scholarly journals Insight into OroxylinA-7-O-β-d-Glucuronide-Enriched Oroxylum indicum Bark Extract in Oral Cancer HSC-3 Cell Apoptotic Mechanism: Role of Mitochondrial Microenvironment

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7430
Author(s):  
Sharmila Kameyanda Poonacha ◽  
Madhyastha Harishkumar ◽  
Madhyastha Radha ◽  
Remya Varadarajan ◽  
Suchetha Kumari Nalilu ◽  
...  
Keyword(s):  
Incubation Time ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Squamous Carcinoma ◽  
Stem Bark ◽  
Cell Number ◽  
Bark Extract ◽  
Dna Ladder ◽  
Oroxylum Indicum ◽  
Squamous Carcinoma Cells

Oroxylum indicum, of the Bignoniaceae family, has various ethnomedical uses such as an astringent, anti-inflammatory, anti-bronchitis, anti-helminthic and anti-microbial, including anticancer properties. The druggability of OI stem bark extract was determined by its molecular docking interactions with PARP and Caspase-3, two proteins involved in cell survival and death. Note that 50 µg/mL of Oroxylum indicum extract (OIE) showed a significant (p < 0.05%) toxicity to HSC-3 cells. MTT aided cell viability and proliferation assay demonstrated that 50 µg/mL of OIE displayed significant (p < 0.5%) reduction in cell number at 4 h of incubation time. Cell elongation and spindle formation was noticed when HSC-3 cells were treated with 50 µg/mL of OIE. OIE initiated DNA breakage and apoptosis in HSC-3 cells, as evident from DNA ladder assay and calcein/EB staining. Apoptosis potential of OIE is confirmed by flow cytometer and triple-staining (live cell/apoptosis/necrosis) assay. Caspase-3/7 fluorescence quenching (LANCE) assay demonstrated that 50 µg/mL of OIE significantly enhanced the RFU of caspases-3/7, indicating that the apoptosis potential of OIE is probably through the activation of caspases. Immuno-cytochemistry of HSC-3 cells treated with 50 µg/mL of OIE showed a significant reduction in mitochondrial bodies as well as a reduction in RFU in 60 min of incubation time. Immunoblotting studies clearly showed that treatment of HSC-3 cells with OI extract caused caspase-3 activation and PARP deactivation, resulting in apoptotic cell death. Overall, our data indicate that OIE is an effective apoptotic agent for human squamous carcinoma cells and it could be a future cancer chemotherapeutic target.

Biological Species and Environment Study in Microsystins Causing Apotosis in Heart

2014 ◽  
Vol 886 ◽  
pp. 341-344
Author(s):  
Tong Qiu
Keyword(s):  
Caspase 3 ◽  
Apoptotic Cell ◽  
Cell Number ◽  
Biological Species ◽  
Freshwater Ecosystems ◽  
Cyanobacterial Blooms ◽  
Caspase 9 ◽  
Gene Expressions ◽  
Genes Expression ◽  
Environment Study

The occurrence of heavy cyanobacterial blooms in eutrophic freshwater ecosystems has been a worldwide problem. Microcystins, the predominant toxins of cyanobacterial blooms, are associated with mortality and illness in both animals and human. In present study, we monitored the apoptosis of heart from MCs intoxication, and evaluated the roles of main apoptosis-related genes expression in cardiotoxic effects. The results revealed that MCs exposure led to the gradually rise in apoptotic cell number. Meanwhile, Bax, Bcl-2, p53, Caspase-3 and Caspase-9 gene expressions were significantly elevated simultaneously with the extension of the time. It suggested that MCs can cause damage to heart directly.

scholarly journals Acacia catechu ethanolic bark extract induces apoptosis in human oral squamous carcinoma cells

2017 ◽  
Vol 8 (4) ◽  
pp. 143 ◽  
Author(s):  
Devaraj Ezhilarasan ◽  
Thangavelu Lakshmi ◽  
Rajagopal Vijayaragavan ◽  
SukhwinderKaur Bhullar ◽  
Ramasamy Rajendran
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Bark Extract ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
Acacia Catechu

scholarly journals MicroRNA-155 Promotes Myocardial Infarction-Induced Apoptosis by Targeting RNA-Binding Protein QKI

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jing Guo ◽  
Hui-Bin Liu ◽  
Chuan Sun ◽  
Xiu-Qing Yan ◽  
Juan Hu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Rna Binding ◽  
Apoptotic Cell ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Cell Number ◽  
Neonatal Rat

Acute myocardial infarction (AMI) is the leading cause of sudden death worldwide. MicroRNA-155 (miR-155) has been reported to target antiapoptotic genes in various diseases models, but the functional role of miR-155 in response to MI injury needs further investigations. This study investigated the role of miR-155 in myocardial ischemia injury. TUNEL and flow cytometry were performed to measure cell apoptosis. Western blot analysis was employed to detect protein expressions of Bcl-2, XIAP, Bax, and caspase-3. qRT-PCR was used to quantify miRNA levels. We showed that miR-155 was dynamically elevated in murine hearts subjected to MI and in neonatal rat ventricular cardiomyocyte (NRVM) injury induced by hydrogen peroxide (H2O2). In response to H2O2, the silencing of miR-155 using AMO-155 (antisense inhibitor oligodeoxyribonucleotides) significantly increased cell viability and reduced cell apoptosis. Moreover, AMO-155 reversed the H2O2-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3. Further study revealed that AMO-155 resulted in a decrease of H2O2-induced JC-1-labelled monomeric cell number. In addition, AMO-155 markedly decreased infarct size, ameliorated impaired cardiac function, and significantly reduced apoptotic cell percentages in MI mice heart. The RNA-binding protein Quaking (QKI) was predicted as a target gene of miR-155 through bioinformatic analysis, and AMO-155 attenuated the downregulation of QKI in H2O2-treated cardiomyocytes and MI mice heart. Knockdown of QKI by siRNA abolished the antiapoptotic effects of AMO-155. Taken together, miR-155 is upregulated in the MI heart and NRVMs in response to H2O2 stress, and downregulating of miR-155 protects cardiomyocytes against apoptosis. Mechanistically, it is probably due to the repression of QKI signaling pathway.

scholarly journals Novel Apoptosis-Inducing Activity inBacteroides forsythus: a Comparative Study with Three Serotypes of Actinobacillus actinomycetemcomitans

2000 ◽  
Vol 68 (8) ◽  
pp. 4611-4615 ◽  
Author(s):  
Shinichi Arakawa ◽  
Takuma Nakajima ◽  
Hiroaki Ishikura ◽  
Shizuko Ichinose ◽  
Isao Ishikawa ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Apoptotic Cell ◽  
White Blood Cells ◽  
Membrane Integrity ◽  
Cytolytic Activity ◽  
Actinobacillus Actinomycetemcomitans ◽  
Leukemic Cells ◽  
Dna Ladder ◽  
Serotype A ◽  
Serotype B

ABSTRACT Bacteroides forsythus, which has been reported to be associated with periodontitis but has not been recognized as a key pathogen, was found to induce cytolytic activity against HL-60 and other human leukemic cells. This cytolytic activity was demonstrated according to three different criteria: (i) loss of both mitochondrial membrane potential and membrane integrity in cells treated with bacterial extracts and then with Rh123 and propidium iodide, respectively, as demonstrated by flow cytometry; (ii) damage to cytoplasmic membrane, as revealed by scanning electron microscopy (SEM); and (iii) DNA ladder formation and activation of caspase-3. These results indicate that B. forsythus produced an apoptosis-inducing factor(s) found to be composed of protein as judged by heat and trypsin sensitivity. In addition to extracts from B. forsythus, the culture supernatant of this bacterium has the ability to induce a cytolytic effect against peripheral white blood cells, especially lymphocytes. For comparison with B. forsythus, the same analyses were applied to two strains with different serotypes ofActinobacillus actinomycetemcomitans, serotypes a (ATCC 43717) and c (ATCC 43719), in addition to previously reported apoptosis-inducing serotype b (ATCC 43718), which was used as a positive control. The strains of A. actinomycetemcomitansserotypes a and b induced apoptosis in HL-60 cells as judged by the above three criteria but to a slightly lesser extent than did B. forsythus, while the serotype c strain produced apoptosis to a negligible extent. Detailed SEM images showed that the A. actinomycetemcomitans serotype a strain induced large-pore formation and the serotype b strain produced small pores with typical blebbing, while B. forsythus induced severe membrane ruffling. Further DNA ladder formation and caspase-3 activation were observed in the serotype a and b strains but not in the serotype c strain. The present paper is the first report of a protein factor(s) from B. forsythus and the A. actinomycetemcomitans serotype a strain which induces apoptotic cell death.

Fisetin Inhibits Cell Proliferation through the Induction of G0/G1 Phase Arrest and Caspase-3-Mediated Apoptosis in Mouse Leukemia Cells

2019 ◽  
Vol 47 (04) ◽  
pp. 841-863 ◽  
Author(s):  
Yu-Hsiang Tsai ◽  
Jen-Jyh Lin ◽  
Yi-Shih Ma ◽  
Shu-Fen Peng ◽  
An-Cheng Huang ◽  
...  
Keyword(s):  
Fruits And Vegetables ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Human Cancer ◽  
Cell Number ◽  
Viable Cell Number ◽  
Mouse Leukemia ◽  
Human Cancer Cell Lines ◽  
Phase Arrest ◽  
Apoptotic Protein

Fisetin, a naturally occurring flavonoid, is found in common fruits and vegetables and has been shown to induce cytotoxic effects in many human cancer cell lines. No information has shown that fisetin induced cell cycle arrest and apoptosis in mouse leukemia WEHI-3 cells. We found that fisetin decreased total viable cells through G0/G1 phase arrest and induced sub-G1 phase (apoptosis). We have confirmed fisetin induced cell apoptosis by the formation of DNA fragmentation and induction of apoptotic cell death. Results indicated that fisetin induced intracellular Ca[Formula: see text] increase but decreased the ROS production and the levels of [Formula: see text]m in WEHI-3 cells. Fisetin increased the activities of caspase-3, -8 and -9. Cells were pre-treated with inhibitors of caspase-3, -8 and -9 and then treated with fisetin and results showed increased viable cell number when compared to fisetin treated only. Fisetin reduced expressions of cdc25a but increased p-p53, Chk1, p21 and p27 that may lead to G0/G1 phase arrest. Fisetin inhibited anti-apoptotic protein Bcl-2 and Bcl-xL and increased pro-apoptotic protein Bax and Bak. Furthermore, fisetin increased the protein expression of cytochrome c and AIF. Fisetin decreased cell number through G0/G1 phase arrest via the inhibition of cdc25c and induction of apoptosis through caspase-dependent and mitochondria-dependent pathways. Therefore, fisetin may be useful as a potential therapeutic agent for leukemia.

Prostacyclin-induced peroxisome proliferator-activated receptor-α translocation attenuates NF-κB and TNF-α activation after renal ischemia-reperfusion injury

2009 ◽  
Vol 297 (4) ◽  
pp. F1109-F1118 ◽  
Author(s):  
Hsi-Hsien Chen ◽  
Tzen-Wen Chen ◽  
Heng Lin
Keyword(s):  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Cell Number ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nitrogen Levels ◽  
Tnf Α

Prostacyclin and peroxisome proliferator-activated receptors (PPAR) protect against ischemia-reperfusion (I/R) injury by the induction of an anti-inflammatory pathway. In this study, we examined the prostacyclin-enhanced protective effect of PPARα in I/R-induced kidney injury. PPAR-α reduced the NF-κB-induced overexpression of TNF-α and apoptosis in cultured kidney cells. In a murine model, pretreating wild-type (WT) mice with a PPAR-α activator, docosahexaenoic acid (DHA), significantly reduced I/R-induced renal dysfunction (lowered serum creatinine and urea nitrogen levels), apoptotic responses (decreased apoptotic cell number and caspase-3, -8 activation), and NF-κB activation. By comparison, I/R-induced injury was exacerbated in PPAR-α knockout mice. This indicated that PPAR-α attenuated renal I/R injury via NF-κB-induced TNF-α overexpression. Overexpression of prostacyclin using an adenovirus could also induce PPAR-α translocation from the cytosol into the nucleus to inhibit caspase-3 activation. This prostacyclin/PPAR-α pathway attenuated TNF-α promoter activity by binding to NF-κB. Using a cAMP inhibitor (CAY10441) and a prostacyclin receptor antibody, we also found that there was another prostacyclin/IP receptor/cAMP pathway that could inhibit TNF-α production. Taken together, our results demonstrate for the first time that prostacyclin induces the translocation of PPAR-α from the cytosol into the nucleus and attenuates NF-κB-induced TNF-α activation following renal I/R injury. Treatments that can augment prostacyclin, PPAR-α, or the associated signaling pathways may ameliorate conditions associated with renal I/R injury.

scholarly journals Anti-Cancer Activity Of Luvunga Scandens Extract Against Squamous Cell Carcinoma

2017 ◽  
Vol 16 (2) ◽  
Author(s):  
Sama Naziyah Shaban ◽  
Solachuddin Icwan ◽  
Muhamamd Taher Bakhtiar
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Caspase 3 ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Cell Cycle Analysis ◽  
Squamous Carcinoma Cells ◽  
Anti Cancer

Introduction: Squamous cell carcinoma is reported as one of the most common types of cancer with increasing numbers of occurrence. Luvunga scandens is a plant possessing many bioactivities and general health effects, yet its anti-proliferative effect is under reported and need to be scientifically evaluated. Materials and Methods: MTT assay was used to assess the cytotoxicity of the plant against human squamous carcinoma cells in addition to the safety assessment for human dermal fibroblast cell line (HDF). The morphological changes of L. scandens treated squamous carcinoma cells has been confirmed by SEM, the apoptosis of the plant against squamous carcinoma cells has been tested using caspase 3/7 assay, followed by cell cycle analysis done using a flowcytometer on squamous carcinoma cells treated with the IC50 dose of L. scandens plant. Results: The plant's extract possesses cytotoxic effect against squamous carcinoma cells with IC50 readings; (methanol= 37.5 mg/mL, dichloromethane= 38 mg/mL, hexane= 37.5 mg/mL), and safe on HDF cells. The SEM results demonstrate that L. scandens treated cells showed an overall change in the cell shape, alteration of surface morphology, absence of microvilli and appearance of blebs. Caspase 3/7 assay results show that L. scandens dichloromethane extract produces the highest level of apoptosis against squamous carcinoma cells. For cell cycle analysis, all the L. scandens treated squamous carcinoma cells show high readings in the sub-G1 phase. Conclusion(s): This in vitro study has proved that L. scandens plant exhibit anti-proliferative effects against Squamous carcinoma cells, hence, it can be considered as a new promising potential anti-cancer therapy.

scholarly journals Capsaicin Potentiates Anticancer Drug Efficacy Through Autophagy-Mediated Ribophorin II Downregulation and Necroptosis in Oral Squamous Cell Carcinoma Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Yi-Ching Huang ◽  
Tien-Ming Yuan ◽  
Bang-Hung Liu ◽  
Kai-Li Liu ◽  
Chiung-Hua Wung ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Anticancer Drugs ◽  
Apoptotic Cell ◽  
Squamous Carcinoma ◽  
Chemotherapeutic Agents ◽  
Carcinoma Cells ◽  
Down Regulation ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

The ability of capsaicin co-treatment to sensitize cancer cells to anticancer drugs has been widely documented, but the detailed underlying mechanisms remain unknown. In addition, the role of ribophorin II turnover on chemosensitization is still uncertain. Here, we investigated capsaicin-induced sensitization to chemotherapeutic agents in the human oral squamous carcinoma cell lines, HSC-3 and SAS. We found that capsaicin (200 μM) did not induce remarkable apoptotic cell death in these cell lines; instead, it significantly enhanced autophagy with a concomitant decrease of ribophorin II protein. This capsaicin-induced decrease in ribophorin II was intensified by the autophagy inducer, rapamycin, but attenuated by the autophagy inhibitors, ULK1 inhibitor and chloroquine, indicating that the autophagic process was responsible for the capsaicin-induced down-regulation of ribophorin II. Co-administration of capsaicin with conventional anticancer agents did, indeed, sensitize the cancer cells to these agents. In co-treated cells, the induction of apoptosis was significantly reduced and the levels of the necroptosis markers, phospho-MLKL and phospho-RIP3, were increased relative to the levels seen in capsaicin treatment alone. The levels of DNA damage response markers were also diminished by co-treatment. Collectively, our results reveal a novel mechanism by which capsaicin sensitizes oral cancer cells to anticancer drugs through the up-regulation of autophagy and down-regulation of ribophorin II, and further indicate that the induction of necroptosis is a critical factor in the capsaicin-mediated chemosensitization of oral squamous carcinoma cells to conventional anticancer drugs.

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