apoptosis

Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion

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Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion by Deng-ming Wei, Guang-zhao Huang, Yi-gu Zhang, Guang-xun Rao.

Objective: To study effect of triptolide(TL) on neuronal apoptosis in cerebral tissue rat after ischemia-reperfusion. Method: Triptolide at dose 0.2 or 0.4 mg·kg -1was intr aperitoneally injected once a day for 4 d. The focal ischemia-rep erfusion model was established with thread embolism middle artery before trip tolide injection the fourth day. Neurological deficit score rats eval uated; and immunohistochemical techniques were used to count positive cells express MPO TUNEL tissue. Result: Compare d control group, neural function significantly impr oved, number infiltrate neutrophil cere bral remarkably reduced two TL-treated groups. Conclusio n: results suggested that TL can inhibit infiltration decrease degree [

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Expression of GATA6 in insulinoma and its relationship with proliferation and apoptosis of insulinoma cells

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Expression of GATA6 in insulinoma and its relationship with proliferation and apoptosis of insulinoma cells by 魏美林, 韩峻峰, 魏丽, 王倩倩, 李旭.

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PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress

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PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress by Heyu Zhang, Xi Ma, Xuan Deng, Yiyu Chen, Xiaoning Mo, Yingmei Zhang, Hongshan Zhao, Dalong Ma.

An apoptosis-related protein, cerebral cavernous malformation 3 (CCM3 or PDCD10), has recently been implicated in mutations associated with malformation. Herein, we show that PDCD10 interacts serine/threonine kinase 25 (STK25), an oxidant stress response related to sterile-20 (Ste20) is activated by oxidative and induces apoptotic cell death. Functional investigations indicate STK25 protein are up-regulated H2O2 stimulation, co-expression of the proteins accelerates apoptosis. The induction small interfering (siPDCD10) siSTK25 results decreased endogenous expression, which accompanied attenuated Interaction between modulates ERK activity under stress. stabilizes through a proteasome-dependent pathway. Our findings suggest might be regulatory adaptor required for functions, differ distinctly depending on redox status cells may potentially tumor progression.

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Regulation of apoptosis signal‐regulating kinase 1 degradation by Gα13

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Regulation of apoptosis signal‐regulating kinase 1 degradation by Gα13 by Mikhail A. Kutuzov, Alexandra V. Andreeva, Tatyana A. Voyno-Yasenetskaya.

Apoptosis signal-regulating kinase (ASK1) is a mitogen-activated protein (MAPK) that transduces apoptotic signals from variety of stresses. We have shown previously alpha subunits heterotrimeric G12 and G13 proteins stimulate ASK1 activity ASK1-dependent apoptosis. Here, we report novel mechanism G-protein-dependent regulation ASK1. demonstrated G alpha13 forms complex with in an activation-independent manner. Both N- C-terminal regulatory domains were essential for the efficient interaction, while its domain was not required. Formation alpha13-ASK1 enhanced by JNK-interacting leucine zipper protein, JLP. Constitutively activated alpha13Q226L increased expression. Short-term activation serotonin 5-HT4 receptor coupled to also Importantly, prolonged COS-7 cells or treatment human umbilical vein endothelial thrombin concomitantly down-regulated both Data showed reduced rate degradation, decreased ubiquitination, association E3 ubiquitin ligase CHIP, mediate degradation. Our findings indicate expression levels can be regulated alpha13, at least part via control ubiquitination

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Regulation of the Intrinsic Apoptosis Pathway by Reactive Oxygen Species

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Regulation of the Intrinsic Apoptosis Pathway by Reactive Oxygen Species by Chu Chiao Wu, Shawn B. Bratton.

The intrinsic apoptosis pathway is conserved from worms to humans and plays a critical role in the normal development homeostatic control of adult tissues. As result, numerous diseases cancer neurodegeneration are associated with either too little or much apoptosis.B cell lymphoma-2 (BCL-2) family members regulate death, primarily via their effects on mitochondria. In stressed cells, proapoptotic BCL-2 promote mitochondrial outer membrane permeabilization (MOMP) cytochrome c (cyt c) release into cytoplasm, where it stimulates formation “apoptosome.” This large, multimeric complex composed adapter protein, apoptotic protease-activating factor-1, cysteine protease, caspase-9. Recent studies suggest that proteins involved processes leading up (and including) apoptosome subject various forms post-translational modification, including proteolysis, phosphorylation, some cases, direct oxidative modification.Despite intense investigation pathway, significant questions remain regarding how cyt released mitochondria, formed regulated, caspase-9 activated within complex.Further biochemistry MOMP needed understand mechanisms underpin these processes, novel animal models will be necessary future ascertain importance many posttranslational modifications reported for components apoptosome.

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S9.4b Trimetallic Cu-Zn-Fe nanoparticles induced apoptosis and cell cycle arrest in multidrug-resistant Candida auris S9.4 Free oral presentations (late breaking), September 23, 2022, 4:45 PM – 6:15 PM

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S9.4b Trimetallic Cu-Zn-Fe nanoparticles induced apoptosis and cell cycle arrest in multidrug-resistant Candida auris S9.4 Free oral presentations (late breaking), September 23, 2022, 4:45 PM – 6:15 PM by Hammad Alam, Aijaz Ahmad.

Abstract Background Candida species are opportunistic fungus that can cause serious infections, particularly in immunocompromised population. The number of fungal infections has increased steadily with being responsible for ˃ 70% these instances, hospitalized patients significant underlying conditions. Pharmacological resistance and the advent auris have elevated candidiasis to a major public health concern. is an emerging multidrug-resistant catastrophic bloodstream high fatality rates, medical issues. Antifungal study trimetallic nanoparticles (NPs) various types been studied as therapy option efficient safe control candidiasis. These NPs were highlighted environmentally friendly sustainable synthetic preparative possibilities. Objective: This work aimed synthesize characterize novel Cu-Zn-Fe determine their vitro antifungal activity mechanism action against isolates. Methods synthesis characterization was done by standard methods. capability determined calculating minimum inhibitory concentrations (MIC) fungicidal (MFC) following CLSI recommended guidelines. Susceptibility on planktonic cells biofilms further confirmed MuseTM cell count viability assay scanning electron microscopy (SEM) respectively. For insight mechanisms, apoptosis cycle arrest exploring different apoptotic markers analyzer. Results Characterizations Fourier-transform infrared spectroscopy (FTIR), diffuse reflectance UV-visible spectroscopy, X-ray diffraction (XRD), (SEM), transmission (TEM) successful biosynthesis NPs. MIC MFC values 12.5 25 μg/ml results reporting 45.5%, 13.5%, 1.8% when C. treated 1/2 MIC, 2MIC Cell analysis revealed 91.2% healthy developing untreated G0/G1 phase, whereas 5.2% 3.7% S phase G2/M In contrast, NP-treated observed be arrested 49.3% at 2MIC. To physiology death caused NPs, we investigated mitochondrial membrane potential (∆ψm), live having stable (∆ψm) showed loss (∆ψm). Another important parameter yeast release cytochrome C from mitochondria cytosol resulting decreased cytosolic levels. Both test causing auris. Conclusion (Cu-Zn-Fe) displayed strong auris, S-phase, which could linked DNA damage. Important suggested apotosis All findings suggest taken next level research development medications.

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Antitumor activity of conventional and supercritical extracts from Piper nigrum L. cultivar Bragantina through cell cycle arrest and apoptosis induction

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Antitumor activity of conventional and supercritical extracts from Piper nigrum L. cultivar Bragantina through cell cycle arrest and apoptosis induction by Valdelúcia M.A.S. Grinevicius, Kátia S. Andrade, Fabiana Ourique, Gustavo Amadeu Micke, Sandra R.S. Ferreira, Rozangela Curi Pedrosa.

Abstract Herbal formulae with black pepper have been used to cancer treatment. The aim of this work was evaluate antitumor activity ethanolic and high pressure extracts produced from ( Piper nigrum L. cultivar Bragantina). were obtained by Supercritical Fluid extraction (SFE) at different conditions. Phytochemical analysis the showed presence piperine terpenoids. However, extract 200 bar 40 °C (SFE200) had higher content lowest monoterpenes/sesquiterpenes ratio, compared others extracts, also presented more cytotoxicity after 72 h (EC 50 14.40 ± 3.30 μg/ml), probably due synergy between sesquiterpenes. SFE200 contain phytocompounds able intercalate causing oxidative DNA damage. In vivo treatment 10 mg/kg/day for isogenic Balb-c mice bearing Ehrlich ascites carcinoma tumor inhibition increased survival time extract, related cell cycle arrest apoptosis.

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Letrozole Inhibits Cells Apoptosis Through the Down-Regulation of Bcl-2 Expression and Up-Regulation of Caspase-3 Expression in Human Uterine Leiomyoma Cells

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Letrozole Inhibits Cells Apoptosis Through the Down-Regulation of Bcl-2 Expression and Up-Regulation of Caspase-3 Expression in Human Uterine Leiomyoma Cells by Zhou Shou-hong.

Objective To explore the effect of letrozole on proliferation,apoptosis and expression bcl-2 caspase-3 in human uterine leiomyoma cells.Methods Primary culture leimyoma cells were treated with letrozole(10-8,10-7,10-6 10-5 mol/L) for 24,48 72 hours MTT assay was used to detect growth curve.The rates apoptosis measured by flow cytometry.The level estradiol medium radio-immunity assay.The detected Real-time PCR Western blot.Results The proliferations significantly inhibited markedly increased treatment 10-7,10-6 mol/L 48 a dose-dependent time-dependent manner.The levels decreased manner hours.The manner.Conclusions Letrozole inhibits proliferation,promotes apoptosis,which mechanism may be related decrease secretion,the increase induced cells.

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Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome

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Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome by Rainer Seidl, Michal Bajo, K. Böhm, E. C. LaCasse, A. E. MacKenzie, N. Cairns, Gert Lubec.

In Down syndrome (DS), enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration Alzheimer-type. The human IAP (inhibitor proteins) genes (NAIP, c-IAP-2/HIAP-1, c-IAP-1/Hiap-2, XIAP, survivin) are an evolutionary conserved family proteins which prevent death across species, implying that they act at central, highly point cascade. Evidence for downregulation NAIP-mRNA fetal DS (23rd week gestation), as found by subtractive hybridization technique challenged studies protein level adult brain specimen. NAIP-like immunoreactivity was determined four different regions cerebral cortex cerebellum 9 patients with Alzheimer-like neuropathologic lesions, Alzheimer disease (AD) compared to controls. For first time, NAIP-IR could be demonstrated cortical brain. Compared control subjects, western blotting significantly decreased levels parietal occipital frontal AD. While mode NAIP action is unknown, inhibition certain caspases has already been other IAP-family members (c-IAP1, c-IAP2 XIAP). Although AD awaits further confirmation, results suggest alterations regulatory (inhibitory) another feature

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Experimental study on apoptosis of MCF-7 breast cancer cells induced by Interferon-γ through the Fas/FasL

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Experimental study on apoptosis of MCF-7 breast cancer cells induced by Interferon-γ through the Fas/FasL by Sun Li-xin.

Objective:To investigate the mechanism of apoptosis MCF-7 treated by interferon-γ.Methods:Detected control group and experimental groups flow cytometry(FCM).Results:The percentage apoptotic cells increased after interferon-γ(P0.05),and FasL interferon-γ(P0.05).Conclusion:Interferon-γ can induced breast cancer through Fas/FasL.

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