APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
·
2021
·Vol. 105
·期 5
·2033-2042
·
IF 4.813
Wang Xiao,Xu Na,Li Qinglin,Chen Shengqi,Cheng Hui,Yang Mo,Jiang Ting,Chu Jun,Ma Xiaojing,Yin Dengke
Liver cancer, one of the most common types of cancer in the world, is the second leading cause of death for cancer patients. For liver cancer, there is an urgent need for an effective treatment with no or less toxic side effects. Lactonic sophorolipids (LSL), as a potential anticancer drug, has attracted wide attention of pharmaceutical researchers with its good biological activities. The effects of LSL and cell death inhibitors were measured by MTT test on HepG2 cells. Meanwhile, the morphology of the cells was observed under a microscope. The apoptosis rate was detected by flow cytometry, and the expression levels of enzyme activity of Caspase-3 and Caspase-9 were measured by detection kits. Meanwhile, mRNA levels of Apaf-1 , Caspase-3 , Bax , and Bcl-2 were measured by quantitative real-time RT-PCR; protein levels of Caspase-3, Cleaved Caspase-3, Bax, and Bcl-2 were measured by western blot. LSL can inhibit the proliferation of cells, and it is possible to induce apoptosis in cells. The HepG2 cells with LSL co-culture exhibited typical apoptotic morphology, and the expression levels of enzyme activity of Caspase-3 and Caspase-9 increased ( P < 0.05). We also found that LSL increases cell apoptosis rate and regulates the expression of genes and proteins associated with apoptosis through the Caspase-3 pathway. These results indicate that LSL may be one of the potential drug candidates to inhibit the proliferation and induce apoptosis in HepG2 cells.
Key points
• LSL, which is of good biological activities such as anti-bacterium, virus elimination, and inflammatory response elimination, has been firstly used to intervene in vitro to investigate its effect on HepG2 cell proliferation. • LSL can inhibit the proliferation of cells, and it is possible to induce apoptosis in HepG2 cells through the Caspase-3 pathway. • The mechanism of LSL action on HepG2 cell proliferation was firstly also discussed, which provides a certain experimental reference for the clinical treatment of liver cancer. Graphical abstract
研究领域:
肿瘤学
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药理学
·
细胞生物学
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产品关联
DOI
PubMed
高影响因子
Materials Express
·
2023
·Vol. 13
·期 8
·1339-1345
·
IF 0.7
Liao Wanrong,Fang Wang,Xu Juan
Lung cancer is a common malignancy of the respiratory system with a high morbidity and mortality. We intended to identify the apoptosis-promoting role of tripterine in lung cancer. Lung cancer SPC-A-1 cells were exposed to low, moderate, and high dosage of tripterine (2, 5 and 10 μmol/L)
with the model group not being intervened. After treatment, the role of tripterine in SPC-A-1 cell apoptosis was observed. In addition, lung cancer cells were transfected with TNF-α mimic (pc-TNF-α group) and TNF-α inhibitor (si-TNF-α group).
Tripterine +pc-TNF-α group was set up to determine the interaction between tripterine and TNF-α. The cell survival rate, TNF-α and Caspase-3 expression levels then were detected by MTT and flow cytometry. Tripteryglide treatment dose-dependently decreased
lung cancer cell viability and induced cell apoptosis, resulting in an increase of TNF-α expression. However, when TNF-α expression was inhibited upon transfection, SPC-A-1 cell apoptosis was suppressed. TNF-α mimics activated apoptosis and up-regulated
Caspase-3 expression. Combination of tripteryglide and TNF-α mimics more significantly elevated apoptotic rate of lung cancer cells when elevating the content of Caspase-3. SPC-A-1 cells are highly sensitive to TNF-α and TNF-α significantly increases
the activity and expression of Caspase-3. Tripteryglide can up-regulate TNF-α expression to facilitate lung cancer cell apoptosis and increase Caspase-3 expression.
研究领域:
肿瘤学
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药理学
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细胞生物学
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DOI
高影响因子
Frontiers in Chemistry
·
2022
·
IF 5.545
Fan Zhang,Changqing Mao,Siyu Cao,Runchi Zhang,Yi Guo,Guifang Chen,Chang Feng
Bio-nanomicelles based on biomaterials such as nucleic acids, peptides, glycans, and lipids have developed rapidly in the field of bioanalysis. Although DNA and peptides have unique advantages, unfortunately, there are few bio-nanomicelles integrating DNA with peptides. Here, we designed a peptide-DNA hybrid bio-nanomicelle for the activity detection of caspase-3. The detection mechanism is based on caspase-3 specific recognition and cleavage of peptide substrates, which owns high sensitivity and selectivity. Under optimal conditions, the detection of caspase-3 activity can be achieved using our designed bio-nanomicelles and the detection limit is 0.72 nM. Furthermore, the proposed method was also successfully applied for the detection of caspase-3 in cell lysate samples after apoptosis-inducing.
研究领域:
生物分析
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纳米技术
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
ANALYTICAL CHEMISTRY
·
2020
·
IF 6.785
Guohua Qi,Dan Sun,Yu Tian,Chen Xu,Ying Zhang,Dandan Wang,Kongshuo Ma,Shuping Xu,Yongdong Jin
Caspase-3 is considered as one of the key proteases that can spontaneously regulate the life activities of cells, and its activation (usually is a slow process) will execute the apoptosis process of cells. Rapid activation of caspase-3 on demand in living-cells is therefore highly desired toward precise cancer therapy but it is still a key challenge. Herein, we applied electrostimulus (ES) to achieve fast activation of caspase-3 and trigger cell apoptosis, and developed a smart magnetic-plasmonic assembly nanoprobes (A-nanoprobes) to real-time trace cellular caspase-3 activation at the single cell level. The designer core–satellite A-nanoprobe, working specific to the activated caspase-3 via a disassembly tactic, provides strong “hot spots” to improve the sensitivity and therefore enables SERS sensing of cellular caspase-3 upon activated by ES. Single-cell analysis revealed that the ES can rapidly activate the apoptosis pathway of caspase-3 on demand to make the DNA fragmentation and ultimately induce the cell apoptosis. Such method and nanoplatform were further used to monitor ES-triggered caspase-3 activation in cell apoptosis process of different cell types, revealing that more caspase-3 will be activated for cancerous cells than normal cells during the ES to induce cells apoptosis. This strategy and platform are promising for detecting cellular caspase-3 and other enzymes in the process of cancer diagnosis and treatments.
研究领域:
生物医学工程
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纳米技术
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癌症研究
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Experimental and Therapeutic Medicine
·
2017
·Vol. 14
·期 5
·4307-4311
·
IF 1.261
Tao Zhou,Shanliang Guo,Shaolin Wang,Qiong Li,Mingsheng Zhang
This study was designed to investigate possible protective effects of sevoflurane on myocardial ischemia-reperfusion injury (MIRI) and its impact on expression of HIF-1α and caspase-3 in rats, so as to provide new insights for the treatment of MIRI. Forty SD rats were randomly divided into four groups (n=10) including Sham operation (Sham), ischemia-reperfusion (IR), sevoflurane preconditioning group (Sevo-Pre) and sevoflurane post-conditioning (Sevo-Post) groups. Perfusion was performed using ex vivo heart perfusion. The baseline values of cardiac function were recorded in each group at the end of balanced perfusion and after 60 min of reperfusion. Myocardial infarct size (MIS) was calculated at the end of perfusion using TTC staining. Levels of HIF-1α and caspase-3 protein and HIF-1α (western blotting) and Bcl-2 mRNA (RT-qPCR) were detected at the end of reperfusion. Our results showed no significant differences in cardiac function between the groups at the end of the balanced perfusion. After reperfusion for 60 min, however, the cardiac functions of the Sevo-Pre and Sevo-Post groups were significantly better than those in the IR group, and the MIS at the end of reperfusion was significantly decreased. Western blotting and RT-qPCR showed that expression of HIF-1α protein was significantly increased, expression of caspase-3 protein was significantly decreased and expression of HIF-1α and Bcl-2 mRNA were significantly increased in Sevo-Pre and Sevo‑Post groups compared with the levels in the IR group at the end of reperfusion. There were no significant differences in experimental results between Sevo-Pre and Sevo-Post groups. Our data support the idea that sevoflurane can improve MIRI in rats by improving cardiac function and reducing MIS. This protective effect seems to be achieved by activation of HIF-1α and inhibition of caspase-3.
研究领域:
药理学
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心脏病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2018
·
IF 3.997
Juang Wang,Zilong Zhou,Fang Zhang,Hui Xu,Wenli Chen,Tingting Jiang
We demonstrated a novel nanocomposite based on fluorescent turn-on gold nanostars for simultaneous tumor targeting photothermal therapy (PTT) and feedback apoptosis imaging of the self-therapeutic effect. In this theranostic agent ( [email protected] ), gold nanostars (AuNSs) and fluorescent dye Atto 655, as a fluorophore/quencher pair, were conjugated to form intermolecular fluorescence quenching in virtue of the linkage of a caspase-3 responsive peptide. Folic acid targeting moiety facilitated the selective accumulation in cancer cells via receptor-mediated endocytosis. Upon photo irradiation, [email protected] demonstrated excellent photothermal effect and induced cell death with apoptosis related mechanism. The typical apoptosis-effector proteases, caspase-3, was subsequently activated and terminated intramolecular fluorescent quenching process. Obvious fluorescence recovery could be applied to precisely assess the activated caspase-3 expression and the real time therapeutic efficacy. This novel versatile nanocomposite could serve as a theranostic agent for tumor targeting PTT and also provide self-therapeutic monitoring for precise cancer therapeutic applications.
研究领域:
纳米技术
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癌症治疗
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生物医学工程
·
分子生物学
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产品关联
DOI
PubMed
高影响因子
BIOMATERIALS
·
2017
·
IF 8.402
Na Zhao,Baoyan Wu,Xianglong Hu,Da Xing
Stimuli-responsive nanoparticles with multiple therapeutic/diagnostic functions are highly desirable for effective tumor treatment. Herein novel caspase-3 responsive functionalized upconversion nanoparticles (CFUNs) were fabricated with three-in-one functional integration: near-infrared (NIR) triggered photodynamic damage along with caspase-3 activation, subsequent caspase-3 responsive drug release, and cascade chemotherapeutic activation. CFUNs were formulated from the self-assembly of caspase-3 responsive doxorubicin (DOX) prodrug tethered with DEVD peptide (DEVD-DOX), upconversion nanoparticles (UCNP), a photosensitizer (pyropheophorbide-a methyl ester, MPPa), and tumor-targeting cRGD-PEG-DSPE to afford multifunctional CFUNs, MPPa/UCNP-DEVD-DOX/cRGD. Upon cellular uptake and NIR irradiation, the visible light emission of UCNP could excite MPPa to produce reactive oxygen species for photodynamic therapy (PDT) along with the activation of caspase-3, which further cleaved DEVD peptide to release DOX within tumor cells, thus accomplishing NIR-triggered PDT and cascade chemotherapy. CFUNs presented silent therapeutic potency and negligible cytotoxicity in the dark, whereas in vitro and in vivo experiments demonstrated the NIR-triggered cascade therapeutic activation and tumor inhibition due to consecutive PDT and chemotherapy. Current NIR-activated cascade tumor therapy with two distinct mechanisms is significantly favorable to overcome multidrug resistance and tumor heterogeneity for persistent tumor treatment.
研究领域:
纳米技术
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癌症治疗
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药学
·
生物医学工程
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产品关联
DOI
PubMed
高影响因子
Food Science & Nutrition
·
2025
·Vol. 13
·期 8
·e70756
·
IF 3.8
Jie Shi,Jingyi Ge,Zhenghai Zhang,Lianhui Wei,Yan Dong,Guowei Li,Qingli Yang,Jing Pan,Yanru Ji
This study aimed to investigate the antithrombotic activity of hemp seed peptides derived from trypsin hydrolysates and elucidate their molecular mechanisms using a ponatinib-induced zebrafish ( Danio rerio ) thrombosis model. Through ultrafiltration and LC–MS/MS analysis, we identified 1741 peptide sequences (< 3 kDa), with 67% distributed in the 0.5–1.5 kDa range. In vivo experiments demonstrated that 125 μg/mL hemp seed peptides significantly ameliorated ponatinib-induced thrombosis by increasing 16.55% cardiac erythrocyte staining intensity, enhancing 54.8% blood flow velocity, and restoring 11.2% intersegmental blood vessel diameters. In addition, the observed anticoagulant effect may be partially attributed to upregulated expression levels of vascular endothelial growth factor receptor 1 ( vegfr1 ) and down-regulated expression levels of cysteinyl aspartate-specific proteinase-3 ( caspase-3 ) at the mRNA level. These findings propose hemp seed peptides as novel dietary antithrombotic agents with potential applications in functional food development.
研究领域:
药理学
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分子生物学
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心血管研究
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食品科学
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生物技术
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动物学
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产品关联
DOI
PubMed
高影响因子
ANALYTICAL CHEMISTRY
·
2017
·
IF 6.32
Hong Cheng,Shi-Ying Li,Hao-Ran Zheng,Chu-Xin Li,Bo-Ru Xie,Ke-Wei Chen,Bin Li,Xian-Zheng Zhang
A novel single-molecular fluorescent probe was developed for spatiotemporal matrix metalloproteinase-2 (MMP-2) and caspase-3 imaging with distinct fluorescence signals. Due to the multi-Förster resonance energy transfer (FRET) processes, the probe could respond to MMP-2 and caspase-3 independently with high signal-to-noise ratio. Moreover, the overexpression of MMP-2 in cancer cell lines and the cisplatin induced cell apoptosis were spatiotemporal imaged with distinct fluorescence emissions. Because of the independent process of the probe for MMP-2 and caspase-3 imaging, the probe could meet the demands for precise disease diagnosis and cancer theranostic applications, which could extensively simplify the processes for precise cancer diagnosis and imaging.
研究领域:
生物医学工程
·
分子生物学
·
癌症研究
·
成像科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CELLULAR SIGNALLING
·
2026
·
IF 4.7
Guangyuan Li,Mingyu Peng,Mengxue Li,Ruoyu Hu,Chunxiao Gao,Yamin Xing,Ting Zhang,Jixuan Xu,Miaoran Fu,Wulong Liang,Pengya Feng,Hongqiao Zhang,Zisen Zhang,Pengyuan Zheng,Xiufeng Chu
Pyroptosis is a form of programmed cell death mediated by gasdermin proteins, with GSDMD and GSDME being the most extensively studied. Inflammatory caspases-1 or caspases-4/5/11 cleave GSDMD and release its pore-forming fragment GSDMD-NT, whereas the apoptotic caspase-3, cleaves GSDME and releases its pore-forming fragment GSDME-NT. In this study, we observed that caspase-3 is activated during GSDMD-mediated pyroptosis. Interestingly, downregulation of caspase-3 activity either through RNAi or caspase-3 inhibitor significantly increased cell death. Furthermore, we found that caspase-3 physically interacts with GSDMD-NT and cleaves it at a site distinct from those targeted by caspase-1 or caspases-4/5/11. This alternative cleavage generates a non-functional fragment of GSDMD-NT, thereby disrupting its integrity. Consequently, we demonstrate that caspase-3 activation serves as a negative feedback mechanism to regulate the intensity of GSDMD-NT-mediated pyroptosis.
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产品关联
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2026
·
IF 3.6
Shangxiang Feng,Kun Song,Hao Zhang,Zhuoqun Wang,Yuchi Zhao,Zhongyuan Zhao,Chao Wan
This study investigated the effects of Aureusidin on extracellular matrix (ECM) degradation and pyroptosis of chondrocytes in osteoarthritis. Network pharmacology, molecular docking, and pull-down assays were initially conducted to explore the target of Aureusidin. Subsequently, Sprague-Dawley rats underwent anterior cruciate ligament transection (ACLT) received oral administration of Aureusidin. Cartilage damage was evaluated histopathologically by H&E and Safranin O-fast green staining. Primary rat chondrocytes were treated with Aureusidin under IL-1β stimulation. Pyroptotic morphology was observed under light microscopy. Propidium iodide staining and flow cytometry were conducted to evaluate membrane rupture. The expression of markers associated with ECM degradation and pyroptosis was analyzed by qRT-PCR, Western blot, immunohistochemistry, and ELISA. Caspase-3 was identified as a target for Aureusidin. Aureusidin (5, 10, 20 mg/kg) alleviated ACLT-induced cartilage damage and ECM degradation. It reduced the OARSI score and serum levels of CTX-II and COMP, while upregulating the expression of Col2a1 and Acan , and downregulating Adamts5 , Mmp13 , and Mmp3 . Aureusidin also mitigated atypical pyroptosis, evidenced by inhibited expression of GSDME-N, Caspase-3, and Cleaved-Caspase-3, and decreased levels of IL-1β and IL-18. In IL-1β-stimulated primary chondrocytes, Aureusidin (5, 10, 20 μM) attenuated ECM degradation and Caspase-3/GSDME-mediated pyroptosis. Treating chondrocytes with the Caspase-3 inhibitor Z -DEVD-FMK under IL-1β-stimulated conditions alleviated ECM degradation and pyroptosis, but the additional application of Aureusidin did not provide further inhibition. Aureusidin has the potential to inhibit ECM degradation and Caspase-3/GSDME-mediated chondrocyte pyroptosis during osteoarthritis progression. Its therapeutic effects are dependent on binding to and modulating the Caspase-3.
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DOI
PubMed
高影响因子
JOURNAL OF NATURAL PRODUCTS
·
2021
·
IF 4.05
Yaling Hui,Ting Tang,Jing Wang,Huanhuan Zhao,Hong-Ying Yang,Junmin Xi,Baoxin Zhang,Jianguo Fang,Kun Gao,Yueting Wu
Nonsmall cell lung cancer (NSCLC) has been a fatal and refractory disease worldwide. Novel therapeutic developments based on fundamental investigations of anticancer mechanisms underlie substantial foundations to win the fight against cancer diseases. In this study, we isolated a natural product fusaricide (FCD) from an endophytic fungus of Lycium barbarum, identified as Epicoccum sp. For the first time, we discovered that FCD potently inhibited proliferation in a variety of human NSCLC cell lines, with relatively less toxicity to normal cells. Our study exhibited that FCD induced apoptosis, caused DNA damage and cell cycle arrest in G0/G1 phase, and activated caspase-3 as well as other apoptosis-related factors in human NSCLC NCI-H460 cells. FCD was proven to be an iron chelator that actively decreased levels of cellular labile iron pool in NCI-H460 cells in our study. FeCl3 supplement reversed FCD-induced apoptosis. The upregulation of transferrin receptor 1 (TfR1) and downregulation of ferritin heavy chain (FTH) expression were observed after FCD treatment. In summary, our study highlighted the potential anticancer effects of FCD against human NSCLCs and demonstrated that the FCD-mediated apoptosis depended on binding to intracellular iron.
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DOI
PubMed
高影响因子
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