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Role of apoptosis-inducing factor in perinatal hypoxic-ischemic brain injury 被引量:15
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作者 Juan Rodriguez Tao Li +2 位作者 Yiran Xu Yanyan Sun Changlian Zhu 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第2期205-213,共9页
Perinatal complications,such as asphyxia,can cause brain injuries that are often associated with subsequent neurological deficits,such as cerebral palsy or mental retardation.The mechanisms of perinatal brain injury a... Perinatal complications,such as asphyxia,can cause brain injuries that are often associated with subsequent neurological deficits,such as cerebral palsy or mental retardation.The mechanisms of perinatal brain injury are not fully understood,but mitochondria play a prominent role not only due to their central function in metabolism but also because many proteins with apoptosis-related functions are located in the mitochondrion.Among these proteins,apoptosis-inducing factor has already been shown to be an important factor involved in neuronal cell death upon hypoxia-ischemia,but a better understanding of the mechanisms behind these processes is required for the development of more effective treatments during the early stages of perinatal brain injury.In this review,we focus on the molecular mechanisms of hypoxic-ischemic encephalopathy,specifically on the importance of apoptosis-inducing factor.The relevance of apoptosis-inducing factor is based not only because it participates in the caspase-independent apoptotic pathway but also because it plays a crucial role in mitochondrial energetic functionality,especially with regard to the maintenance of electron transport during oxidative phosphorylation and in oxidative stress,acting as a free radical scavenger.We also discuss all the different apoptosis-inducing factor isoforms discovered,focusing especially on apoptosis-inducing factor 2,which is only expressed in the brain and the functions of which are starting now to be clarified.Finally,we summarized the interaction of apoptosis-inducing factor with several proteins that are crucial for both apoptosis-inducing factor functions(prosurvival and pro-apoptotic)and that are highly important in order to develop promising therapeutic targets for improving outcomes after perinatal brain injury. 展开更多
关键词 apoptosis apoptosis inducing factor ASPHYXIA cell death free radical HYPOXIA-ISCHEMIA mitochondria NEONATES oxidative stress
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Poly(ADP-ribosyl)ation of Apoptosis Antagonizing Transcription Factor Involved in Hydroquinone-Induced DNA Damage Response 被引量:6
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作者 ling xiao xuan liu jia xian +5 位作者 yun lin du yu jun chen shao qian chen jia long tang huan wen liu lin hua 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2016年第1期80-84,共5页
The molecular mechanism of DNA damage induced by hydroquinone (HQ) remains unclear. Poly(ADP-ribose) polymerase-1 (PARP-1) usually works as a DNA damage sensor, and hence, it is possible that PARP-1 is involved ... The molecular mechanism of DNA damage induced by hydroquinone (HQ) remains unclear. Poly(ADP-ribose) polymerase-1 (PARP-1) usually works as a DNA damage sensor, and hence, it is possible that PARP-1 is involved in the DNA damage response induced by HQ. In TK6 cells treated with HQ, PARP activity as well as the expression of apoptosis antagonizing transcription factor (AATF), PARP-1, and phosphorylated H2AX (v-H2AX) were maximum at 0.5 h, 6 h, 3 h, and 3 h, respectively. To explore the detailed mechanisms underlying the prompt DNA repair reaction, the above indicators were investigated in PARP-l-silenced cells. PARP activity and expression of AATF and PARP-1 decreased to 36%, 32%, and 33%, respectively, in the cells; however, y-H2AX expression increased to 265%. Co-immunoprecipitation (co-IP) assays were employed to determine whether PARP-1 and AATF formed protein complexes. The interaction between these proteins together with the results from IP assays and confocal microscopy indicated that poly(ADP-ribosyl)ation {PARylation) regulated AATF expression, in conclusion, PARP-1 was involved in the DNA damage repair induced by HQ via increasing the accumulation of AATF through PARylation. 展开更多
关键词 PARP DNA DDR Figure ADP-ribosyl)ation of apoptosis Antagonizing Transcription factor Involved in Hydroquinone-Induced DNA Damage Response
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Expression of tumor necrosis factor related apoptosis inducing ligand receptor in glioblastoma
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作者 Dongling Gao Zhongwei Zhao Hongxin Zhang Lan Zhang Kuisheng Chen Yunhan Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第5期538-541,共4页
BACKGROUND: Receptors for tumor necrosis factor related apoptosis inducing ligand (TRAIL) include death receptor 4, death receptor 5, decoy receptor 1, and decoy receptor 2. Activation of death receptor 4 and 5 sel... BACKGROUND: Receptors for tumor necrosis factor related apoptosis inducing ligand (TRAIL) include death receptor 4, death receptor 5, decoy receptor 1, and decoy receptor 2. Activation of death receptor 4 and 5 selectively kills tumor cells. OBJECTIVE: To detect TRAIL receptor expression in glioblastoma by immunohistochemistry and RT-PCR, and to compare this expression to that in normal brain tissue. DESIGN: Observational analysis. SETTING: Department of Pathology, the First Affiliated Hospital of Zhengzhou University; Henan Tumor Pathology Key Laboratory. PARTICIPANTS: Twenty-five patients (17 males and 8 females) who received glioblastoma resection were selected from the Fifth Affiliated Hospital of Zhengzhou University, between September 2003 to June 2004. All glioblastoma samples were diagnosed pathologically. Twenty patients (12 males and 8 females) with craniocerebral injury who received normal brain tissue resection were selected in the same time period. There were no significant differences in sex and age between glioblastoma patients or between craniocerebral injury patients (P 〉 0.05). All patients and appropriate relatives provided informed consent, and this study was approved by the local research ethics committee. METHODS: Polyclonal antibody against TRAIL receptors and an immunohistochemical kit (batch number: 200502) were purchased from Boster Company, Wuhan. Immunohistochemistry: Expression of death receptor 4, death receptor 5, decoy receptor l, and decoy receptor 2 were observed in both glioblastoma and normal brain tissue. The experiment was performed according to the kit instructions, and positive staining was brown-yellow. Assessment: There were no positive signals (-); weakly positive signals, positive cells 〈 25% (+); weakly positive signals, positive cells 25%-50% (++); strongly positive signals, positive cells 50%-75% (+++); strongly positive signals, positive cells 〉 75% (++++). Evaluation: Expression levels of TRAIL receptors were estimated in both normal brain tissue and glioblastoma. Expression of decoy receptor 1 and decoy receptor 2 mRNA in glioblastoma were detected by reverse transcription polymerase chain reaction, and expression of decoy receptor in glioblastoma was estimated. MAIN OUTCOME MEASURES: Comparison of death receptor and decoy receptor protein expression between glioblastoma and normal brain tissue; decoy receptor mRNA expression in glioblastoma. RESULTS: Death receptor protein expression was strongly positive (+++) in glioblastoma, while it was weakly positive (+, ++) in normal brain tissue. Therefore, expression rate of death receptor protein in the glioblastoma was significantly higher than that in the normal brain tissue (.~ 2 = 18.48, 23.03, P 〈 0.01). Decoy receptor protein expression in the glioblastoma was significantly lower than that in the normal brain tissue ( x2 = 6.65, 18.76, P 〈 0.01). The level of decoy receptor mRNA expression in glioblastoma was significantly higher than those of protein expression ( x 2 = 9.82, 10.09, P〈 0.01). CONCLUSION: High expression of death receptor and low expression of decoy receptor are frequently observed in glioblastoma, suggesting that TRAIL receptor genes show an anti-tumor and expressive response during the initiation and development of the tumor. There are significant differences in decoy receptor expression between normal brain tissue and glioblastoma, suggesting that the restricted expression of decoy receptor in glioblastoma is regulated at the post-transcriptional level. 展开更多
关键词 GLIOBLASTOMA tumor necrosis factor related apoptosis inducing ligand apoptosis IMMUNOHISTOCHEMISTRY reverse transcription polymerase chain reaction
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How do Chinese medicines that tonify the kidney inhibit dopaminergic neuron apoptosis? 被引量:10
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作者 Shaogang Lin Shuifen Ye +6 位作者 Jinmu Huang Yun Tian Yihui Xu Mengqi Wu Jingxia Wang Songying Wu Jing Cai 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第30期2820-2826,共7页
Wistar rats were intragastrical y perfused with Chinese medicines used for tonifying the kidney. These included 0.180 g/mL of Herba Epimedi (Epimedium), Semen Cuscutae (Dodder Seed), or Herba Cistanches (Desertli... Wistar rats were intragastrical y perfused with Chinese medicines used for tonifying the kidney. These included 0.180 g/mL of Herba Epimedi (Epimedium), Semen Cuscutae (Dodder Seed), or Herba Cistanches (Desertliving Cistanche), 0.04 mg/mL monoamine oxidase-B inhibitor selegiline, or distil ed water for 14 consecutive days to prepare drug-containing serum or blank serum. MES23.5 cells in the logarithmic phase were cultured in media supplemented with 15%drug-containing serum for 24 hours, fol owed by incubation in culture solution containing 100μmol/L H2O2 for 3 hours. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow tometry results showed that al drug-containing serums improved the survival rate of H 2 O 2-injured MES23.5 cells, inhibited pro-apoptotic FasL and caspase-3 expression, promoted anti-apoptotic Bcl-2 expression. However, drug-containing serums had little influence on Fas expression in H 2 O 2-injured MES23.5 cells. Enzyme-linked immunosorbent assay results showed that serum containing Herba Cistanches or Herba Epimedi increased the expression of nerve growth factor, brain-derived neurotrophic factor, and glial cellline-derived neurotrophic factor in injured MES23.5 cells;serum containing Semen Cuscutae only increased brain-derived neurotrophic factor expres-sion; while expression of the above neurotrophic factors remained the same in cells treated with serum containing selegiline. These findings indicate that Chinese medicines used to tonify the kid-ney can protect nerve cells by regulating the expression of apoptosis-related factors and neuro-trophic factors in MES23.5 cells. 展开更多
关键词 neural regeneration traditional Chinese medicine drug-containing serum MES23.5 dopaminergicnerve cells neurotrophic factors apoptosis factors Parkinson's disease NEUROPROTECTION
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Apoptosis and Expression of Protein TRAIL in Granulosa Cells of Rats with Polycystic Ovarian Syndrome 被引量:5
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作者 张娟 朱桂金 +2 位作者 王昕荣 徐蓓 胡琳莉 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2007年第3期311-314,共4页
The relationship between apoptosis of granulosa cells and follicle development arrest in polycystic ovarian syndrome (PCOS) rats, and the contribution of tumor necrosis factor related apoptosis inducing ligand (TRAIL)... The relationship between apoptosis of granulosa cells and follicle development arrest in polycystic ovarian syndrome (PCOS) rats, and the contribution of tumor necrosis factor related apoptosis inducing ligand (TRAIL) in apoptosis of granulosa cells were explored. By using sodium prasterone sulfate rat PCOS model was induced. The apoptosis of granulosa cells in ovaries of rats was observed by TdT-mediated dUTP-biotin nick end-labeling (TUNEL), and the expression of TRAIL protein and mRNA in granulosa cells was detected by using immunhistochemical staining and reverse transcription polymerase chain reaction (RT-PCR) respectively. The apoptotic rate and the expression of protein TRAIL in granulosa cells were significantly higher in antral follicles from the PCOS rats than in those from the control rats (P<0.01, P<0.05). There was no significant difference in apoptotic rate and the expression of TRAIL protein in granulosa cells of preantral follicles between the PCOS rats and the control rats (P>0.05). No apoptosis and the expression of TRAIL protein in granulosa cells of primordial follicles were found in the two groups. The expression of TRAIL mRNA was significantly stronger in granulosa cells from the PCOS rats than in those from the con- trol rats (P<0.01). It was suggested that the apoptotic rate in granulosa cells was significantly higher in antral follicle from the PCOS rats than in those from the control rats. TRAIL played a role in regu- lating the apoptosis of granulosa cells in PCOS rats. 展开更多
关键词 tumor necrosis factor related apoptosis inducing ligand granulosa cell apoptosis polycystic ovarian syndrome RAT
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Chloride channel blocker 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid inhibits nitric oxide-induced apoptosis in cultured rat hippocampal neurons 被引量:2
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作者 Jinbao Yin Lijuan Xu +5 位作者 Shuling Zhang Yuanyin Zheng Zhichao Zhong Hongling Fan XiLi Quanzhong Chang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第2期121-126,共6页
Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2'-disulfonic ... Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2'-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly(adenosine diphosphate-ribose)polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2'-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly(adenosine diphosphate-ribose)polymerase-1 and apoptosis-inducing factor. 展开更多
关键词 neural regeneration brain injury chloride channel 3-morpholinosydnonimine hippocampus poly(adenosine diphosphate-ribose)polymerase-1 apoptosis inducing factor neuronal apoptosis grants-supported paper photographs-containing paper neuroregeneration
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Effects of 3-aminobenzamide on expressions of poly(ADP ribose) polymerase and apoptosis inducing factor in cardiomyocytes of rats with acute myocardial infarction 被引量:10
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作者 ZHAO Yu-juan WANG Jian-hua +4 位作者 FU Bing MA Mu-xin LI Bao-xin HUANG Qi YANG Bao-feng 《Chinese Medical Journal》 SCIE CAS CSCD 2009年第11期1322-1327,共6页
Background Poly(ADP-ribose) polymerase (PARP) plays an important role in cell survival and death. However, the mechanisms involved are not fully understood. Therefore, we investigated the effect of inhibition of P... Background Poly(ADP-ribose) polymerase (PARP) plays an important role in cell survival and death. However, the mechanisms involved are not fully understood. Therefore, we investigated the effect of inhibition of PARP on acute myocardial infarction (AMI) at different time points in rats. Methods AMI was induced in rats by ligating the left anterior descending coronary artery. One group received 3-aminobenzamide (3-AB, a kind of PARP inhibitor) (30 mg/kg) by intraperitoneal injection. The changes of ultramicrostructure of cardiocytes in infarction region were noted, PARP cleavage was measured by Western blotting, and expressions of protein of PARP and apoptosis inducing factor (AIF) were measured by immunohistochemical staining after treatment with 3-AB for 2 hours, 4 hours, 6 hours, 1 week, 4 weeks and 8 weeks. Results Few damages to the ultramicrostructure of cardiocytes were observed after treatment with 3-AB. PARP cleavage was detected as early as 4 hours and markedly increased by 6 hours following AMI without 3-AB, but was not found until 6 hours following AMI treated with 3-AB. There were significant differences between 3-AB and AMI groups at the same time points. The expression of PARP was observed gradually increased, but that of AIF was suppressed for 6 hours after treatment of 3-AB, compared with AMI groups in positive cells at the same time points. There was significantly less cleavage of PARP and more PARP expression in 3-AB treated group compared with AMI and control groups at all matched time points. Conclusions Our results suggest that 3-AB inhibits degradation of PARP, increases the expression of PARP protein, and suppresses the expression of AIF protein. Inhibition of PARP activity may protect cardiocytes in rats with AMI and reduce apoptosis. 展开更多
关键词 3-AMINOBENZAMIDE acute myocardial infarction poly(ADP-ribose) polymerase apoptosis inducing factor DNA repair apoptosis
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Effects of decompression joint Governor Vessel electro-acupuncture on rats with acute upper cervical spinal cord injury 被引量:8
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作者 Yan-Lei Wang Ying-Na Qi +5 位作者 Wei Wang Chun-Ke Dong Ping Yi Feng Yang Xiang-Sheng Tang Ming-Sheng Tan 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第7期1241-1246,共6页
Decompression is the major therapeutic strategy for acute spinal cord injury,but there is some debate about the time window for decompression following spinal cord injury.An important goal and challenge in the treatme... Decompression is the major therapeutic strategy for acute spinal cord injury,but there is some debate about the time window for decompression following spinal cord injury.An important goal and challenge in the treatment of spinal cord injury is inhibiting or reversing secondary injury.Governor Vessel electroacupuncture can improve symptoms of spinal cord injury by inhibiting cell apoptosis and improving the microenvironment of the injured spinal cord.In this study,Governor Vessel electroacupuncture combined with decompression at different time points was used to treat acute spinal cord injury.The rat models were established by inserting a balloon catheter into the atlanto-occipital space.The upper cervical spinal cord was compressed for 12 or 48 hours prior to decompression.Electroacupuncture was conducted at the acupoints Dazhui(GV14) and Baihui(GV 20)(2 Hz,15 minutes) once a day for 14 consecutive days.Compared with decompression alone,hind limb motor function recovery was superior after decompression for 12 and 48 hours combined with electroacupuncture.However,the recovery of motor function was not significantly different at 14 days after treatment in rats receiving decompression for 12 hours.Platelet-activating factor levels and caspase-9 protein expression were significantly reduced in rats receiving electroacupuncture compared with decompression alone.These findings indicate that compared with decompression alone,Governor Vessel electroacupuncture combined with delayed decompression(48 hours) is more effective in the treatment of upper cervical spinal cord injury.Governor Vessel electroacupuncture combined with early decompression(12 hours) can accelerate the recovery of nerve movement in rats with upper cervical spinal cord injury.Nevertheless,further studies are necessary to confirm whether it is possible to obtain additional benefit compared with early decompression alone. 展开更多
关键词 nerve regeneration acute spinal cord injury decompression Governor Vessel electroacupuncture platelet-activating factor apoptosis methylprednisolone caspase family upper cervical spine animal model Basso Beattie and Bresnahan locomotor scale neural regeneration
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Effects of moxibustion at bilateral Feishu(BL13)and Xinshu(BL15)combined with benazepril on myocardial cells apoptosis index and apoptosis-related proteins cytochrome c and apoptosis-inducing factor in rats with chronic heart failure 被引量:1
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作者 WANG Wei LI Qingling +4 位作者 MA Qiang XIA Ran GAO Bing WANG Yi WANG Jing 《Journal of Traditional Chinese Medicine》 SCIE CSCD 2022年第2期227-233,共7页
OBJECTIVE:To observe the effects of moxibustion at bilateral Feishu(BL13)and Xinshu(BL15)combined with benazepril on myocardial cells apoptosis index,the expression levels of apoptosis-related proteins cytochrome c(Cy... OBJECTIVE:To observe the effects of moxibustion at bilateral Feishu(BL13)and Xinshu(BL15)combined with benazepril on myocardial cells apoptosis index,the expression levels of apoptosis-related proteins cytochrome c(Cyt-C)and apoptosis-inducing factor(AIF)in chronic heart failure(CHF)rats.METHODS:Sixty-five rats were randomly divided into normal group(n=10)and model-I group(n=55).After modeling,CHF rats in model-I group were divided into model group,moxibustion group,benazepril group,moxibustion plus benazepril group(abbreviated as aibei group,the same below),10 rats in each group.Echocardiogram index was examined by echocardiography.Hemodynamic indices were measured by rat cardiac function meter.Serum B-type brain natriuretic peptide(BNP)was detected by enzymelinked immunosorbent assay.Myocardial cells apoptosis index was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling staining.Pathological changes of myocardial tissues were observed by hematoxylin and eosin staining.The expression levels of Cyt-C and AIF in myocardial tissues were detected by Western blot.RESULTS:Compared with normal group,ejection fraction and left ventricular diameter shortening rate in model-Ⅰgroup were significantly reduced,myocardial cells of rats in model group exhibited unclear transverse striations,cells swellings and vacuoles,cardiac functions were deteriorated,serum BNP level,myocardial cells apoptosis index,and the expression levels of Cyt-C and AIF were significantly increased.Compared with model group,myocardial cells of rats in moxibustion group,benazepril group,and aibei group were dyed more evenly,muscle fibers were arranged relatively neatly,cardiac functions were improved,serum BNP level,myocardial cells apoptosis index,and the expression levels of Cyt-C and AIF were significantly decreased.Compared with aibei group,cardiac functions were worsened,myocardial cells apoptosis index,and the expression levels of Cyt-C and AIF were increased.CONCLUSION:Moxibustion at bilateral Feishu(BL13)and Xinshu(BL15)combined with benazepril could improve CHF better than moxibustion at bilateral Feishu(BL13)and Xinshu(BL15)or benazepril alone.The mechanisms might be that they can inhibit the expressions of Cyt-C and AIF,and inhibit the apoptosis of cardiomyocytes. 展开更多
关键词 heart failure MOXIBUSTION point BL13(Feishu) point BL15(Xinshu) cytochromes c apoptosis inducing factor
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Noise exposure induced cochlear hair cell death pathways in guinea pig
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作者 Alfred Nuttall 《Journal of Otology》 2010年第1期51-56,共6页
Objective To understand the mechanism of noise exposure induced outer hair cells(OHCs) death pathways. Methods Thirty two guinea pigs were used in this study. The animals were either exposed for 4 h/day to broadband n... Objective To understand the mechanism of noise exposure induced outer hair cells(OHCs) death pathways. Methods Thirty two guinea pigs were used in this study. The animals were either exposed for 4 h/day to broadband noise at 122 dB SPL (A-weighted) for 2 consecutive days or perfused with MNNG. After auditory test, the cochleae of animals were dissected. Propidium iodide (PI), a DNA intercalating fluorescent probe, was used to trace morphological changes in OHC nuclei. F-actin staining was used to determine missing OHCs. Caspase-3 was detected in living organ of Corti whole mounts using the fluorescent probe. The single strand DNA (ssDNA) in apoptotic OHCs in guinea pigs and apoptosis inducing factor (AIF) in hair cells in guinea pigs were examined by immunohistology method. Whole mounts of organ of Corti were prepared. Morphological and fluorescent changes were examined under a confocal microscope. Results (1) Both apoptotic and necrotic hair cells appeared following noise exposure. (2) Noise exposure induced single strand DNA in apoptotic OHCs but not in the normal OHCs. (3) Either after noise exposure or after MNNG perfusion, apoptotic OHCs were featured by nuclear condensation or fragmentation with caspase-3 activation, whereas necrotic OHCs were characterized by nuclear swelling without caspase-3 activation. (4) In normal organ of Corti, AIF was located in the mitochondria areas. After noise exposure, AIF was translocated from mitochondria in apoptotic and necrotic OHCs. Conclusion These findings indicate that noise exposure damages DNA in the OHC, which triggers action of Caspase-3. Subsequently, AIF is translocated to the nucleus, leading to DNA damage and OHCs death. 展开更多
关键词 Noise exposure Outer hair cell Single strand DNA apoptosis induced factor Caspase.
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Effects of Shen-Fu Injection (参附注射液) on Apoptosis of Regulatory T Lymphocytes in Spleen during Post-Resuscitation Immune Dysfunction in A Porcine Model of Cardiac Arrest 被引量:11
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作者 顾伟 张茜 李春盛 《Chinese Journal of Integrative Medicine》 SCIE CAS CSCD 2016年第9期666-673,共8页
Objective: To investigate whether Shen-Fu Injection(参附注射液, SFI) reduces post-resuscitation immune dysfunction in a porcine model of cardiac arrest by modulating apoptosis of regulatory T lymphocytes(Treg) in... Objective: To investigate whether Shen-Fu Injection(参附注射液, SFI) reduces post-resuscitation immune dysfunction in a porcine model of cardiac arrest by modulating apoptosis of regulatory T lymphocytes(Treg) in the spleen. Methods: After 8-min untreated ventricular fibrillation and 2-min basic life support, 24 pigs were divided into 3 groups with a random number table, i.e. SFI group, epinephrine(EP) group, and saline(SA) group(8 in each group), which received central venous injection of SFI(1.0 m L/kg), EP(0.02 mg/kg) and SA, respectively. The same procedure without CA initiation was achieved in the sham-operated(sham) group(n=6). After successful return of spontaneous circulation(ROSC), apoptosis rate of splenic Treg was detected by flow cytometry; and the m RNA expression of forkhead/winged helix transcription factor(Foxp3) of splenic Treg was detected by real time-polymerase chain reaction; and the levels of interleukin-4(IL-4) and interferon-γ(IFN-γ) in porcine splenic Treg were detected by using enzyme-linked immunosorbent assay(ELISA). Results: Compared with the sham group, the apoptosis rate of Treg was significantly decreased, and the levels of Foxp3 m RNA expression, IFN-γ, IL-4 and IFN-γ/IL-4 were increased in the SA group(P〈0.05 or P〈0.01). Compared with the EP and SA groups, SFI treatment increased the apoptosis rate of Treg and reduced the levels of Foxp3 m RNA expression, IFN-γ and IFN-γ/IL-4(P〈0.05). Conclusions: SFI has significant effects in attenuating post-resuscitation immune dysfunction by modulating apoptosis of Treg in the spleen. 展开更多
关键词 Shen-Fu Injection cardiopulmonary resuscitation post-resuscitation immune dysfunction regulatory T lymphocytes apoptosis forkhead/winged helix transcription factor Chinese medicine
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