scholarly journals Evaluation of the Apoptotic and Scolicidal Effects of Crude and Flavonoid Extracts of Allium noeanum on Protoscolices and Hydatid Cyst Wall

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Zahra Salemi ◽  
Mehrdad Goudarzi ◽  
Reza Hajihossein ◽  
Mitra Noori ◽  
Saeid Babaei ◽  
...  
Keyword(s):  
Crude Extract ◽  
Caspase 3 ◽  
Statistical Significance ◽  
Herbal Extract ◽  
Hydatid Cysts ◽  
Traditional Treatment ◽  
Larval Phase ◽  
Apoptotic Effect ◽  
Cyst Rupture ◽  
Apoptotic Effects

Background: Hydatidosis is a disease, caused by the larval phase of Echinococcus granulosus. It is considered a serious condition, as cyst rupture can release protoscolices into the host body, leading to the formation of secondary cysts. Surgery is the main approach for the treatment of this disease. Some natural compounds, which are safe options with few side effects, have been assessed for their scolicidal activities. Objectives: Allium noeanum is a native herb of Markazi Province, Iran, which has been used for the traditional treatment of certain diseases. However, its anti-parasitic property has not been investigated so far. The present study aimed to evaluate the anti-parasitic property of this plant by evaluating the scolicidal and apoptotic effects of two types of this herbal extract (crude and flavonoid) on hydatid cysts. Methods: The hydatid cysts were obtained from abattoirs, and protoscolices were drained under sterile conditions. The protoscolices suspension and cyst walls were used for scolicidal and immunohistochemical evaluations. In addition, A. noeanum was collected from Shazand Mountains. The crude and flavonoid extracts of this plant were prepared by maceration and chromatography methods, respectively. Immunohistochemistry was conducted for the detection of caspase-3 activity using a commercial kit. Data were analyzed in Excel and SPSS, and statistical significance was defined as P < 0.05. Results: The 100% concentration (0.49 gr/mL) of the crude A. noeanum extract caused the death of 100% of protoscolices. On the other hand, all concentrations of the flavonoid extract led to the death of 100% of parasites. According to the statistical analyses, each type of the extract showed different dose- and time-dependent rates of scolicidal activity (P < 0.001). Immunohistochemistry showed lower caspase-3 activity in cyst walls exposed to flavonoids, compared to those exposed to the crude extract. Conclusions: In the present study, the scolicidal activity of the flavonoid extract of A. noeanum against protoscolices was confirmed. It was also found that the apoptotic effect of the crude extract of this herb was more than its flavonoid extract.

Nitric oxide-dependent pro-oxidant and pro-apoptotic effect of metallothioneins in HL-60 cells challenged with cupric nitrilotriacetate

2001 ◽  
Vol 354 (2) ◽  
pp. 397-406 ◽  
Author(s):  
Shang-Xi LIU ◽  
Kazuaki KAWAI ◽  
Vladimir A. TYURIN ◽  
Yulia Y. TYURINA ◽  
Grigory G. BORISENKO ◽  
...  
Keyword(s):  
Dna Cleavage ◽  
Caspase 3 ◽  
Protective Role ◽  
Membrane Phospholipids ◽  
No Donor ◽  
Redox Active ◽  
Apoptotic Effect ◽  
Transition And Heavy Metals ◽  
Apoptotic Effects

Intracellular safeguarding functions of metallothioneins (MTs) include sequestering transition and heavy metals, scavenging free radicals and protecting against electrophiles. We report that MT protection against Cu-induced cytotoxicity can be reversed and pro-oxidant and pro-apoptotic effects can be induced in HL-60 cells exposed to NO. We demonstrate that in ZnCl2-pretreated HL-60 cells loaded with copper nitrilotriacetate (Cu-NTA), exposure to an NO donor, S-nitroso-N-acetyl penicillamine, resulted in S-nitrosylation and oxidation of MT cysteines. This disruption of MT Cu-binding thiolate clusters caused loosening and release of redox-active Cu, enhanced redox-cycling activity of Cu and increased peroxidation of major classes of membrane phospholipids. We also found that Cu-induced oxidative stress in ZnCl2-pretreated/Cu-NTA-loaded HL-60 cells was accompanied by apoptosis documented by characteristic changes of nuclear morphology, internucleosomal DNA cleavage, externalization of phosphatidylserine, release of cytochrome c from mitochondria into cytosol and activation of caspase-3. We conclude that in Cu-challenged cells, NO can reverse the protective role of MTs and convert them into pro-oxidant, pro-apoptotic implements.

scholarly journals Apoptotic Effects of Anthocyanins from Vitis coignetiae Pulliat Are Enhanced by Augmented Enhancer of the Rudimentary Homolog (ERH) in Human Gastric Carcinoma MKN28 Cells

2021 ◽  
Vol 22 (6) ◽  
pp. 3030
Author(s):  
Cheol Park ◽  
Won Sup Lee ◽  
Se-Il Go ◽  
Sang-Ho Jeong ◽  
Jiyun Yoo ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Ros Generation ◽  
Human Gastric Cancer ◽  
Oxygen Species ◽  
Mitochondrial Depolarization ◽  
Gastric Cancer Cells ◽  
Anticancer Efficacy ◽  
Antiapoptotic Proteins ◽  
Apoptotic Effect ◽  
Apoptotic Effects

Evidence suggests that augmented expression of a certain gene can influence the efficacy of targeted and conventional chemotherapies. Here, we tested whether the high expression of enhancer of the rudimentary homolog (ERH), which serves as a prognostic factor in some cancers, can influence the efficacy of anthocyanins isolated from fruits of Vitis coignetiae Pulliat, Meoru in Korea (AIMs) on human gastric cancer cells. The anticancer efficacy of AIMs was augmented in ERH-transfected MKN28 cells (E-MKN28 cells). Molecularly, ERH augmented AIM-induced caspase-dependent apoptosis by activating caspase-3 and -9. The ERH-augmented apoptotic effect was related to mitochondrial depolarization and inhibition of antiapoptotic proteins, XIAP, and Bcl-2. In addition, reactive oxygen species (ROS) generation was augmented in AIMs-treated E-MKN28 cells compared to AIMs-treated naïve MKN28 cells. In conclusion, ERH augmented AIM-induced caspase-dependent mitochondrial-related apoptosis in MKN28 cells. A decrease in expression of Bcl-2 and subsequent excessive ROS generation would be the mechanism for ERH-augmented mitochondrial-related apoptosis in AIMs-treated MKN28 cells. A decrease in expression of XIAP would be another mechanism for ERH-augmented caspase-dependent apoptosis in AIMs-treated MKN28 cells.

scholarly journals Cytotoxic and apoptotic effect of nanoclinoptilolite on canine osteosarcoma cell lines

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Pınar Alkım Ulutaş ◽  
Funda Kıral ◽  
Bülent Ulutaş ◽  
Gamze Sevri Ekren Aşıcı
Keyword(s):  
Cell Culture ◽  
Cell Viability ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Biological Activities ◽  
Osteosarcoma Cell ◽  
Canine Osteosarcoma ◽  
Anticancer Properties ◽  
Apoptotic Effect ◽  
Apoptotic Effects

AbstractIntroductionClinoptilolite has antiviral, antibacterial, anti-inflammatory, antidiabetic, and anticancer properties due to its biological activities. In various cancer cell culture studies, it has been reported effective against tumour cells and gave positive results in treatment of various tumours in dogs. No study was found on the effects of the nanoparticulate form, nanoclinoptilolite, on cancer cells. The aim of this study was to determine its cytotoxic and apoptotic effects in canine osteosarcoma (OSA) cell culture.Material and MethodsDoses at 50% inhibitory concentration were determined by measuring the dose- and duration-dependent cytotoxicity of nanoclinoptilolite on canine D-17 osteosarcoma cells by methylthiazol tetrazolium (MTT) test for 24 h, 48 h, and 72 h. Murine caspase-3 and -7 activity and expression levels of the BAX and BCL2 genes were measured using RT-PCR to investigate the apoptotic effect.ResultsNanoclinoptilolite decreased cell viability and induced caspase-3- and -7-mediated apoptosis in treated canine OSA cells. Furthermore, its application to canine OSA cells downregulated the expression of BCL2 and upregulated the expression of proapoptotic BAX.ConclusionClinoptilolite, which was previously demonstrated to have anticancer properties, decreased cell viability effectively and rapidly and increased the apoptotic cell ratio in a novel use in nanoparticle form, exhibiting this effect by increasing the BAX/BCL2 ratio.

scholarly journals Apoptotic Effects of Xanthium strumarium via PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Juyoung Kim ◽  
Kyung Hee Jung ◽  
Hyung Won Ryu ◽  
Doo-Young Kim ◽  
Sei-Ryang Oh ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Caspase 3 ◽  
Mtor Pathway ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Mechanistic Study ◽  
Migration And Invasion ◽  
Xanthium Strumarium ◽  
Apoptotic Effects ◽  
Hcc Cells

Xanthium strumarium (XS) has been traditionally used as a medicinal herb for treating inflammatory diseases, such as appendicitis, chronic bronchitis, rheumatism, and rhinitis. In this study, we yielded ethanol extracts from XS and investigated whether they could inhibit the progression of hepatocellular carcinoma (HCC) and its underlying mechanism. The XS-5 and XS-6 extracts dose-dependently inhibited the growth and proliferation in HCC cell lines. The apoptotic effects of them were observed via increased levels of cleaved caspase-3 and cleaved PARP, as well as elevated numbers of terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling- (TUNEL-) positive apoptotic cells. They also decreased XIAP and Mcl-1 expression via loss of mitochondrial membrane potential. Additionally, they inhibited the invasion and migration of HCC cells. In an ex vivo model, the extracts significantly inhibited tumor cell growth and induced apoptosis by increasing the expression of the cleaved caspase-3. A mechanistic study revealed that they effectively suppressed PI3K/AKT/mTOR signaling pathways in HCC cells. Taken together, our findings demonstrate that they could efficiently not only induce apoptosis but also inhibit cell growth, migration, and invasion of human HCC cells by blocking the PI3K/AKT/mTOR pathway. We suggest XS-5 and XS-6 as novel natural anti-HCC agents.

Abstract 203: Glucose Stimulated Endothelial Microparticles Increase Endothelial Cell Apoptotic Susceptibility

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Tyler Bammert ◽  
Jamie Hijmans ◽  
Whitney Reiakvam ◽  
Ma’ayan Levy ◽  
Kelly Stockelman ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Caspase 3 ◽  
Cell Function ◽  
Culture Media ◽  
Umbilical Vein ◽  
Endothelial Cell Function ◽  
Cellular Expression ◽  
Apoptotic Effect ◽  
Clinical Interest ◽  
Umbilical Vein Endothelial Cells

Clinical interest in endothelial cell-derived microparticles (EMPs) has increased due to their role in the pathogenesis of vascular disease. Although released by the endothelium, EMPs have autocrine properties that can significantly impact endovascular health. Hyperglycemic conditions, such as diabetes, are known to stimulate EMP release; however, the effects of these glucose-related microparticles on endothelial cell function are not well understood. High glucose concentrations induce endothelial cell apoptosis through a caspase-3-dependent mechanism. The aim of this study was to determine the effect of EMPs derived from a hyperglycemic condition on endothelial cell susceptibility to apoptosis. Human umbilical vein endothelial cells (HUVECs) were cultured (3 rd passage) and plated in 6-well plates at a density of 5.0 x 10 5 cell/condition. Cells were incubated with RPMI 1640 media containing 25mM D-glucose (concentration representing a diabetic glycemic state) or 5mM D-glucose (control, normoglycemic, condition) for 48 h to generate EMPs. EMPs derived from both conditions were pelleted by centrifugation and resuspended in culture media. EMP identification (CD144 + expression) and number was determined by flow cytometry. HUVECs (2 x10 6 cells/condition) were treated with EMPs (2:1 ratio) generated from either the hyperglycemic or normoglycemic conditions for 24 h. Thereafter, cells were treated with staurosporine (1μmol/L) for 3 h at 37°C and biotin-ZVKD-fmk inhibitor for 1 h at 37°C. Intracellular concentration of active caspase-3 was determined by enzyme immune assay. Cellular expression of miR-Let7a, an anti-apoptotic microRNA, was determined by RT-PCR using the ΔΔCT normalized to RNU6. Hyperglycemic EMPs resulted in significant increase in basal (1.5 + 0.1 vs 1.0 + 0.1 ng/mL) and staurosporine-stimulated (2.2 + 0.2 vs 1.4 + 0.1 ng/mL) caspase-3 activity compared with normoglycemic EMPs. Additional, the expression of miR-Let7a was markedly reduced (~140%) in response to hyperglycemic EMPs (0.43 + 0.17 fold vs control). These results demonstrate that hyperglycemic-induced EMPs increase endothelial cell apoptotic susceptibility. This apoptotic effect may be mediated, at least in part, by a reduction in miR-Let7a expression.

scholarly journals Modulatory effect of Persea Americana oil against diethylnitrosamine-induced hepatotoxicity in rats: a proposed mechanism

2021 ◽  
Vol 45 (1) ◽  
Author(s):  
Omayma A. R. Abozaid ◽  
Lobna M. Anees ◽  
Gehan R. Abdel-Hamed
Keyword(s):  
Nadph Oxidase ◽  
Caspase 3 ◽  
Persea Americana ◽  
Gene Expressions ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Apoptotic Effect ◽  
Oxide Synthase ◽  
Parp 1 ◽  
Inducible Nitric Oxide

Abstract Background The purpose of this study was to investigate the effectiveness of Persea Americana (avocado) oil against diethylnitrosamine (DEN)-induced hepatotoxicity in rats. Methods For the induction of hepatotoxicity, DEN was administrated orally in a dose of 20 mg/kg B.wt for 6 successive weeks, and then the animals were gavaged with Persea Americana oil in a dose of 4 mL/kg b.wt. daily for another 6 weeks. Serum caspase-3 activity and poly (ADP-ribose) polymerase-1 (PARP-1) levels were estimated; in addition to gene expressions for NADPH oxidase, inducible nitric oxide synthase (iNOS), Bcl-2, and Bax were detected. Results The DEN-intoxicated group exhibited a remarkable increase in NADPH oxidase and iNOS expression combined with over-activation of PARP-1 and increased antiapoptotic Bcl-2 gene expression, whereas the expression of apoptotic biomarkers significantly decreased. On the other hand, treatment with Persea Americana oil significantly suppressed the elevated levels of hepatic enzymes and improved histopathological alterations in the liver. Furthermore, these groups displayed marked downregulation in NADPH oxidase and iNOS expressions. Persea Americana oil suppressed the expression of the antiapoptotic Bcl-2, activated the intrinsic mitochondrial apoptosis pathway through upregulation of pro-apoptotic Bax, and induced an obvious increase in caspase-3 activity. Moreover, Persea Americana oil administration markedly inhibited the activity of PARP-1. Conclusions This study indicated the promising potential of Persea Americana oil against DEN-induced hepatic injury through its anti-oxidative activity and pro-apoptotic effect via caspase activation and PARP-1 inhibition.

scholarly journals An Insight into the Mechanism of Holamine- and Funtumine-Induced Cell Death in Cancer Cells

Molecules ◽  
2020 ◽  
Vol 25 (23) ◽  
pp. 5716
Author(s):  
Jelili A. Badmus ◽  
Okobi E. Ekpo ◽  
Jyoti R. Sharma ◽  
Nicole Remaliah S. Sibuyi ◽  
Mervin Meyer ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Anticancer Agents ◽  
Topoisomerase I ◽  
Caspase 3 ◽  
Steroidal Alkaloids ◽  
Antiproliferative Effects ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
Apoptotic Effect ◽  
Mcf 7

Holamine and funtumine, steroidal alkaloids with strong and diverse pharmacological activities are commonly found in the Apocynaceae family of Holarrhena. The selective anti-proliferative and cell cycle arrest effects of holamine and funtumine on cancer cells have been previously reported. The present study evaluated the anti-proliferative mechanism of action of these two steroidal alkaloids on cancer cell lines (HT-29, MCF-7 and HeLa) by exploring the mitochondrial depolarization effects, reactive oxygen species (ROS) induction, apoptosis, F-actin perturbation, and inhibition of topoisomerase-I. The apoptosis-inducing effects of the compounds were studied by flow cytometry using the APOPercentageTM dye and Caspase-3/7 Glo assay kit. The two compounds showed a significantly greater cytotoxicity in cancer cells compared to non-cancer (normal) fibroblasts. The observed antiproliferative effects of the two alkaloids presumably are facilitated through the stimulation of apoptosis. The apoptotic effect was elicited through the modulation of mitochondrial function, elevated ROS production, and caspase-3/7 activation. Both compounds also induced F-actin disorganization and inhibited topoisomerase-I activity. Although holamine and funtumine appear to have translational potential for the development of novel anticancer agents, further mechanistic and molecular studies are recommended to fully understand their anticancer effects.

scholarly journals Apoptotic effects of hsian‐tsao ( Mesona procumbens Hemsley) on hepatic stellate cells mediated by reactive oxygen species and ERK, JNK, and caspase‐3 pathways

2019 ◽  
Vol 7 (5) ◽  
pp. 1891-1898
Author(s):  
Yung‐Hsiang Yeh ◽  
Chun‐Ya Liang ◽  
Mao‐Liang Chen ◽  
Fu‐Ming Tsai ◽  
Yi‐Ying Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hepatic Stellate Cells ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Stellate Cells ◽  
Oxygen Species ◽  
Apoptotic Effects

scholarly journals Anti-Apoptotic Effect of G-Protein-Coupled Receptor 40 Activation on Tumor Necrosis Factor-α-Induced Injury of Rat Proximal Tubular Cells

2019 ◽  
Vol 20 (14) ◽  
pp. 3386
Author(s):  
Chang Kim ◽  
Soo Joo ◽  
In Kim ◽  
Hoon-In Choi ◽  
Eun Bae ◽  
...  
Keyword(s):  
Protein Expression ◽  
Tumor Necrosis ◽  
Caspase 3 ◽  
Expression Ratio ◽  
Tnf Α ◽  
Apoptotic Effect ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
G Protein Coupled ◽  
Necrosis Factor

G-protein-coupled receptor 40 (GPR40) has an anti-apoptotic effect in pancreatic β-cells. However, its role in renal tubular cell apoptosis remains unclear. To explore the role of GPR40 in renal tubular apoptosis, a two-week unilateral ureteral obstruction (UUO) mouse model was used. The protein expression of GPR40 was decreased, while the Bax/Bcl-2 protein expression ratio, the expression of tumor necrosis factor (TNF)-α mRNA, and angiotensin II type 1 receptor (AT1R) protein were increased in mice with UUO. In vitro, pretreatment of rat proximal tubular (NRK52E) cells with GW9508, a GPR40 agonist, attenuated the decreased cell viability, increased the Bax/Bcl-2 protein expression ratio, increased protein expression of cleaved caspase-3 and activated the nuclear translocation of nuclear factor-κB (NF-κB) p65 subunit induced by TNF-α treatment. TNF-α treatment significantly increased the expression of AT1R protein and the generation of reactive oxygen species (ROS), whereas GW9508 treatment markedly reversed these effects. Pretreatment with GW1100, a GPR40 antagonist, or silencing of GPR40 in NRK52E cells promoted the increased expression of the cleaved caspase-3 protein by TNF-α treatment. Our results demonstrate that decreased expression of GPR40 is associated with apoptosis via TNF-α and AT1R in the ureteral obstructed kidney. The activation of GPR40 attenuates TNF-α-induced apoptosis by inhibiting AT1R expression and ROS generation through regulation of the NF-κB signaling pathway.

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