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1.
J Neurol Sci ; 410: 116679, 2020 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-31951835

RESUMO

Paraquat has dopaminergic neurotoxicity and potentially contributes to Parkinson's disease (PD) as a risk factor. However, the cellular and molecular mechanisms of PQ-induced neurodegeneration have not been clearly elucidated. Studies have shown that PQ induces microglial neuroinflammation through toll-like receptor 4 (TLR4)-nuclear factor-κB pathway, resulting in neuronal cell loss. Mitogen-activated protein kinases (MAPKs) are involved in the production of pro-inflammatory cytokines in microglia, and in this study, the role of MAPKs in PQ-activated microglial inflammation was investigated. Murine BV2 microglial cells were treated with 40 µM of PQ following pretreatment of the cells with selective inhibitor of MAPKs phosphorylation for blockage of the phosphorylation of ERK, JNK and P38, or a specific TLR4 inhibitor for blocking the activation of TLR4. The protein expression of phosphorylated ERK, JNK and p38, and the transcription expression of pro-inflammatory mediators were assessed with Western blotting and qRT-PCR technique, respectively. The results indicated that PQ significantly induced the phosphorylation of ERK, JNK and P38 in microglia, while MAPKs inhibitors suppressed PQ-induced phosphorylation of ERK, JNK and P38, and reduced the transcription level of pro-inflammatory cytokines. PQ-stimulated phosphorylation of ERK, JNK and P38 was also reduced by TLR4 inhibitor. The inhibited intensity in the level of pro-inflammatory cytokine transcription was obviously greater in TLR4 inhibitor + PQ group than in each MAPK inhibitor + PQ group. Taken together, inhibition of MAPKs phosphorylation partially attenuates PQ-induced microglial inflammation, which may become a potential intervention strategy for PQ neurotoxicity.

2.
Chembiochem ; 20(21): 2767-2776, 2019 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-31119850

RESUMO

Iridium(III) complexes have attracted more and more attention in the past few years because of their potential antineoplastic activity. In this study, four IrIII complexes of the types [(η5 -Cpx )Ir(N^N)Cl]PF6 (complexes 1 and 2) and [Ir(Phpy)2 (N^N)]PF6 (complexes 3 and 4) have been synthesized and characterized. They exhibit potential antineoplastic activity towards A549 cells, especially in the case of complex 1 [IC50 =(3.56±0.5) µm], which was nearly six times as effective as cisplatin [(21.31±1.7) µm]. Additionally, these complexes show some selectivity towards cancer cells over normal cells. They could be transported by serum albumin (binding constants were changed from 0.37×105 to 81.71×105 m-1 ). IrIII complexes 1 and 2 could catalyze the transformation of nicotinamide adenine dinucleotide reduced form (NADH) into NAD+ (turnover numbers 43.2, 11.9] and induce the accumulation of reactive oxygen species, thus confirming their antineoplastic mechanism of oxidation, whereas the cyclometalated complexes 3 and 4 were able to target the lysosome [Pearson co-localization coefficient (PCC)=0.73], cause lysosomal damage, and induce apoptosis. Understanding the mechanism of action would help further structure-activity optimization on these IrIII complexes as emerging cancer therapeutics.

3.
Angew Chem Int Ed Engl ; 58(28): 9414-9418, 2019 Jul 08.
Artigo em Inglês | MEDLINE | ID: mdl-31041835

RESUMO

Interfacial charge collection efficiency has demonstrated significant effects on the power conversion efficiency (PCE) of perovskite solar cells (PSCs). Herein, crystalline phase-dependent charge collection is investigated by using rutile and anatase TiO2 electron transport layer (ETL) to fabricate PSCs. The results show that rutile TiO2 ETL enhances the extraction and transportation of electrons to FTO and reduces the recombination, thanks to its better conductivity and improved interface with the CH3 NH3 PbI3 (MAPbI3 ) layer. Moreover, this may be also attributed to the fact that rutile TiO2 has better match with perovskite grains, and less trap density. As a result, comparing with anatase TiO2 ETL, MAPbI3 PSCs with rutile TiO2 ETL delivers significantly enhanced performance with a champion PCE of 20.9 % and a large open circuit voltage (VOC ) of 1.17 V.

4.
Org Lett ; 21(5): 1534-1537, 2019 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-30775925

RESUMO

Garsubelone A (1), the first dimeric polycyclic polyprenylated acylphloroglucinols type metabolite featuring a complicated 6/6/6/6/6/6/6 heptacyclic architecture containing 10 stereogenic centers, was isolated from Garcinia subelliptica. Biogenetically, this compound was constructed by the plausible monomeric precursor, garsubelone B (2) and secohyperforin, via a key Diels-Alder cycloaddition to form an unique 2-oxabicyclo[3.3.1]nonane core. Their structures and absolute configurations were determined by comprehensive spectroscopic and X-ray diffraction techniques. The cytotoxic activities of these isolates were also evaluated.


Assuntos
Antineoplásicos Fitogênicos/química , Antineoplásicos Fitogênicos/metabolismo , Garcinia/química , Floroglucinol/análogos & derivados , Compostos Policíclicos/química , Compostos Policíclicos/metabolismo , Terpenos/química , Antineoplásicos Fitogênicos/isolamento & purificação , Ensaios de Seleção de Medicamentos Antitumorais , Estrutura Molecular , Floroglucinol/química , Compostos Policíclicos/isolamento & purificação , Difração de Raios X
5.
Chem Biol Interact ; 299: 179-185, 2019 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-30584891

RESUMO

Accumulating evidences suggest that heat shock protein 60 (HSP60) and toll-like receptor 4 (TLR4) are involved in triggering inflammatory response in microglia. Paraquat (PQ) evokes microglial inflammation by up-regulating expression of HSP60-TLR4-myeloid differentiation factor 88 (Myd88)-nuclear factor-kappa B (NF-κB) in vitro. The aim of this study is to investigate the potential modulatory roles of HSP60 and TLR4 in PQ-induced inflammation. Before treated with PQ, microglia BV2 cells were pretreated using siRNA to knockdown HSP60 or with specific inhibitor to inhibit TLR4 expression. Expression of TLR4 and MyD88, and nuclear translocation of NF-κB subunit p65 were studied with immunoblotting and immunofluorescence, respectively. Expression of pro-inflammatory factors was assessed with quantitative real-time PCR. Knockdown of HSP60 or inhibition of TLR4 significantly reduced the expression of TLR4 and MyD88 and decreased the accumulation of NF-κB p65 in the nucleus. Gene expression of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) were also significantly decreased in response to PQ. These results suggest that HSP60 and TLR4 can modulate intracellular signaling of PQ-induced inflammation. Inhibiting HSP60 or TLR4 reduces significantly the intensity of inflammation in PQ-activated microglia.


Assuntos
Chaperonina 60/metabolismo , Herbicidas/toxicidade , Paraquat/toxicidade , Receptor 4 Toll-Like/metabolismo , Animais , Chaperonina 60/antagonistas & inibidores , Chaperonina 60/genética , Regulação para Baixo/efeitos dos fármacos , Inflamação/metabolismo , Inflamação/patologia , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Camundongos , Microglia/citologia , Microglia/efeitos dos fármacos , Microglia/metabolismo , Fator 88 de Diferenciação Mieloide/metabolismo , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo II/metabolismo , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Sulfonamidas/farmacologia , Receptor 4 Toll-Like/antagonistas & inibidores , Fator de Transcrição RelA/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo
7.
Acta Biochim Biophys Sin (Shanghai) ; 50(11): 1131-1140, 2018 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-30215665

RESUMO

Myocardial damage caused by myocardial ischemia-reperfusion injury (MIRI) is difficult to be alleviated because cardiomyocyte necrosis is an irreversible and unregulated death form. Recently, necroptosis, a necrosis form caused by tumor necrosis factor-α (TNF-α) and Fas ligand (FasL), was found to be regulated by receptor interacting protein 3 (RIP3) and RIP3-receptor interacting protein 1 (RIP1)-mixed lineage kinase domain like protein (MLKL) pathway. But it is unclear whether they also play a regulatory role in MIRI-induced necroptosis. Our previous results showed that in rat MIRI, RIP3 could translocate and express highly in mitochondria. Therefore, it is important to explore proteins that interact with RIP3 which was translocated to mitochondria. The aim of this study was to explore the role of RIP3 in cardiomyocyte necrosis induced by mitochondrial damage of hypoxia/reoxygenation (H/R). Our results showed that H/R could cause RIP3-depended mitochondrial fragmentation and necrosis-based death; and RIP3-promoted H/R-induced necroptosis in H9c2 cells through increasing lactate dehydrogenase release and inhibiting cell viability. This process did not require RIP1 or MLKL but dynamin-related protein 1 (Drp1), which was related to Drp1 activation, reactive oxygen species elevation, and ΔΨm decline. This study provides novel insights into the role of RIP3 in cardiomyocyte injury during H/R. RIP3 may serve as a potential target for the treatment of MIRI.


Assuntos
Mitocôndrias/metabolismo , Miócitos Cardíacos/metabolismo , Oxigênio/metabolismo , Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo , Animais , Apoptose , Hipóxia Celular , Linhagem Celular , Sobrevivência Celular/genética , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Miócitos Cardíacos/citologia , Necrose , Interferência de RNA , Ratos , Espécies Reativas de Oxigênio/metabolismo , Proteína Serina-Treonina Quinases de Interação com Receptores/genética
8.
Cell Physiol Biochem ; 46(5): 2187-2196, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29730656

RESUMO

BACKGROUND/AIMS: MicroRNAs (miRNAs) are non-coding single stranded RNAs of 17-25 nucleotides in size, and their altered expression has been observed in various cancers. Previous studies have confirmed that miR-433-3p has effects on cancer cell proliferation, invasion, and migration, and its expression also correlates with sensitivity to chemotherapy. However, to date, there have been no studies on the biological functions of miR-433-3p in esophageal squamous cell carcinoma (ESCC). METHODS: The Cell Counting Kit-8, transwell, and matrigel assays were used to test the effects of miR-433-3p and its predicted target, growth factor receptor-bound protein 2 (GRB2), on the proliferation, migration, and invasion of Eca109 and KYSE30 cells, two types of esophageal cancer cell lines. The miR-433-3p binding site in the 3' untranslated region (UTR) region of GRB2 was predicted and verified using miRNA target site prediction software and structuring correct mutant examination. Western blotting and fluorescent quantitative PCR (FQ-PCR) techniques were employed to evaluate GRB2 expression. The inhibitory effects of miR-433-3p on tumor growth were investigated using a tumor xenograft model. RESULTS: The binding site of miR-433-3p was identified in the 3'UTR region of GRB2. Western blotting and FQ-PCR showed that miR-433-3p inhibited the mRNA and protein expression of GRB2. Overexpression of GRB2 inhibited tumorigenesis in nude mice. MiR-433-3p overexpression inhibited the proliferation, migration, and invasion of ESCC cells by suppressing GRB2 gene expression. CONCLUSIONS: Our findings suggest that targeting miR-433-3p may have therapeutic benefits in ESCC.


Assuntos
Carcinoma de Células Escamosas/genética , Neoplasias Esofágicas/genética , Proteína Adaptadora GRB2/genética , Regulação Neoplásica da Expressão Gênica , MicroRNAs/metabolismo , Invasividade Neoplásica/genética , Animais , Carcinoma de Células Escamosas/patologia , Linhagem Celular Tumoral , Proliferação de Células , Neoplasias Esofágicas/patologia , Carcinoma de Células Escamosas do Esôfago , Humanos , Camundongos Nus , Invasividade Neoplásica/patologia
9.
Artigo em Inglês | MEDLINE | ID: mdl-30643539

RESUMO

Objective. The randomized controlled trial was to evaluate the efficacy of topical Chinese herbal Zhangpi Ointment for hydroxyurea-induced leg ulcers in patients with myeloproliferative neoplasms. Patients and Methods. This single-center, prospective, randomized, open-label, controlled clinical trial conducted at Shanghai Ninth People's Hospital enrolled 54 patients with hydroxyurea-induced leg ulcers. Patients were randomly assigned to the control group (n = 27) treated with chlorhexidine dressing or the intervention group (n = 27) treated with the Zhangpi Ointment. Finally, 26 patients in the control group and 23 patients in the intervention group completed 8 weeks of observation. Results. The rate of complete healing was 100% for the intervention group, which was significantly higher than that of the control group (96.15%) (P<0.05). Furthermore, the intervention group achieved a significantly higher rate of wound healing (95.56%) than the control group (69.02%) at week 4 (P<0.01). The intervention group took 34 ± 5 days to achieve complete healing while the control group took 41 ± 7 days (P < 0.01). Moreover, grade 3/4 side effects were observed in neither group. Conclusion. The Zhangpi Ointment is effective in promoting the healing of hydroxyurea-induced leg ulcers in patients with myeloproliferative neoplasms, providing a therapeutic option for a condition that is recalcitrant to conventional therapy.

10.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 33(4): 308-313, 2017 Apr 08.
Artigo em Chinês | MEDLINE | ID: mdl-29926635

RESUMO

OBJECTIVE: To investigate the effects of adiponectin(ADP) postconditioning against myocardial ischemia/reperfusion injury(MIRI) in rats and role of ADP/PI3K/Akt pathway in ADP postconditioning. METHODS: SD rat was connected to ventilator by tracheal intubation under anesthesia, then left anterior descending coronary artery (LAD) was threaded between left auricle and pulmonary artery cone after exposing heart by surgery. MIRI model was induced by ligation of LAD for 30 min and the following reperfusion for 120 min. Rats were divided randomly into 5 groups (n=12):① Sham group:LAD was threaded without ligation; ② MIRI group; ③ADP group (ADP postconditioning) were subjected to intravenous injection of ADP when LAD ligation for 10 min and the ligation held for 20 min after that, then reperfusion for 120 min; ④ ADP+LY294002 group were subjected to injection of ADP and LY294002 when LAD ligation for 10 min, the other steps were the same as ADP group; ⑤ LY294002 group were subjected to injection of LY294002 when LAD ligation for 10 min, the other steps were the same as ADP group. Titers of lactate dehydrogenase(LDH) and cardiac troponin I(cTnI) in plasma were observed, expressions of PI3K, Akt, phosphorylated-Akt(p-Akt), ADP mRNA, ADPR1 mRNA and PI3k mRNA in myocardial tissue were measured. RESULTS: Compared with sham group, the levels of LDH and cTnI in MIRI group were increased (P<0.05); Compared with MIRI group, the levels of LDH and cTnI in ADP group were decreased (P<0.05); Compared with ADP group, the levels of LDH and cTnI were increased in LY294002 applying groups(P<0.05). Compared with MIRI group, the expressions of PI3K, p-Akt, ADP mRNA, ADPR1 mRNA and PI3K mRNA were increased in ADP group (P<0.05), the above mentioned 5 parameters in LY294002 applying groups were decreased(P<0.05). CONCLUSIONS: ADP postconditioning could reduce MIRI in rats, the protective effect might have relation to ADP/PI3k/Akt pathway.


Assuntos
Adiponectina/farmacologia , Pós-Condicionamento Isquêmico , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Animais , Cromonas/farmacologia , L-Lactato Desidrogenase/sangue , Morfolinas/farmacologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Ratos , Ratos Sprague-Dawley , Troponina I/sangue
11.
Acta Biochim Biophys Sin (Shanghai) ; 48(12): 1075-1084, 2016 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-27797717

RESUMO

Myocardial ischemia is a heart condition caused by reduction of blood flow to the heart, preventing heart from receiving enough oxygen. Myocardial ischemia is the most common cause of death globally. Heart ischemic preconditioning (IPC) has a protective effect against myocardial cell death induced by ischemia and ischemia-reperfusion injury. WDR26 has recently been identified as a protein that is increased following rat cardiac IPC. WDR26 can promote the proliferation of H9c2 cells and protect cardiomyocytes against oxidative stress through inhibiting apoptosis. However, its role in myocardial ischemia is unclear. The aim of this study was to explore the role of WDR26 in myocardial ischemia and H9c2 cell hypoxia. Our results showed that WDR26 is induced by myocardial ischemia and H9c2 cell hypoxia. WDR26 protects H9c2 cells against hypoxia injury through inhibiting LDH release and increasing cell viability. WDR26 promotes hypoxia-induced autophagy in hypoxia of H9c2 cells. We further demonstrated that in H9c2 cell hypoxia, WDR26 increases mitochondrial membrane potential, thereby increases Parkin translocation of mitochondria. After Parkin is translocated at mitochondria, WDR26 can increase mitochondrial protein ubiquitination in hypoxia of H9c2 cells. WDR26 is a mediator of response to hypoxia, and WDR26 plays an important role in hypoxia-mediated autophagy and mitophagy. This study provides novel insights into the protective role of WDR26 in cardiomyocyte injury during hypoxia. WDR26 may serve as a potential target for the treatment of myocardial ischemia.


Assuntos
Hipóxia Celular , Miócitos Cardíacos/citologia , Proteínas/fisiologia , Ubiquitina-Proteína Ligases/metabolismo , Animais , Linhagem Celular , Potencial da Membrana Mitocondrial , Miócitos Cardíacos/metabolismo , Transporte Proteico , Ratos , Ratos Sprague-Dawley
12.
Oncol Lett ; 9(1): 295-299, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25435978

RESUMO

The aim of the present study was to explore the effects of curcumin in combination with bevacizumab on the vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR)/K-ras pathway in hepatocellular carcinoma. A total of 30 Sprague Dawley (SD) rats were randomly divided into five groups: Control, model, curcumin, VEGF blocker, and curcumin + VEGF blocker groups. The mRNA levels of VEGF and VEGFR in all groups were subsequently measured by quantitative reverse transcriptase-polymerase chain reaction and the protein expression of K-ras was detected by western blot analysis. Compared with the control group, the mRNA levels of VEGF and VEGFR were revealed to be significantly increased in the model, curcumin and VEGF blocker groups. The VEGF mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were all decreased when compared with the model group. In addition, the VEGF mRNA levels in the curcumin + VEGF blocker group were significantly lower compared with the curcumin group (P<0.05). The VEGF mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were decreased when compared with the model group (P=0.0001). No significant differences in VEGF mRNA levels were identified between the VEGF blocker and curcumin groups (P=0.863), whereas the VEGF mRNA levels in the curcumin + VEGF blocker group were significantly lower than that of the curcumin group (P=0.025). Curcumin and the VEGF blocker are each capable of inhibiting hepatocellular carcinoma progression by regulating the VEGF/VEGFR/K-ras pathway. The combination of the two compounds has a synergistic effect on the inhibition of the effects of the VEGF signaling pathways in hepatocellular carcinoma progression.

13.
Exp Ther Med ; 5(5): 1305-1309, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23737869

RESUMO

The aim of this study was to investigate the effect of limb ischemic preconditioning (LIPC) on myocardial apoptosis in myocardial ischemia-reperfusion injury (MIRI), as well as the regulation of caspase-3 and the B cell lymphoma 2 (Bcl-2) gene in LIPC. A total of 50 rats were divided randomly into 5 groups (n=10). Four rats in each group were drawn out for detection of apoptosis. The sham, MIRI and LIPC groups underwent surgery without additional treatment. In the LY294002 group, LY294002 preconditioning was administered 15 min before reperfusion. In the LY294002+LIPC group, following LIPC, LY294002 was administered 15 min before reperfusion. The relative expression of myocardial Bcl-2 and caspase-3 mRNA and the apoptotic index for each group were determined by reverse transcription-polymerase chain reaction (RT-PCR) and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. The ultrastructure of the cardiac muscle tissues was observed by election microscopy. Compared with the sham group, the expression of caspase-3 mRNA in the MIRI group significantly increased (P<0.05) and the expression of Bcl-2 mRNA clearly decreased. Compared with the MIRI group, LIPC reduced the expression of caspase-3 and increased the expression of Bcl-2 mRNA (P<0.05). There were no significant differences between the LY294002+LIPC group and the MIRI group. Compared with the sham group, the apoptotic index of myocardial cells in the MIRI group significantly increased (P<0.05). Compared with the MIRI group, LIPC significantly decreased the apoptotic index of myocardial cells (P<0.05) and LY294002 increased the apoptotic index of myocardial cells. Compared with the LIPC group, LY294002+LIPC significantly increased the apoptotic index of myocardial cells (P<0.05). There were no significant differences between the LY294002+LIPC and MIRI groups. In conclusion, LIPC increased the expression of Bcl-2 and decreased caspase-3 mRNA and apoptosis in myocardial tissue following MIRI. Therefore, LIPC plays a protective role in myocardial tissue.

14.
Chin J Physiol ; 51(6): 357-62, 2008 Dec 31.
Artigo em Inglês | MEDLINE | ID: mdl-19280879

RESUMO

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is one of the hormone nuclear receptors. Recent data have shown that activation of PPARgamma signal pathway has many positive effects on cardiovascular system. The goals of this study were to determine whether PPARgamma activator affects cardiac fibrosis and the possible mechanisms. Cardiac fibroblasts (CFs) of SD neonate rats were used in the study. Cells were divided into 4 groups: I--control group; II--pioglitazone group (Piog--PPARgamma agonist); III--angiotensin II (Ang II) group; and IV--Piog + Ang II group (Piog plus angiotensin II). mRNA and protein expression of collagen type I, III and angiotensin II type 1 receptor (AT1-R) were tested by reverse transcription--polymerase chain reaction and Western blotting. With the inhibition of actinomycin D, we investigated the impacts of Piog on the stability of AT1-RmRNA. Compared with group I, the mRNA and protein expression of collagen type I, III and AT1-R were up-regulated in group III (P < 0.05). However with the effects of Piog in group IV, the expressions mentioned above were attenuated significantly (P < 0.05). With the effects of actinomycin D, AT1-RmRNA was reduced at the same degree in control and Piog groups at the same time points. These results indicated that treatment with Piog can attenuate Ang II-induced collagen synthesis in CFs through down-regulation of the AT1-R expression. With the intervention of actinomycin D, we suggested that PPARgamma agonist didn't affect the stability of AT1-RmRNA.


Assuntos
Regulação para Baixo , Miocárdio/metabolismo , PPAR gama/metabolismo , Receptor Tipo 1 de Angiotensina/metabolismo , Transdução de Sinais , Animais , Animais Recém-Nascidos , Sobrevivência Celular , Células Cultivadas , Colágeno Tipo I/genética , Colágeno Tipo III/genética , Fibroblastos , Estabilidade de RNA , Ratos , Ratos Sprague-Dawley , Receptor Tipo 1 de Angiotensina/genética
16.
Biol Trace Elem Res ; 113(3): 231-45, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-17194924

RESUMO

The mechanism of Cd2+ on the DNA cleavage and Ce3+ on the DNA repair in the kidney of silver crucian carp (Carassius auratus gibelio) is investigated by agarose gel electrophoresis methods and assaying biochemical indexes. It proves that Cd2+ induces the classical laddering degradation of DNA in vivo, but DNA cleavage is repaired after injecting with a low Ce3+ concentration under various Cd2+ concentrations. The DNA cleavage caused by Cd2+ is the result of the activation of deoxyribonuclease (DNase) and accumulation of reactive oxygen species (ROS), and Cd2+ destroys the antioxidant system, which diminishes the activities of superoxide dismutase, catalase, and peroxidase, and the increase of the lipid peroxidation (LPO) level. However, Ce3+ could inhibit activation of Cd2+ on DNase activity, relieve inhibition of Cd2+ on activities of the antioxidant enzyme, and diminish ROS accumulation. The results show that Ce3+ could relieve the toxicity of Cd2+ to silver crucian carp.


Assuntos
Cádmio/toxicidade , Césio/metabolismo , Rim/efeitos dos fármacos , Rim/metabolismo , Animais , Antioxidantes/química , Antioxidantes/metabolismo , Cádmio/metabolismo , Carpas , Dano ao DNA , Desoxirribonucleases/metabolismo , Elétrons , Eletroforese em Gel de Ágar , Íons , Peroxidação de Lipídeos , Lipídeos/química , Metais , Espécies Reativas de Oxigênio
17.
Lin Chuang Er Bi Yan Hou Ke Za Zhi ; 16(2): 56-7, 2002 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-15510627

RESUMO

OBJECTIVE: To analyze the experience and curative effect in treating chronic dacrocystitis by dacryocystorhinotomy with Ho:YAG laser under endoscope. METHOD: 20 patients of chronic dacryocystitis were treated by dacryocystorhinotomy with Ho:YAG laser under endoscope, followed-up for 1 approximately 2 years to observe the curative effects. RESULT: One was unplugged 8 months after the operation, six after 6 months, four after 4 months and nine after 3 months. No recidivations was found one year after the operation and the effective rate was 100%. There was no complications in all of the cases. CONCLUSION: The technique of dacryocystorhinotomy with Ho: YAG laser under endoscope overcomes the disadvantages of traditional method of operation.


Assuntos
Dacriocistite/cirurgia , Dacriocistorinostomia/métodos , Terapia a Laser , Adulto , Doença Crônica , Endoscópios , Feminino , Seguimentos , Hólmio/uso terapêutico , Humanos , Masculino
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