scholarly journals Immunocytochemical indicators of apoptosis in gingival tissues of patients with chronic periodontitis

2014 ◽  
Vol 83 (1) ◽  
pp. 37-46
Author(s):  
Aldona Kasprzak ◽  
Miłosz Hausmann ◽  
Agata Małkowska-Lanzafame ◽  
Joanna Surdyk-Zasada ◽  
Wiesława Przybyszewska ◽  
...  
Keyword(s):  
Chronic Periodontitis ◽  
Caspase 3 ◽  
Tissue Expression ◽  
P53 Expression ◽  
Effector Phase ◽  
Apoptotic Protein ◽  
Gingival Cells ◽  
Apoptotic Proteins ◽  
Inflammatory Infiltrates ◽  
And Control

Introduction. Inflammatory mechanisms of chronic periodontitis (CP) may be linked to various forms of disturbances in apoptosis.Aim. The study aimed at comparison of tissue expression of anti-apoptotic protein (Bcl-2) and proapoptotic proteins (p53, caspase-3) in gingival tissues of 30 patients with CP and of 15 with healthy periodontium.Material and methods. Gingival samples (n = 68) were obtained during the open curettage procedure with gingivectomy of adult patients (18 women and 12 men) with CP. Classical immunocytochemical (IHC) method was used to detect apoptotic proteins, and the obtained expression was evaluated using semi-quantitative IRS scale.Results. No differences could be revealed in expression intensity or reciprocal correlations between apoptotic proteins within the group of patients with CP. Greater expression of the two apoptotic proteins (Bcl-2 and p53) were detected in patients with CP than in control individuals. Moreover, a more pronounced expression of Bcl-2 was demonstrated in gingival samples of patients with localised form as compared to generalised form of CP. Expression of caspase-3 (effector phase of apoptosis) manifested no differences between CP and control individuals. Greater expression of the anti-apoptotic protein Bcl-2 and caspase-3 was detected in cells of inflammatory infiltrates in lamina propria than in keratinocytes.Conclusions. In CP significant alterations developed in expression of indicators of apoptosis, with prevalence of Bcl-2 and p53 expression, as compared to the control. The localised form of CP was linked to higher proportion of Bcl-2-positive cells of inflammatory infiltrates, suggesting that apoptosis was inhibited mainly in this form of CP. The comparable expression of caspase-3 in gingival cells with CP and in control and absence of correlation with clinical data suggested that the process of apoptosis did not play a significant role in destruction of periodontium tissues in CP.

Yuk-Hap-Tang Induces Apoptosis by Intervening Mn-SOD in Human Cervical Carcinoma HeLa Cells

2004 ◽  
Vol 32 (06) ◽  
pp. 883-895 ◽  
Author(s):  
H. J. Chae ◽  
J. M. Park ◽  
G. Y. Lee ◽  
H. R. Park ◽  
S. W. Chae ◽  
...  
Keyword(s):  
Cell Death ◽  
Cervical Carcinoma ◽  
Anticancer Agents ◽  
Hela Cells ◽  
Caspase 3 ◽  
Reduced Glutathione ◽  
Cleavage Product ◽  
P53 Expression ◽  
Human Cervical Carcinoma ◽  
Apoptotic Protein

Yuk-Hap-Tang (YHT) induces cell death in human cervical carcinoma HeLa cells. Caspase-3, -6 and -9 were markedly activated in HeLa cells treated with YHT. The preferred substrate for caspase-3 cysteine protease, PARP, was cleaved to its 85-kDa cleavage product. YHT increased the amount of the anti-apoptotic protein, Bcl-2, and the pro-apoptotic protein, Bax. Although p53 has been reported to accumulate in cancer cells in response to anticancer agents, the p53 expression level was not changed in HeLa cells treated with YHT. Manganese (Mn)-TBAP, a mitochondria-specific SOD mimetic agent and NAC/GSH (N-acetyl cysteine/reduced glutathione) reduced the YHT-induced cytotoxicity and decreased the number of the YHT-induced apoptotic cells. Furthermore, YHT reduced the expression of Mn-SOD protein and its activity in HeLa cells. The data demonstrate that YHT induces the apoptosis of human cervical carcinoma HeLa cells by intervening Mn-SOD.

Effects of Papaya Leaf Extract (Carica papaya L.) on Cellular Proliferation and Apoptosis in Cervical Cancer Mice Model

2019 ◽  
Vol 17 (5) ◽  
pp. 265-275
Author(s):  
Y. Peristiowati ◽  
Y. Puspitasari ◽  
Indasah
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Hela Cells ◽  
Leaf Extract ◽  
Caspase 3 ◽  
Methanol Extract ◽  
Negative Control ◽  
Proliferation Index ◽  
Control Group ◽  
P53 Expression

This study is aimed at analyzing the anticancer properties of papaya leaf extract, specifically the inhibition of cell proliferation and apoptotic induction through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and p53 pathways. Twenty-five mice (Mus musculus), aged 2 months and weighing 20–30 g, was injected with 0.5 mg dexamethasone for 7 days. The mice were then injected intracutaneously with 1 ml of HeLa cells (8 × 106 HeLa cells/microliter). The mice were divided into five groups (5 each): negative control (P1) (5% CMC-Na, sodium carboxymethyl cellulose), treatment II (225 mg/kg BW (body weight) papaya leaves methanol extract), treatment III (450 mg/kg BW), treatment IV (750 mg/kg BW), and treatment PV (2 mg alcohol anticancer drug). Papaya leaf extract treatments were applied for 2 weeks. Then, the tumor tissue was isolated for hematoxylin and eosin staining. Immunohistochemical imaging was used to detect Ki-67, caspase-3, NF-κB, and p53 expression. Further analysis was undertaken using the ImmunoRatio software program. The results indicated that administration of papaya leaf methanol extract significantly increased the expression of NF-κB and p53 at a dose of 450 mg/kg BW. Our results also showed that the mice treated with 450 mg of papaya leaf extract per kg of BW (P3) had the largest increase of caspase-3 expression compared to the negative control group. Papaya leaf ethanol extract decreased the cancer cell proliferation index and increased apoptosis of cancer cells in animal models of cervical cancer; it may also work to increase NF-kB expression and expression of the p53 gene.

The Anti-Proliferative Activity of Anisosciadone: A New Guaiane Sesquiterpene from Anisosciadium lanatum

2019 ◽  
Vol 19 (9) ◽  
pp. 1114-1119 ◽  
Author(s):  
Ahmed A. Mahmoud ◽  
Wael M. El-Sayed
Keyword(s):  
Anticancer Agents ◽  
Antiproliferative Activity ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Chemical Constituents ◽  
Spectroscopic Techniques ◽  
Significant Activity ◽  
Caspase 9 ◽  
P53 Expression ◽  
Expression And Activity

Background: The increase in cancer rate and the development of resistant tumors require a continuous search for new anticancer agents. Aims: This study aimed to analyze and identify the chemical constituents of Anisosciadium lanatum, and to investigate the antiproliferative activity of the identified constituents against various human cell lines (HepG2, MCF7, HT29, A549, and PC3) along with the possible molecular mechanisms involved. Methods: The structure of the isolated compounds was determined by spectroscopic techniques including HRFABMS, GC-MS, IR, and 400 MHz 1D and 2D NMR analyses (1H, 13C NMR, DEPT, 1H-1H COSY, HMQC, HMBC and NOESY). The antiproliferative activity and IC50 value of the isolated compounds were measured and compared to doxorubicin. Results: A new guaiane sesquiterpene containing a rare epoxide structural element, 10β,11β−epoxy−1α,4β,5β,7αΗ- guaiane-9-one, anisosciadone (1), and stigmasterol (2) have been isolated from the plant. Anisosciadone (1) showed a significant antiproliferative activity against liver, colon, and lung cells only, while stigmasterol (2) had a significant activity against liver, colon, and breast cells. Both 1 and 2 caused no cytotoxicity to normal fibroblasts. Anisosciadone elevated the expression and activity of Caspase 3 as well as p53 expression without affecting Caspase 9 in HepG2 cells. It also caused ~ 50% downregulation in cdk1 expression. Conclusion: Taken together, anisosciadone was specific in action against cancer cells and induced apoptosis in liver cells. It also has a unique feature by elevating the expression and activity of Caspase 3 without affecting the initiator Caspase 9. Therefore, anisosciadone deserves more investigation as a targeted therapy for cancer.

scholarly journals Implant Treatment with 12-Year Follow-Up in a Patient with Severe Chronic Periodontitis: A Case Report and Literature Review

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Keisuke Seki ◽  
Yoshiyuki Hagiwara
Keyword(s):  
Periodontal Disease ◽  
Chronic Periodontitis ◽  
Case Reports ◽  
English Literature ◽  
Supportive Therapy ◽  
Periodontal Treatment ◽  
Periodontal Tissues ◽  
Severe Periodontitis ◽  
And Control ◽  
Implant Treatment

Tooth loss among adults is associated with progressive periodontitis. Implant prosthetic treatment has long been utilized in periodontal patients. Even when the implants are applied, ongoing management of periodontal disease and control of inflammation is necessary to maintain a healthy oral cavity. Lack of appropriate periodontal treatment can result in recurrence of periodontal disease during a maintenance period; loss of the supportive capacity of the periodontal tissues will increase the susceptibility of residual teeth to traumatic force. For this reason, it is worthwhile to improve oral function by applying implants as a fixed device. Here, we report that implant treatment in a patient with generalized severe chronic periodontitis helped maintain the periodontal and peri-implant tissue for a long term. We propose that initial periodontal treatment and ongoing supportive therapy can help maintain implants in patients with severe periodontitis. In addition, we reviewed case reports in the English literature so far.

scholarly journals 7β-(3-Ethyl-cis-crotonoyloxy)-1α-(2-methylbutyryloxy)-3,14-dehydro-Z Notonipetranone Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Protein Expressions

Molecules ◽  
2021 ◽  
Vol 26 (1) ◽  
pp. 181
Author(s):  
Amna Khan ◽  
Adnan Khan ◽  
Sidra Khalid ◽  
Bushra Shal ◽  
Eunwoo Kang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuropathic Pain ◽  
Interleukin 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Glutathione S Transferase ◽  
Quinone Oxidoreductase ◽  
Apoptotic Protein ◽  
Apoptotic Proteins ◽  
Apoptosis And Inflammation

7β-(3-Ethyl-cis-crotonoyloxy)-1α-(2-methylbutyryloxy)-3,14-dehydro-Z-notonipetranone (ECN), a sesquiterpenoid obtained from a natural source has proved to be effective in minimizing various side effects associated with opioids and nonsteroidal anti-inflammatory drugs. The current study focused on investigating the effects of ECN on neuropathic pain induced by partial sciatic nerve ligation (PSNL) by mainly focusing on oxidative stress, inflammatory and apoptotic proteins expression in mice. ECN (1 and 10 mg/kg, i.p.), was administered once daily for 11 days, starting from the third day after surgery. ECN post-treatment was found to reduce hyperalgesia and allodynia in a dose-dependent manner. ECN remarkably reversed the histopathological abnormalities associated with oxidative stress, apoptosis and inflammation. Furthermore, ECN prevented the suppression of antioxidants (glutathione, glutathione-S-transferase, catalase, superoxide dismutase, NF-E2-related factor-2 (Nrf2), hemeoxygenase-1 and NAD(P)H: quinone oxidoreductase) by PSNL. Moreover, pro-inflammatory cytokines (tumor necrotic factor-alpha, interleukin 1 beta, interleukin 6, cyclooxygenase-2 and inducible nitric oxide synthase) expression was reduced by ECN administration. Treatment with ECN was successful in reducing the caspase-3 level consistent with the observed modulation of pro-apoptotic proteins. Additionally, ECN showed a protective effect on the lipid content of myelin sheath as evident from FTIR spectroscopy which showed the shift of lipid component bands to higher values. Thus, the anti-neuropathic potential of ECN might be due to the inhibition of oxidative stress, inflammatory mediators and pro-apoptotic proteins.

Abstract WP62: Enhanced Neuroprotection of Normobaric Oxygenation with Ethanol Conferred by Apoptosis Reduction in Acute Ischemic Stroke

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Sweena Parmar ◽  
Xiaokun Geng ◽  
Changya Peng ◽  
Murali Guthikonda ◽  
Yuchuan Ding
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Neuroprotective Effect ◽  
Apoptotic Cell Death ◽  
Ethanol Administration ◽  
Sprague Dawley ◽  
Apoptotic Proteins

Objectives: Normobaric oxygenation (NBO) has been shown to provide neuroprotection in vivo and in vitro . Yet, a recent Phase 2 clinical trial investigating NBO therapy in acute ischemic stroke was terminated due to questionable therapeutic benefit. NBO therapy alone may be insufficient to produce improved outcomes. In our recent study, we demonstrated a strong neuroprotective effect of ethanol at a dose of 1.5 g/kg (equivalent to the human legal driving limit). In this study, we sought to identify whether low-dose ethanol administration enhances the neuroprotection offered by NBO and whether combined administration of NBO with ethanol is associated with reduced apoptosis. Methods: Sprague-Dawley rats were subjected to right middle cerebral artery occlusion (MCAO) for 2 h, followed by reperfusion. Ischemic animals received either an intraperitoneal injection of 1.0 g/kg ethanol, 2 h of 100% NBO, or both ethanol and NBO. The Cell Death Detection ELISA Assay (Roche) was performed to determine apoptotic cell death at 24 h after reperfusion. Levels of pro-apoptotic (Caspase-3, Bcl-2-associated X-BAX, and Apoptosis-Inducing Factor-AIF) and anti-apoptotic proteins (Bcl-2 and Bcl-xL) were determined by Western blot analysis at 3 and 24 h after reperfusion. Results: As expected, untreated ischemic rats had the highest apoptotic cell death. Combined NBO/ethanol therapy decreased cell death by 48%, as compared to 29% with ethanol and 22% with NBO. Similarly, combined NBO/ethanol therapy promoted the greatest expression of anti-apoptotic factors and the lowest expression of pro-apoptotic proteins at 3 h after reperfusion. This effect was maintained at 24 h and even more pronounced for AIF and Caspase-3. Conclusions: Given singularly, NBO and ethanol improved the degree of cell death, decreased the expression of pro-apoptotic proteins, and increased the expression of anti-apoptotic proteins. Yet, when administered together, their effects largely compounded. These results suggest a synergistic neuroprotection offered by NBO with ethanol, which may be attributed at least in part to their shared role in modulating neuronal apoptosis.

4-Acetyl-12,13-Epoxyl-9-Trichothecene-3,15-Diol from Isaria japonica Mediates Apoptosis of Rat Bladder Carcinoma NBT-II Cells by Decreasing Anti-apoptotic Bcl-2 Expression and Increasing Pro-apoptotic Bax Expression

2004 ◽  
Vol 32 (03) ◽  
pp. 377-387 ◽  
Author(s):  
Hyung-Jin Kim ◽  
Seon Il Jang ◽  
Young-Jun Kim ◽  
Hyun-Ock Pae ◽  
Hae-Young Won ◽  
...  
Keyword(s):  
Cell Death ◽  
Bladder Carcinoma ◽  
Cytotoxic Effect ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Morphological Changes ◽  
Rat Bladder ◽  
Apoptotic Protein ◽  
Induction Of Apoptosis ◽  
Induced Apoptosis

We studied the effect of 4-acetyl-12,13-epoxyl-9-trichothecene-3,15-diol (AETD) isolated from Isaria japonica, one of the most popular Chinese fungal medicines, on the induction of apoptosis in rat bladder carcinoma NBT-II cells. AETD was cytotoxic to NBT-II cells, and this cytotoxic effect appears to be attributed to its induction of apoptotic cell death, as AETD induced nuclear morphological changes and internucleosomal DNA fragmentation, and increased the proportion of hypodiploid cells and activity of caspase-3. AETD treatment also decreased the expression of the anti-apoptotic protein Bcl-2 and increased the expression of the pro-apoptotic protein Bax. These results provide important information in understanding the mechanism(s) of AETD-induced apoptosis.

scholarly journals Proposed megakaryocytic regulon of p53: the genes engaged to control cell cycle and apoptosis during megakaryocytic differentiation

2012 ◽  
Vol 44 (12) ◽  
pp. 638-650 ◽  
Author(s):  
Pani A. Apostolidis ◽  
Stephan Lindsey ◽  
William M. Miller ◽  
Eleftherios T. Papoutsakis
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Cell Line ◽  
Target Genes ◽  
Control Cell ◽  
P53 Expression ◽  
Megakaryocytic Differentiation ◽  
Knock Down ◽  
Cell Cycling ◽  
And Control

During endomitosis, megakaryocytes undergo several rounds of DNA synthesis without division leading to polyploidization. In primary megakaryocytes and in the megakaryocytic cell line CHRF, loss or knock-down of p53 enhances cell cycling and inhibits apoptosis, leading to increased polyploidization. To support the hypothesis that p53 suppresses megakaryocytic polyploidization, we show that stable expression of wild-type p53 in K562 cells (a p53-null cell line) attenuates the cells' ability to undergo polyploidization during megakaryocytic differentiation due to diminished DNA synthesis and greater apoptosis. This suggested that p53's effects during megakaryopoiesis are mediated through cell cycle- and apoptosis-related target genes, possibly by arresting DNA synthesis and promoting apoptosis. To identify candidate genes through which p53 mediates these effects, gene expression was compared between p53 knock-down (p53-KD) and control CHRF cells induced to undergo terminal megakaryocytic differentiation using microarray analysis. Among substantially downregulated p53 targets in p53-KD megakaryocytes were cell cycle regulators CDKN1A (p21) and PLK2, proapoptotic FAS, TNFRSF10B, CASP8, NOTCH1, TP53INP1, TP53I3, DRAM1, ZMAT3 and PHLDA3, DNA-damage-related RRM2B and SESN1, and actin component ACTA2, while antiapoptotic CKS1B, BCL2, GTSE1, and p53 family member TP63 were upregulated in p53-KD cells. Additionally, a number of cell cycle-related, proapoptotic, and cytoskeleton-related genes with known functions in megakaryocytes but not known to carry p53-responsive elements were differentially expressed between p53-KD and control CHRF cells. Our data support a model whereby p53 expression during megakaryopoiesis serves to control polyploidization and the transition from endomitosis to apoptosis by impeding cell cycling and promoting apoptosis. Furthermore, we identify a putative p53 regulon that is proposed to orchestrate these effects.

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