in SH values in the presence of MB and this decrease was maintained in the I/R group. AST levels were increased in all ischemic with or without MB. Conclusions: The methylene blue was not able to restore the mitochondrial parameters studied. Also, it was able to decrease lipid peroxidation, preventing the formation of reactive oxygen species.
Тема - темы
Humans , Animals , Male , Reperfusion Injury/prevention & control , Enzyme Inhibitors/therapeutic use , Liver/blood supply , Methylene Blue/therapeutic use , Oxygen Consumption , Aspartate Aminotransferases/blood , Reference Values , Time Factors , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Lipid Peroxidation/drug effects , Reperfusion Injury/metabolism , Reproducibility of Results , Reactive Oxygen Species/analysis , Reactive Oxygen Species/metabolism , Rats, Wistar , Cell Respiration , Alanine Transaminase/blood , Enzyme Inhibitors/pharmacology , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Liver/metabolism , Malondialdehyde/analysis , Methylene Blue/pharmacology , Mitochondrial Swelling/drug effectsРеферат
OBJECTIVES: The objective of the present study was to evaluate the protective effect of pre-conditioning treatment with laser light on hepatic injury in rats submitted to partial ischemia using mitochondrial function and liver fatty acid binding protein as markers. METHODS: Rats were divided into four groups (n=5): 1) Control, 2) Control + Laser, 3) Partial Ischemia and 4) Partial Ischemia + Laser. Ischemia was induced by clamping the hepatic pedicle of the left and middle lobes of the liver for 60 minutes. Laser light at 660 nm was applied to the liver immediately prior to the induction of ischemia at 22.5 J/cm2, with 30 seconds of illumination at five individual points. The animals were sacrificed after 30 minutes of reperfusion. Blood and liver tissues were collected for analysis of mitochondrial function, determination of malondialdehyde and analysis of fatty acid binding protein expression by Western blot. RESULTS: Mitochondrial function decreased in the Partial Ischemia group, especially during adenosine diphosphate-activated respiration (state 3), and the expression of fatty acid binding protein was also reduced. The application of laser light prevented bioenergetic changes and restored the expression of fatty acid binding protein. CONCLUSION: Prophylactic application of laser light to the livers of rats submitted to partial ischemia was found to have a protective effect in the liver, with normalization of both mitochondrial function and fatty acid binding protein tissue expression.
Тема - темы
Animals , Reperfusion Injury/prevention & control , Ischemic Preconditioning/methods , Low-Level Light Therapy/methods , Fatty Acid-Binding Proteins/metabolism , Liver/radiation effects , Liver/blood supply , Aspartate Aminotransferases/blood , Blotting, Western , Reproducibility of Results , Rats, Wistar , Alanine Transaminase/blood , Mitochondrial Membranes/drug effects , Fatty Acid-Binding Proteins/analysis , Liver/metabolism , Malondialdehyde/analysis , Malondialdehyde/radiation effects , Mitochondrial Swelling/radiation effectsРеферат
BACKGROUND: Intravenous palonosetron-HCl, a second-generation antagonist of selective serotonin type 3 (5-HT3) receptors, can prevent chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea and vomiting (PONV). 5-HT3 receptors are abundant in the lower brainstem and the substantia gelatinosa of the spinal cord, which provides a theoretical rationale for neuraxial administration of 5-HT3 receptor antagonists for CINV, PONV, and opioid-induced nausea and vomiting. However, there are no reports of neuraxial administration of palonosetron-HCl. Before neuraxial administration of a drug is accepted for clinical use, its safety must be proven. This study was conducted to determine whether neuraxial administration of palonosetron-HCl produces neurologic injury. METHODS: Male Sprague-Dawley rats under general anesthesia were catheterized intrathecally and the catheter tip was advanced caudally to the L1 vertebra. After 7 days, 20 µl of normal saline (N group, n = 6) or 20 µl (1 µg) of palonosetron-HCl (P group, n = 6) were injected intrathecally once per day for 2 weeks. Neurotoxic changes were evaluated by light microscopy (LM) and electron microscopy (EM) of the spinal cord. Behavioral changes were also evaluated in both groups. RESULTS: One of the N group rats and three of the P group rats demonstrated abnormal behavior during intrathecal drug injection, but otherwise their behavior was normal. The spinal cords of the N group did not have any abnormal findings by LM or EM. The spinal cords of the P group had multiple vacuoles in the white matter by LM, especially in the dorsal funiculus, and EM revealed myelin, axonal, and mitochondrial swelling. CONCLUSIONS: Results suggest that chronic intrathecal administration of palonosetron-HCl produced microscopic morphologic changes in the spinal cords of rats.
Тема - темы
Animals , Humans , Male , Rats , Anesthesia, General , Axons , Brain Stem , Catheters , Injections, Spinal , Microscopy , Microscopy, Electron , Mitochondrial Swelling , Myelin Sheath , Nausea , Postoperative Nausea and Vomiting , Rats, Sprague-Dawley , Receptors, Serotonin, 5-HT3 , Serotonin , Spinal Cord , Spine , Substantia Gelatinosa , Vacuoles , Vomiting , White MatterРеферат
PURPOSE: To assess the effect of two laser wavelengths, either separate or combined, on intact rat livers. METHOD: Nineteen male Wistar rats (200-300 g) were submitted to laser irradiation at 5 different sites on the liver surface.Wavelengths 660 and 780 nm were used, with a dose of irradiation of 60 J/cm2/site.The animals were divided into the groups:control (C) and animals irradiated with 660 nm laser (L1), with 780 nm laser (L2) or withboth wavelengths (L3).Mitochondrial function, mitochondrial swelling, and hepatocellular malondialdehyde (MDA) levels were determined.Data were analyzed by the Mann-Whitney test, with the level of significance set at 5%. RESULTS: There was a reduction of ADP-activated respiration (state 3) in group L1 compared to group C (p=0.0016), whereas the values of group L2 were similar to control.Group L3 also showed a reduction of state 3 (p=0.0159).There was a reduction of RCR in group L1 compared to control (p=0.0001) and to group L2 (p=0.0040).Mitochondrial swelling only differed between group L3 and control (p=0.0286).There was a increase in MDA levels in group L3 compared to control (p=0.0476) and to group L2 (p=0.0286) and in group L1 compared to group L2 (p=0.0132). CONCLUSION: Although laser irradiation reduced mitochondrial function,it did not interfere with the hepatocellular energy status.
Тема - темы
Animals , Male , Mitochondria, Liver/radiation effects , Oxidative Stress/radiation effects , Lasers, Semiconductor , Liver/radiation effects , Radiation Dosage , Spectrophotometry , Time Factors , Rats, Wistar , Low-Level Light Therapy , Dose-Response Relationship, Radiation , Malondialdehyde/analysis , Mitochondrial Swelling/drug effectsРеферат
PURPOSE: Cell-in-cell structures are created by one living cell entering another homotypic or heterotypic living cell, which usually leads to the death of the internalized cell, specifically through caspase-dependent cell death (emperitosis) or lysosome-dependent cell death (entosis). Although entosis has attracted great attention, its occurrence is controversial, because one cell line used in its study (MCF-7) is deficient in caspase-3. METHODS: We investigated this issue using MCF-7 and A431 cell lines, which often display cell-in-cell invasion, and have different levels of caspase-3 expression. Cell-in-cell death morphology, microstructures, and signaling pathways were compared in the two cell lines. RESULTS: Our results confirmed that MCF-7 cells are caspase-3 deficient with a partial deletion in the CASP-3 gene. These cells underwent cell death that lacked typical apoptotic properties after staurosporine treatment, whereas caspase-3-sufficient A431 cells displayed typical apoptosis. The presence of caspase-3 was related neither to the lysosome-dependent nor to the caspase-dependent cell-in-cell death pathway. However, the existence of caspase-3 was associated with a switch from lysosome-dependent cell-in-cell death to the apoptotic cell-in-cell death pathway during entosis. Moreover, cellular hypoxia, mitochondrial swelling, release of cytochrome C, and autophagy were observed in internalized cells during entosis. CONCLUSION: The occurrence of caspase-independent entosis is not a cell-specific process. In addition, entosis actually represents a cellular self-repair system, functioning through autophagy, to degrade damaged mitochondria resulting from cellular hypoxia in cell-in-cell structures. However, sustained autophagy-associated signal activation, without reduction in cellular hypoxia, eventually leads to lysosome-dependent intracellular cell death.
Тема - темы
Apoptosis , Autophagy , Caspase 3 , Cell Death , Cell Hypoxia , Cell Line , Cytochromes c , Entosis , MCF-7 Cells , Mitochondria , Mitochondrial Swelling , StaurosporineРеферат
BACKGROUND: Despite manifold benefits of nanoparticles (NPs), less information on the risks of NPs to human health and environment has been studied. Cobalt oxide nanoparticles (Co3O4-NPs) have been reported to cause toxicity in several organisms. In this study, we have investigated the role of Co3O4-NPs in inducing phytotoxicity, cellular DNA damage and apoptosis in eggplant (Solanum melongena L. cv. Violetta lunga 2). To the best of our knowledge, this is the first report on Co3O4-NPs showing phytotoxicity in eggplant. RESULTS: The data revealed that eggplant seeds treated with Co3O4-NPs for 2 h at a concentration of 1.0 mg/ml retarded root length by 81.5 % upon 7 days incubation in a moist chamber. Ultrastructural analysis by transmission electron microscopy (TEM) demonstrated the uptake and translocation of Co3O4-NPs into the cytoplasm. Intracellular presence of Co3O4-NPs triggered subcellular changes such as degeneration of mitochondrial cristae, abundance of peroxisomes and excessive vacuolization. Flow cytometric analysis of Co3O4-NPs (1.0 mg/ml) treated root protoplasts revealed 157, 282 and 178 % increase in reactive oxygen species (ROS), membrane potential (APm) and nitric oxide (NO), respectively. Besides, the esterase activity in treated protoplasts was also found compromised. About 2.4-fold greater level of DNA damage, as compared to untreated control was observed in Comet assay, and 73.2 % of Co3O4-NPs treated cells appeared apoptotic in flow cytometry based cell cycle analysis. CONCLUSION: This study demonstrate the phytotoxic potential of Co3O4-NPs in terms of reduction in seed germination, root growth, greater level of DNA and mitochondrial damage, oxidative stress and cell death in eggplant. The data generated from this study will provide a strong background to draw attention on Co3O4-NPs environmental hazards to vegetable crops.
Тема - темы
Oxides/toxicity , DNA Damage/drug effects , Cell Death/drug effects , Cobalt/toxicity , Solanum melongena/drug effects , Nanoparticles/toxicity , Mitochondrial Swelling/drug effects , Nitric Oxide/metabolism , Oxides/metabolism , Analysis of Variance , Reactive Oxygen Species/metabolism , Cobalt/metabolism , Comet Assay , Solanum melongena/metabolism , Microscopy, Electron, Transmission , Nanoparticles/metabolism , Flow Cytometry , Mitochondrial Swelling/physiologyРеферат
PURPOSE: To investigate the consequences of the association between hyperbaric oxygen therapy and hepatic ischemia / reperfusion. METHODS: Wistar rats were divided into three groups: SHAM, rats submitted to surgical stress and anesthetic but not hepatic ischemia or reperfusion, I / R, rats submitted to total hepatic pedicle ischemia for 30 min, followed by 5 min of reperfusion; HBO120, rats submitted to 120 min of hyperbaric oxygen therapy at two absolute atmospheres and immediately after submitted to the experimental protocol of ischemia and reperfusion. The preservation of the hepatic function was evaluated by determining mitochondrial swelling and malondialdehyde tissue level, as well as alanine aminotransferase and aspartate aminotranferase serum levels. The results were analyzed using the Mann-Whitney test and differences were considered significant for p<0.05. RESULTS: There were significant differences in values: mitochondrial swelling of the I / R group compared to SHAM and HBO120; malondialdehyde between SHAM vs. I / R, SHAM vs HBO120, and I / R vs HBO120, alanine aminotransferase between SHAM vs. I / R . There was no significant difference between groups in aspartate aminotransferase serum levels. CONCLUSION: The association between hyperbaric oxygen therapy and hepatic ischemia and reperfusion process was positive.
Тема - темы
Animals , Male , Rats , Hyperbaric Oxygenation , Ischemia/therapy , Liver/blood supply , Reperfusion Injury/therapy , Alanine Transaminase/blood , Aspartate Aminotransferases/blood , Disease Models, Animal , Ischemia/pathology , Liver/pathology , Malondialdehyde/chemistry , Mitochondrial Swelling/physiology , Rats, Wistar , Statistics, NonparametricРеферат
<p><b>OBJECTIVE</b>To observe the impairing effects of triptolide on liver mitochondria in isolated rat-liver mitochondria and human normal liver HL7702 cell line.</p><p><b>METHODS</b>Rat-liver mitochondria were isolated from adult female Sprague-Dawley (SD) rats. Liver mitochondria were incubated with 0, 1.25, 2.5, 5 and 10 μmol/L triptolide for detecting mitochondrial swelling and with 0, 2.5, 5 and 10 μmol/L triptolide for mitochondrial permeability transition pore (MPTP) activity. Mitochondrial swelling was estimated by measuring the apparent absorbance change during 600 s in the mitochondrial suspensions at 520 nm with a mitochondrial swelling examining kit. The effect of triptolide on MPTP was determined with a fluorescence detection kit by detecting the fluorescence intensity at an excitation wavelength of 488 nm emitted at 527 nm. Human normal liver HL7702 cells were treated without or with 0.02, 0.1 and 0.5 μmol/L triptolide for 24 h for analyzing mitochondrial transmembrane potential (Δψm) and reactive oxygen species (ROS). Δψm was measured using the fluorescent probe 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide (JC-1). ROS was measured using fluorescent probe 2',7'-dichlorofluorescin diacetate (DCFH-DA). The cells were harvested and dyed with JC-1 and DCFH-DA, and analyzed by flow cytometry, respectively.</p><p><b>RESULTS</b>Incubation of isolated mitochondria with triptolide results in swollen mitochondria in a concentration-dependent manner. Moreover, triptolide significantly activated mitochondrial permeability transition at 5 and 10 μmol/L (P<0.05 and P<0.01). When HL7702 cells were exposed to a various concentration triptolide for 24 h, mitochondrial membrane depolarization and increase of ROS were caused by triptolide in a concentration-dependent manner. Triptolide significantly induced the mitochondrial membrane depolarization at 0.1 and 0.5 μmol/L (P<0.05 and P<0.01) and the increase of ROS at 0.1 and 0.5 μmol/L (P<0.05 and P<0.01).</p><p><b>CONCLUSION</b>Triptolide could induce mitochondrial impairment, which may be one of the mechanisms by which hepatotoxicity occurs.</p>
Тема - темы
Animals , Female , Humans , Rats , Cell Line , Diterpenes , Chemistry , Pharmacology , Epoxy Compounds , Chemistry , Pharmacology , Membrane Potential, Mitochondrial , Mitochondria, Liver , Metabolism , Mitochondrial Membrane Transport Proteins , Metabolism , Mitochondrial Swelling , Phenanthrenes , Chemistry , Pharmacology , Rats, Sprague-Dawley , Reactive Oxygen Species , MetabolismРеферат
BACKGROUND: Role of cytochrome c (Cyt c) is an apoptogenic agent under certain conditions. The mitochondrial permeability transition pore (MPTP) plays an important role in cell death since it opens, leading to mitochondrial swelling and release of Cyt c, which initiates apoptosis. By inhibiting the opening of MPTP, cyclosporine A (CSA) may contribute to maintaining mitochondrial homeostasis. We investigate the effects of the partial sciatic nerve injury (PSNI)-induced neuropathic pain model on mitochondrial Cyt c release and the effects of CSA on neuroprotection by mitochondrial stabilizing activity in PSNI rats. METHODS: Rats were assigned to two groups that received different operations (Group P; PSNI operation, Group S; sham operation). The changes of cyt c and GABAergic neuron were evaluated in the spinal cord tissue. After which, PSNI rats randomly received CSA (Group C) or saline (Group S), and the changes of mechanical thresholds with Cyt c and GABAergic neuron were checked. RESULTS: PSNI in rats increased the release of cytosolic Cyt c. However, GABAergic cells were not decreased in the spinal cord level on the ipsilateral side to the PSNI. The second experiment reveal a reduction in Cyt c release, using CSA in PSNI model. Rats receiving CSA were afforded the antiallodynia without decrease of GABAergic cell. CONCLUSIONS: The Cyt c probably contributes to nerve dysfunction after PSNI. PSNI induced neuropathic pain was profoundly linked to mitochondrial stabilization. Thus, the potent neuroprotector, CSA, might produce antiallodynia through its capability to inhibit the opening of MPTP.
Тема - темы
Animals , Rats , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine , Apoptosis , Cell Death , Cyclosporine , Cytochromes , Cytochromes c , Cytosol , GABAergic Neurons , Homeostasis , Hyperalgesia , Mitochondrial Membrane Transport Proteins , Mitochondrial Swelling , Neuralgia , Permeability , Salicylamides , Sciatic Nerve , Spinal CordРеферат
Semiconductor nanoparticles, such as quantum dots (QDs), were used to carry out experiments in vivo and ex vivo with Trypanosoma cruzi. However, questions have been raised regarding the nanotoxicity of QDs in living cells, microorganisms, tissues and whole animals. The objective of this paper was to conduct a QD nanotoxicity study on living T. cruzi protozoa using analytical methods. This was accomplished using in vitro experiments to test the interference of the QDs on parasite development, morphology and viability. Our results show that after 72 h, a 200 μM cadmium telluride (CdTe) QD solution induced important morphological alterations in T. cruzi, such as DNA damage, plasma membrane blebbing and mitochondrial swelling. Flow cytometry assays showed no damage to the plasma membrane when incubated with 200 μM CdTe QDs for up to 72 h (propidium iodide cells), giving no evidence of classical necrosis. Parasites incubated with 2 μM CdTe QDs still proliferated after seven days. In summary, a low concentration of CdTe QDs (2 μM) is optimal for bioimaging, whereas a high concentration (200 μM CdTe) could be toxic to cells. Taken together, our data indicate that 2 μM QD can be used for the successful long-term study of the parasite-vector interaction in real time.
Тема - темы
Animals , Mice , Cadmium Compounds/toxicity , Cell Proliferation , DNA Damage , Quantum Dots , Tellurium/toxicity , Trypanosoma cruzi , Cell Membrane , Flow Cytometry , Fluorescent Dyes , Microscopy, Electron, Transmission , Mitochondrial Swelling , Trypanosoma cruzi/ultrastructureРеферат
<p><b>OBJECTIVE</b>To study effects of three pentacyclic triterpenoids, oleanolic acid (OA), ursolic acid (UA) and asiatic acid (AA) on Ca(2+)-induced liver mitochondrial permeability transition (MPT).</p><p><b>METHOD</b>Effects of three compounds on liver MPT induced by Ca2+ were assessed by measuring the change in mitochondrial swelling, mitochondrial membrane potential and release of matrix Ca2+ in vitro.</p><p><b>RESULT</b>Obvious mitochondrial swelling, loss of mitochondrial membrane potential and release of matrix Ca2+ occurred after the addition of 50 micromol x L(-1) Ca2+. However, preincubation with 50 mg x L(-1) OA, UA or AA significantly blocked the above changes. In addition, it was also found that there are differences in the inhibitions of three compounds on liver MPT induced by Ca2+.</p><p><b>CONCLUSION</b>Three pentacyclic triterpenoids, OA, UA and AA, have significant mitochondrial protection through blocking on liver MPT and the inhibition on liver MPT of AA is stronger than that of UA and OA.</p>
Тема - темы
Animals , Mice , Calcium , Metabolism , Pharmacology , Membrane Potential, Mitochondrial , Mice, Inbred ICR , Mitochondria, Liver , Metabolism , Mitochondrial Membrane Transport Proteins , Mitochondrial Swelling , Pentacyclic Triterpenes , PharmacologyРеферат
<p><b>OBJECTIVE</b>To observe the ultrastructural changes of HeLa cells in response to tubeimoside I (TBMS1) treatment and the protective effect of cyclosporine A (CsA), and explore the role of intrinsic apoptosis pathway in TBMS1-induced HeLa cell apoptosis.</p><p><b>METHODS</b>HeLa cells were treated with TBMS1 (10-50 micromo/L) alone or in combination with 2 micromol/L CsA for 12 and 24 h and observed with transmission electron microscope (TEM) for the ultrastructural changes of the cells.</p><p><b>RESULTS</b>TBMS1 induced apoptosis of HeLa cells in a concentration- and time-dependant manner. Under TEM, the treated cells progressively shrunk and the intercellular space widened with loss of microvillus, mitochondrial swelling, rough endoplasmic reticulum enlargement, chromatin condensation, nuclear shrinkage and nuclear pyknosis as TBMS1 concentration increased. At low concentrations, CsA offered partial protection of the mitochondria from TBMS1-induced damage whereas high-concentration CsA did not.</p><p><b>CONCLUSION</b>TBMS1 induces ultrastructural changes typical for apoptosis of the HeLa cells, which provides morphological evidence for the role of intrinsic apoptosis pathway in TBMS1-induced apoptosis.</p>
Тема - темы
Female , Humans , Apoptosis , Cell Nucleus , Cyclosporine , Pharmacology , Dose-Response Relationship, Drug , Endoplasmic Reticulum, Rough , HeLa Cells , Immunosuppressive Agents , Pharmacology , Microscopy, Electron, Transmission , Mitochondrial Swelling , Saponins , Pharmacology , Time Factors , Triterpenes , Pharmacology , Uterine Cervical Neoplasms , PathologyРеферат
Desequilíbrio/acúmulo de ferro tem sido implicado em injúria oxidativa associada a diversas doenças degenerativas tais como, hemocromatose hereditária, b-talassemia e ataxia de Friedreich. As mitocôndrias são particularmente sensíveis a estresse oxidativo induzido por ferro - um carregamento alto de ferro em mitocôndrias isoladas pode causar uma extensiva peroxidação lipídica e a permeabilização de membrana. Nesse estudo, nós detectamos e caracterizamos danos do DNA mitocondrial em mitocôndrias isoladas de fígado de rato, expostas ao complexo Fe2+-citrato, um dos complexos de baixo peso molecular. A intensa fragmentação do DNA foi induzida após a incubação das mitocôndrias com o complexo de ferro. A detecção de finais 3' de fosfoglicolato nas quebras de fitas de DNA mitocondrial pelo ensaio 32P-postlabeling sugere um envolvimento de radicais hidroxila na fragmentação do DNA induzido por complexo Fe2+-citrato. Os níveis elevados de 8-oxo-7,8-diidro-2'-desoxiguanosina também sugerem que o estresse oxidativo induzido por Fe2+-citrato causa danos no DNA mitocondrial. Em conclusão, nossos resultados mostram que a peroxidação lipídica mediada por ferro esteve associada com severos danos do DNA mitocondrial derivados de ataque direto das espécies reativas de oxigênio.
Тема - темы
Animals , Male , Rats , DNA Damage , DNA, Mitochondrial/drug effects , Ferrous Compounds/pharmacology , Lipid Peroxidation/drug effects , Mitochondria, Liver/drug effects , DNA, Mitochondrial/metabolism , Mitochondria, Liver/metabolism , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Mitochondrial Swelling/drug effects , Rats, WistarРеферат
<p><b>OBJECTIVE</b>To elvaulate the antioxidant activity of the pigment of Lycium ruthenicum.</p><p><b>METHOD</b>The antioxidant activities were measured by the effects of the reducing ability, scavenging DPPH. H2O2-induced hemolysis of mice erythrocyte, serum resistance of reactive oxygen species, content of MDA in liver tissue, and swelling effect of mitochondria in liver tissue.</p><p><b>RESULT</b>The pigment of L. ruthenicum could scaveng DPPH* remarkably with IC50 0.164 mg x mL(-1), inhibitte hemolysis of mice erythrocyte evidently with IC50 0.112 mg x mL(-1). The resistant of reactive oxygen species was enhanced by the tested substances, simultanously. The concentration of MDA of peroxidation of lipid in mice liver could be reduced, and the swelling of mice liver mitochondria alse be restrained.</p><p><b>CONCLUSION</b>The pigment of L. ruthenicum has antioxidant activity in tested concentration.</p>
Тема - темы
Animals , Mice , Antioxidants , Pharmacology , Biphenyl Compounds , Metabolism , Erythrocytes , Free Radical Scavengers , Pharmacology , Hemolysis , Hydrazines , Metabolism , Lipid Peroxidation , Liver , Metabolism , Lycium , Chemistry , Malondialdehyde , Metabolism , Mitochondria, Liver , Pathology , Mitochondrial Swelling , Phenols , Pharmacology , Picrates , Pigments, Biological , Pharmacology , Plants, Medicinal , Chemistry , Reactive Oxygen SpeciesРеферат
<p><b>OBJECTIVE</b>To investigate the effects of resveratrol (Res) on mitochondrial opening and Ca(2+)-induced Ca(2+) release (CICR) from rat liver cell mitochondria mediated by Ca(2+).</p><p><b>METHODS</b>Wistar rat liver cell mitochondria was extracted and Res-induced mitochondrial swelling was assessed spectrophotometrically at 540 nm to examine the permeability transition pore (PTP) opening. The membrane potential changes of Res-treated mitochondria were measured with fluorescence spectrophotometery. Ca(2+) uptake and release by the mitochondria was determined by absorbance change of arsenazo III at 685-675 nm monitored by dual wavelength spectrophotometry.</p><p><b>RESULTS</b>Res promoted Ca(2+)-mediated PTP opening, and this effect was completely inhibited by CsA and lowered by trifluoperazine. CICR accelerated by Res treatment was completely blocked by ruthenium red and partly by trifluoperazine.</p><p><b>CONCLUSION</b>Res can promote PTP opening by inducing CICR, which may be one of the pathways that Res induces cell apoptosis.</p>
Тема - темы
Animals , Female , Rats , Calcium , Metabolism , Cells, Cultured , Hepatocytes , Cell Biology , Metabolism , Mitochondria, Liver , Metabolism , Mitochondrial Membrane Transport Proteins , Metabolism , Mitochondrial Swelling , Rats, Wistar , Stilbenes , PharmacologyРеферат
<p><b>OBJECTIVE</b>The aim of this study was to investigate the mechanisms of C. minima in the treatment of allergic rhinitis.</p><p><b>METHOD</b>An allergic rhinitis animal model induced by ragweed pollen was established. After treatment with an active extract of C. minima, histopathological changes in the nasal mucosa of guinea pig were observed by transmission electron microscope.</p><p><b>RESULT</b>In the allergeic rhinitis model group, there appear a large number of lysosomes in the nasal epithelium with organelles vacuolated and nucleus deformed. Cells in the proper lamina of connective tissue were disarranged with organelles damaged, and there was also infiltration of eosinophils and mast cells in the connective tissue. However, in the treatment group receiving C. minima extract, the pathological changes mentioned above were significantly decreased.</p><p><b>CONCLUSION</b>C. minima is effective in treating allergic rhinitis.</p>
Тема - темы
Animals , Female , Male , Asteraceae , Chemistry , Epithelium , Guinea Pigs , Lysosomes , Mitochondrial Swelling , Nasal Mucosa , Pathology , Oils, Volatile , Pharmacology , Phytotherapy , Plants, Medicinal , Chemistry , Rhinitis, Allergic, Seasonal , Drug Therapy , PathologyРеферат
<p><b>AIM</b>To investigate the effect of 3,4-dihydroxyacetophenone (alpha-DHAP) on Na+, K+ -ATPase activity of injured brain mitochondria induced by ascorbate-FeSO4 and the oxygen consumption of rat brain cells stimulated by ADP.</p><p><b>METHODS</b>Na+, K+ -ATPase activity was determined according to the method of inorganic phosphate. Swelling of the brain mitochondria was detected with the method of spectrophotometer. Lipid peroxidation was detected according to the thiobarbituric acid method of spectrophotometer. Oxygen consumption was measured by oxygen electrode method.</p><p><b>RESULTS</b>The decrease of Na+, K+ -ATPase activity, mitochondria swelling and formation of lipid peroxidation were shown in rat brain mitochondria and cells induced by ascorbate-FeSO4. alpha-DHAP was shown to increase the activity of Na+, K+ -ATPase, decrease the mitochondria swelling and inhibit the production of lipid peroxidation of brain mitochondria and cells induced by ascorbate and FeSO4. alpha-DHAP can also reduce the oxygen consumption of brain cells stimulated by ADP.</p><p><b>CONCLUSION</b>alpha-DHAP can protect the structure and the function of brain mitochondria and cells by scavenging the free radical and resisting the reaction of lipid peroxidation.</p>
Тема - темы
Animals , Male , Rats , Acetophenones , Pharmacology , Adenosine Diphosphate , Pharmacology , Brain , Cell Biology , Metabolism , Free Radical Scavengers , Pharmacology , Lipid Peroxidation , Mitochondria , Metabolism , Mitochondrial Swelling , Oxygen Consumption , Rats, Wistar , Sodium-Potassium-Exchanging ATPase , MetabolismРеферат
<p><b>OBJECTIVE</b>To study the relationship between late mRNA and the cytopathic effect(CPE) and ultrastructural features after human cytomegalovirus (HCMV) infection in vitro.</p><p><b>METHODS</b>Human embryo fibroblast cells(HEL) were infected with HCMV AD169 strain. The expression of the HCMV late mRNA was measured by semiquantitative RT-PCR, the cytopathic effect (CPE) and the cell ultrastructure were observed by means of light microscopy and electron microscopy, respectively.</p><p><b>RESULTS</b>The HCMV late mRNA could be detected 12 hours postinfection and increased gradually, but the CPE appeared 48 hours postinfection in HEL cells. The HCMV infected cells exhibited significant mitochondrial enlargement and the number of mitochondrial ridge deletion, the cisternae lumen of endoplasmic reticulum (ER) dilation and vacuolization (at the end age). The mature nucleocapsid could be observed 96 hours postinfection.</p><p><b>CONCLUSION</b>The ultrastructural changes have an intimate correlation with the expression of HCMV late mRNA and play an important role in the life circle of the virus. HCMV late mRNA may serve as a indicator of the clinical effect of treatment in active HCMV infection.</p>
Тема - темы
Humans , Cytomegalovirus , Genetics , Physiology , Cytopathogenic Effect, Viral , Embryo, Mammalian , Endoplasmic Reticulum , Pathology , Virology , Fibroblasts , Metabolism , Virology , Inclusion Bodies , Pathology , Virology , Mitochondrial Swelling , RNA, Messenger , MetabolismРеферат
<p><b>OBJECTIVE</b>To discuss the effect of the association of Shiquandabutang with Hetaokun on the protection to liver and immunity of tumor mouse S180.</p><p><b>METHOD</b>Through the comparison between tumor transplanted and tumor cultured completely out of cell body, the effect was investigated, with Hetaokun singly used and Shiquandabutang associated with Hetaokun, on the level of SGPT, licking up function of monocyte macrophage, thymus index, spleen index and transform percentage of lymphocyte of the mouse S180. The scanning electron micrographs indicated the protective function of the association of Shiquandabutang with Hetaokun for liver.</p><p><b>RESULT</b>12.5 mg x kg(-1) Hetaokun could obviously restrain the tumor when it was singly used at 73.1%, but it increased SGPT at the same time. The association of Shiquandabutang with Hetaokun could protect liver of the mouse S180. SGPT (P > 0.05) was compared with the common ones and the result showed that the association of shiquandabutang with Hetaokun could make K value increase (P > 0.01). Through the scanning electron micrographs, association of two medicines was found to change liver cells little and expansion of rough Neizhiwang was not found. Compared with the control group, the immunity of the two tumor mouse groups taking the medicine mentioned above was promoted obviously.</p><p><b>CONCLUSION</b>The association of Shiquandabutang with Hetaokun can enhance the efficiency and decrease poison of them to body. With the promotion of immunity of the body, the efficiency is enhanced on the whole.</p>