scholarly journals Apigenin Attenuates Oxidative Injury in ARPE-19 Cells thorough Activation of Nrf2 Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Xinrong Xu ◽  
Min Li ◽  
Weiwei Chen ◽  
Haitao Yu ◽  
Yan Yang ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Antioxidant Properties ◽  
Underlying Mechanism ◽  
Current Data ◽  
Cell Viability Assay ◽  
Cytotoxic Effects ◽  
Protein Levels ◽  
Viability Assay ◽  
Mrna And Protein Expression ◽  
Induced Apoptosis

The current study was aimed at evaluating the therapeutic implication of apigenin and to elucidate the underlying mechanism. Thetert-butyl hydroperoxide (t-BHP) at 200 μM was used to induce oxidative stress-associated injury in ARPE-19 cells. Apigenin at concentrations less than 800 μM did not cause cytotoxic effects on ARPE-19 cells. Cell viability assay showed that apigenin at 200 μM significantly promoted cell survival int-BHP-treated ARPE-19 cells. Additionally, apigenin at 100 μM significantly protected ARPE-19 cells fromt-BHP-induced apoptosis. Molecular examinations demonstrated that apigenin at 400 μM significantly upregulated the mRNA and protein expression of Nrf2 and stimulated its nuclear translocation in ARPE-19 cells treated with or withoutt-BHP. Apigenin 400 μM also significantly elevated the expression of HO-1, NQO1, and GCLM at both mRNA and protein levels in the presence or absence oft-BHP. Furthermore, apigenin at 400 μM significantly increased the activities of SOD, CAT, GSH-PX, and T-AOC and reduced the levels of ROS and MDA int-BHP-treated ARPE-19 cells. However, these effects of apigenin were all abolished by being transfected with Nrf2 siRNA. Collectively, our current data indicated that apigenin exerted potent antioxidant properties in ARPE-19 cells challenged witht-BHP, which were dependent on activation of Nrf2 signaling.

scholarly journals Human Recombinant Fab Fragment Neutralizes Shiga Toxin Type 2 Cytotoxic Effects in vitro and in vivo

Toxins ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 508 ◽  
Author(s):  
Daniela Luz ◽  
Maria Amaral ◽  
Flavia Sacerdoti ◽  
Alan Bernal ◽  
Wagner Quintilio ◽  
...  
Keyword(s):  
Shiga Toxin ◽  
Lethal Dose ◽  
Dependent Manner ◽  
Fab Fragment ◽  
Cell Viability Assay ◽  
Cytotoxic Effects ◽  
Morphological Alterations ◽  
Viability Assay

Shiga toxin (Stx) producing Escherichia coli (STEC) is responsible for causing hemolytic uremic syndrome (HUS), a life-threatening thrombotic microangiopathy characterized by thrombocytopenia, hemolytic anemia, and acute renal failure after bacterially induced hemorrhagic diarrhea. Until now, there has been neither an effective treatment nor method of prevention for the deleterious effects caused by Stx intoxication. Antibodies are well recognized as affinity components of therapeutic drugs; thus, a previously obtained recombinant human FabC11:Stx2 fragment was used to neutralize Stx2 in vitro in a Vero cell viability assay. Herein, we demonstrated that this fragment neutralized, in a dose-dependent manner, the cytotoxic effects of Stx2 on human glomerular endothelial cells, on human proximal tubular epithelial cells, and prevented the morphological alterations induced by Stx2. FabC11:Stx2 protected mice from a lethal dose of Stx2 by toxin-antibody pre-incubation. Altogether, our results show the ability of a new encouraging molecule to prevent Stx-intoxication symptoms during STEC infection.

miR-208a-3p promotes NSCLC proliferation and migration by suppressing lncRNA-MEG3 expression

2021 ◽  
Author(s):  
Linfei Yang ◽  
Qian Li ◽  
Hai Zhong ◽  
Liang Ye ◽  
Surong Fang ◽  
...  
Keyword(s):  
Protein Extraction ◽  
Underlying Mechanism ◽  
In Vitro Assays ◽  
Cell Viability Assay ◽  
Migration Assay ◽  
Normal Tissues ◽  
Viability Assay ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background The disordered expression of maternally expressed gene 3 (MEG3) has been observed in non-small-cell lung cancer (NSCLC). However, the molecular mechanism accounting for this abnormal expression is not fully understood. Methods MEG3 expression was detected by qRT-PCR in 51 cases of NSCLC and adjacent normal tissues. Then, the relationship between MEG3 and miR-208a-3p was assessed in vitro by cell viability assay, cell migration assay, protein extraction and western blot analysis. Resoults We observed that MEG3 expression was decreased in NSCLC tissues. And MEG3 expression was negatively related to lymph node metastasis and differentiation. Moreover, MEG3 expression is regulated by miR-208a-3p expression by overexpression and knockout experiments. Furthermore, we focused on the underlying mechanism of MEG3 downregulation. We found that the overexpression of miR-208a-3p reduced the level of MEG3 expression based on computational predictions and in vitro assays. Using CCK-8 and transwell migration assays, we found that the overexpression of miR-208a-3p can increased proliferation and apoptosis in NSCLC cells. Moreover, the depletion of MEG3 rescued the proliferation and migration induced by miR-208a-3p knockdown. Conclusion Taken together, the results of this study reveal that miR-208a-3p promotes NSCLC tumorigenesis by negatively regulating MEG3 expression and functions as an oncogenic miRNA in NSCLC.

scholarly journals Astaxanthin Modulates Apoptotic Molecules to Induce Death of SKBR3 Breast Cancer Cells

Marine Drugs ◽  
2020 ◽  
Vol 18 (5) ◽  
pp. 266 ◽  
Author(s):  
Min Sung Kim ◽  
Yong Tae Ahn ◽  
Chul Won Lee ◽  
Hyungwoo Kim ◽  
Won Gun An
Keyword(s):  
Breast Cancer ◽  
Cell Cycle Progression ◽  
Cellular Proliferation ◽  
Morphological Changes ◽  
Cancer Cell Line ◽  
Cancer Therapies ◽  
Intrinsic Apoptosis ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
Induced Apoptosis

Astaxanthin (AST) is related to apoptosis but the details of the mechanism of how AST makes apoptosis is not clear. The present study investigated apoptotic effects of AST to SKBR3, a breast cancer cell line in detail. Cell viability assay showed cellular proliferation and morphological changes of the cells were observed under AST treatment. FACS analysis indicated that AST blocked cell cycle progression at G0/G1, suppressed proliferation dose-dependently, and induced apoptosis of the cells. The apoptosis of the cells by AST was further demonstrated through the decreased expression level of mutp53 and cleaved a PARP-1 fragment, respectively. In addition, AST induced the intrinsic apoptosis of the cells by activation of Bax/Bcl2, cleaved caspase-3, and cleaved caspase-9 as well as the phosphorylation of ERK1/2, JNK, and p38. Furthermore, AST decreased production of intracellular reactive oxygen species as well as modulated expressions of superoxide dismutases and Pontin, an anti-apoptotic factor. Co-immunoprecipitation assay revealed AST reduced interaction between Pontin and mutant p53. Taken together, these studies proved that AST regulates the expression of apoptotic molecules to induce intrinsic apoptosis of the cells, suggesting AST therapy might provide an alternative for improving the efficacies of other anti-cancer therapies for breast cancer.

scholarly journals Antiproliferative Effects of an Analog of Curcumin in Hep-2 cells: A Comparative Study with Curcumin

2013 ◽  
Vol 8 (2) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Mohankumar Kumaravel ◽  
Pajaniradje Sankar ◽  
Periyasamy Latha ◽  
Chellakan S Benson ◽  
Rajagopalan Rukkumani
Keyword(s):  
Cell Proliferation ◽  
Curcuma Longa ◽  
Antioxidant Properties ◽  
Active Principle ◽  
Cell Cycle Distribution ◽  
Curcumin Analog ◽  
Cell Viability Assay ◽  
Chemopreventive Agents ◽  
Viability Assay ◽  
Cell Counts

Curcumin, the major active principle of Curcuma longa, is one of the promising, plant-derived, chemopreventive agents being studied for its anticarcinogenic and antioxidant properties. Hence, in our study, we aimed at testing the antiproliferative efficacy of an o-hydroxyl substituted analog of curcumin, bis demethoxy curcumin analog (BDMC-A), and comparing its efficacy with that of curcumin. BDMC-A was synthesised with a yield of 78% and 98% purity. Hep-2 cells and the MTT cell viability assay were used to examine cell proliferation. LDH assay and cell counts were performed to assess the cytotoxicity and anti-proliferative effects of the compound, respectively. Flow cytometry followed by Western blot were performed to investigate the cell cycle distribution. BDMC-A inhibited cell proliferation at a much lower concentration (IC50 20 μM) than curcumin (IC50 50 μM). Similar effects were observed in the LDH release and cell count assays. Flow cytometric studies using propidium iodide showed accumulation of cells in the G0/G1 phase and the arrest was further confirmed by immunoblotting of protein cyclin D1. BDMC-A was more potent in inhibiting the cells at a lower dose when compared with curcumin. Our results showed that the analog of curcumin is likely to possess more efficacy compared with curcumin in inhibiting cancer.

scholarly journals Efficient Delivery of Therapeutic siRNA with Nanoparticles Induces Apoptosis in Prostate Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xupeng Mu ◽  
Haibin Lu ◽  
Lianlian Fan ◽  
Shaohua Yan ◽  
Kebang Hu
Keyword(s):  
Sirna Delivery ◽  
Mitochondrial Pathway ◽  
Gene Knockdown ◽  
Hybrid Nanoparticles ◽  
Cell Viability Assay ◽  
Protein Levels ◽  
Viability Assay ◽  
Efficient Delivery ◽  
Du145 Cells

Gene silencing using small interfering RNA (siRNA) has shown significant potential in the treatment of cancer. Herein, we developed the lipid-polymer hybrid nanoparticles (PEG-LP/siRNA NPs) for siRNA delivery. The cell viability assay indicated that PEG-LP/siRNA NPs had negligible cell cytotoxicity. The cellular uptake efficiency of PEG-LP/siRNA NPs measured by flow cytometry was up to 94.4%. Importantly, in vitro gene knockdown experiments demonstrated that PEG-LP/siJnk-1 NPs could significantly downregulate the expression of Jnk-1 at both the mRNA and protein levels in DU145 cells. Gene knockdown of Jnk-1 could activate apoptosis in part by the mitochondrial pathway in DU145 cells. Moreover, the PEG-LP/siJnk-1 NPs could inhibit tumor growth in a DU145 xenograft murine model, suggesting its therapeutic promise in cancer therapy.

Cotreatment with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced apoptosis of Bcr-Abl–positive human acute leukemia cells

Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3236-3239 ◽  
Author(s):  
Ramadevi Nimmanapalli ◽  
Lianne Fuino ◽  
Corinne Stobaugh ◽  
Victoria Richon ◽  
Kapil Bhalla
Keyword(s):  
Histone Deacetylases ◽  
Hydroxamic Acid ◽  
Blast Crisis ◽  
Cell Types ◽  
Suberoylanilide Hydroxamic Acid ◽  
Cytotoxic Effects ◽  
Protein Levels ◽  
Myelocytic Leukemia ◽  
Deacetylase Inhibitor ◽  
Induced Apoptosis

Abstract Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl–expressing K562 and LAMA-84 cells. Cotreatment with SAHA and imatinib (Gleevec) caused more down-regulation of the levels and auto-tyrosine phosphorylation of Bcr-Abl and apoptosis of these cell types, as compared with treatment with either agent alone (P < .05). This finding was also associated with a greater decline in the levels of phospho-AKT and Bcl-xL. Significantly, treatment with SAHA also down-regulated Bcr-Abl levels and induced apoptosis of CD34+ leukemia blast progenitor cells derived from patients who had developed progressive blast crisis (BC) of chronic myelocytic leukemia (CML) while receiving therapy with imatinib. Taken together, these findings indicate that cotreatment with SAHA enhances the cytotoxic effects of imatinib and may have activity against imatinib-refractory CML-BC.

scholarly journals PSAT1 prompted cell proliferation and inhibited cell apoptosis in multiple myeloma through regulating PI3K/AKT pathway

2020 ◽  
Vol 19 (4) ◽  
pp. 745-749
Author(s):  
Hongqing Zhu ◽  
Yejun Si ◽  
Yun Zhuang ◽  
Meng Li ◽  
Jianmin Ji ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Underlying Mechanism ◽  
Akt Pathway ◽  
Protein Levels ◽  
Phosphoserine Aminotransferase ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Polymerase Chain

Purpose: To identify the biological function of phosphoserine aminotransferase 1 (PSAT1) in regulating cell proliferation and apoptosis in multiple myeloma (MM).Methods: The mRNA and protein levels of PSAT1 were determined using quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. Cell proliferation was measured using CCK-8 assay.Results: PSAT1 mRNA and protein expression levels were significantly increased in MM cell lines when compared to control cells. Moreover,  downregulation of PSAT1 inhibited MM cell proliferation and induced cell apoptosis, whereas overexpression of PSAT1 promoted MM cell  proliferation and suppressed cell apoptosis. Further analysis demonstrated that the underlying mechanism was via regulation of PI3K/AKT pathway.Conclusion: The results identified a novel role for PSAT1 in the progression of MM, which may provide a therapeutic and a new anticancer target for the therapy of MM. Keywords: Multiple myeloma, PSAT1, Cell proliferation, PI3K/AKT pathway

scholarly journals Yiqi Huoxue Recipe Improves Liver Regeneration in Rats after Partial Hepatectomy via JNK Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Wen-cong Li ◽  
Su-xian Zhao ◽  
Wei-guang Ren ◽  
Hui-juan Du ◽  
Yu-guo Zhang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Underlying Mechanism ◽  
Mrna Levels ◽  
Protective Effects ◽  
Jnk Pathway ◽  
Expression Levels ◽  
Protein Levels ◽  
Mrna And Protein Expression

The liver is the only visceral organ that exhibits a remarkable capability of regenerating in response to partial hepatectomy (PH) or chemical injury. Improving liver regeneration (LR) ability is the basis for the favourable treatment outcome of patients after PH, which can serve as a potential indicator for postoperative survival. The present study aimed to investigate the protective effects of Yiqi Huoxue recipe (YQHX) on LR after PH in rats and further elucidate its underlying mechanism. A two-thirds PH rat model was used in this study. Wistar rats were randomly divided into four groups: sham-operated, PH, YQHX + PH, and Fuzheng Huayu decoction (FZHY) + PH groups. All rats were sacrificed under anesthesia at 24 and 72 h after surgery. The rates of LR were calculated, and the expression levels of cyclin D1 and c-jun were determined by immunohistochemical staining. The protein levels of p-JNK1/2, JNK1/2, p-c-jun, c-jun, Bax, and Bcl-2 were detected by Western blotting, while the mRNA levels of JNK1, JNK2, c-jun, Bax, and Bcl-2 were examined by real-time polymerase chain reaction (RT-PCR). At the corresponding time points, YQHX and FZHY administration dramatically induced the protein levels of p-JNK1/2 compared to the PH group p<0.05, while FZHY + PH group showed prominently increase in p-JNK1/2 protein levels compared to the YQHX + PH group p<0.05. A similar trend was observed for the expression levels of p-c-jun. Compared to the PH group, YQHX and FZHY markedly reduced the mRNA and protein expression levels of Bax at 24 h after PH, while those in the FZHY + PH group decreased more obviously p<0.05. Besides, in comparison with the PH group, YQHX and FZHY administration predominantly upregulated the mRNA and protein expression levels of Bcl-2 at 24 and 72 h after PH p<0.05. In conclusion, YQHX improves LR in rats after PH by inhibiting hepatocyte apoptosis via the JNK signaling pathway.

Evaluation of the Influence of Ferrite Magnetic Nanoparticle for Cancer Cell

2021 ◽  
Vol 323 ◽  
pp. 146-151
Author(s):  
Khishigdemberel Ikhbayar ◽  
Nomin Myagmar ◽  
Gantulga Davaakhuu ◽  
Uyanga Enkhnaran ◽  
Enkhmend Bekhbaatar ◽  
...  
Keyword(s):  
Cell Viability ◽  
Colony Formation ◽  
Magnetic Nanoparticle ◽  
In Vitro Cytotoxicity ◽  
Colony Formation Assay ◽  
Cell Viability Assay ◽  
Cytotoxic Effects ◽  
Viability Assay ◽  
A Cell

Magnetic nanoparticles for thermotherapy must be biocompatible and possess high thermal efficiency as heating elements. The biocompatibility of Mg 0.8 Ni 0.2 Fe 2 O 4 nanoparticles was studied using a cytotoxicity colony formation assay and a cell viability assay. HeLa cells exhibited cytotoxic effects when exposed to three different concentrations of 150 μg /ml, 100 μg /ml, and 50 μg /ml nanoparticles. Therefor e, c oncentrations of 50 μg /ml showed the lowest cytotoxic activity and the lowest toxicity to living cells. In vitro cytotoxicity of samples was then investigated by two methods, colony formation assay and cell viability assay. The Hela inhibited cell growth as 16.8% during heating by magnetic field generators.

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