Protective Effect of Nerium Oleander Distillate and Tarantula Cubensis Alcoholic Extract on Cancer Biomarkers on Colon and Liver Tissues of Rats with Experimental Colon Cancer

2021 ◽  
Vol 21 ◽  
Author(s):  
Burak Dik ◽  
Devran Coskun ◽  
Ayşe Er
Keyword(s):  
Colon Cancer ◽  
Caspase 3 ◽  
Cancer Biomarkers ◽  
Nerium Oleander ◽  
Control Group ◽  
Alcoholic Extract ◽  
Colon Cancers ◽  
Cancer Types ◽  
Cox 2 ◽  
Liver Tissues

Background: Colon cancers are among the three major cancer types that result in death. The research for effective treatment continues. Objective: The aim of this study is to determine the effects of Tarantula cubensis alcoholic extract (TCAE) and Nerium oleander (NO) distillate on the levels of midkine, TGF-β, VEGF, AFP, COX-2, IGF and caspase 3 in liver and colon tissues of experimentally induced colon cancer in rats. Method: The liver and colon tissues of the rats were divided into Control, Colon Cancer (AZM), AZM+TCAE and AZM+NO groups and they were homogenized. The levels of midkine, TGF-β, VEGF, AFP, COX-2, IGF and caspase 3 in the colon and liver tissues were measured by ELISA kits. Results: All parameters levels of colon and liver tissues in the AZM group were generally higher (p<0.05) than the Control group. TCAE and NO prevented (p<0.05) the increases in midkine, TGF-β, VEGF, AFP, COX-2, IGF and caspase-3 levels in the colon. NO prevented increase of all parameters except for IGF level, while TCAE prevented (p<0.05) the increase of all values apart from COX-2 and IGF levels in the liver. Conclusion: NO and TCAE may prevented at the specified marker levels of colon in the AZM induced colon cancer. The increases the level of parameters in the liver are not as severe as in the colon, due to the 18-week study period may not be sufficient for liver metastasis formationIn the future molecular studies should be done to determine the mechanisms and pathways of them more clearly.

Brucea javanica Oil Induces Apoptosis in T24 Bladder Cancer Cells via Upregulation of Caspase-3, Caspase-9, and Inhibition of NF-κB and COX-2 Expressions

2010 ◽  
Vol 38 (03) ◽  
pp. 613-624 ◽  
Author(s):  
Guo-Guang Lou ◽  
Hang-Ping Yao ◽  
Li-Ping Xie
Keyword(s):  
Caspase 3 ◽  
Flow Cytometric Analysis ◽  
Morphological Characteristics ◽  
Control Group ◽  
Caspase 9 ◽  
Brucea Javanica ◽  
Flow Cytometric ◽  
T24 Cells ◽  
Bladder Cancer Cells ◽  
Cox 2

The potential molecular mechanism of Brucea javanica oil in the induction of apoptosis of T24 bladder cancer cells was investigated in vitro. T24 cells were divided into two groups: one, treated with B. javanica oil and the other, untreated. The cells were maintained in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum (FCS) and 4 mM glutamine. The morphological characteristics of T24 cells were examined microscopically at the 2nd and 5th day of the culture. The drug toxicity spectrum ( IC 50) was estimated by the MTT assay, and viability of T24 cells was assessed on the basis of the percentage of T24 apoptotic cells, as determined by Annexin/PI staining and flow cytometric analysis. The expression of caspase-3, capase-9, NF-κB p65, and COX-2 was analyzed by Western blotting. Morphological characteristics of the cells on the 2nd day showed apoptosis of the treated T24 cells; it was more apparent in the cells on the 5th day. B. javanica oil decreased the cell viability at the testing concentrations spectrum (5–0.156 mg/ml), and this viability was significantly higher as compared to the control group. In this concentration spectrum, B. javanica oil also induced apoptosis of T24 cells, which was analyzed by annexin/PI staining and flow cytometric analysis. These results were also statistically significant as compared to those of the control group. The expressions of caspase-3 and caspase-9 were low in the control T24 cells, while the expressions of NF-κB and COX-2 were high in normal T24 cells. Treatment with B. javanica oil significantly induced the expressions of caspase-3 and caspase-9 proteins in T24 cells, whereas the expressions of NF-κB and COX-2 proteins were inhibited. B. javanica oil significantly reduced the viability of T24 cells and induced T24 cell apoptosis. The molecular mechanism underlying these effects may be the activation of caspase apoptotic pathway by upregulation of the expression of caspase-3 and caspase-9 proteins and inhibition of the expression of NF-κB and COX-2 proteins.

Study of the antineoplastic effect of modulating apoptosis-related noncoding RNA in human hepatocellular carcinoma cell line (HepG2)

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Mai Abdel Azeem Sherif ◽  
Emtiaz Abd-elkawy Ismail ◽  
Samar Kamal Kassim ◽  
Hanan Hussein Shehata ◽  
Marwa Ali Abdel Khalek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Noncoding Rna ◽  
Caspase 3 ◽  
Control Group ◽  
Antineoplastic Effect ◽  
And Control ◽  
Hcc Cells ◽  
Liver Tissues

Abstract MiR-421 is considered an important molecule that can prevent tumor growth. Bioinformatics analysis indicated that mRNA caspase-3 gene is a target gene of miR-421. The current study aimed to explore the functional role of miR-421 in hepatocellular carcinoma (HCC) and explore the interaction between miR-421 and caspase-3. To validate bioinformatics data, RT-qPCR was used to detect the expression of miR-421 and caspase-3 in 10 HCC tissues. The results showed miR-421 expression was significantly higher in HCC than non HCC liver tissues (P&lt;0.01), nevertheless caspase-3 gene expression was markedly lower in HCC than non HCC liver tissues (P&lt;0.01). Besides, miR-421 expression was negatively associated with caspase-3 expression. MiR-421 mimic and inhibitor was transfected into HCC cell lines (HepG2). Proliferation assay, showed that low-expression of miR-421 inhibited the proliferation of HCC cells. RT-qPCR was worked for detection the expression levels of miR-421 and caspase-3 in HepG2 cells before and after transfection. The results showed that miR-421 expression in HepG2 cells was significantly lower in miR-421 inhibitor transfected group than in mimic- transfected and control groups (Mock) (P≤ 0.05), and caspase-3 gene expression in HCC tissues was markedly higher in inhibitor transfected group than those transfected by mimic and control group (Mock) (P≤0.05). Thus, miR-421 inhibitor may inhibit the proliferation of HCC cells via over- expression of caspase-3.

scholarly journals Eleutherine palmifolia (L.) Merr. Extract Increases The Crypts and Caspase-3 Expression in Colitis-Associated Colon Cancer Model

2020 ◽  
pp. 257-265
Author(s):  
Roihatul Mutiah ◽  
Wahyi Yucha Firsyaradha ◽  
Riza Ambar Sari ◽  
Rahmi Annisa ◽  
Risma Aprinda Kristanti ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Caspase 3 ◽  
Positive Control ◽  
Negative Control ◽  
Immunohistochemical Method ◽  
Positive Control Group ◽  
Control Group ◽  
Chemopreventive Agents ◽  
Fecal Occult ◽  
Apoptotic Activity

It is known that Eleutherine palmifolia (L.) Merr contains flavonoid and polyphenol as bioactive compounds that have the ability as chemopreventive agents. This study aims to examine the effect of Eleutherine palmifolia (L.) Merr extract (EPE) on colon histopathology and the enhancement of caspase-3 expression in BALB/c mice of colitis-associated colon cancer (CAC) model. Thirty Balb/c female mice were used in this study and were divided into six groups. Five mice in one group were normal or negative control (given phosphate-buffered saline), and twenty-five mice were induced intraperitoneally with 10 mg/kg BW AOM (Azoxymethane), and it was followed by the administration of 5% DSS (Dextran Sodium Sulfate) every two weeks for 20 weeks. At the sixth week, one mice in each group was sacrificed for the Fecal Occult Bold Test (FOBT) and serum amyloid α (SAA) test to ensure that CAC was indeed formed. The administration of EPE with varying doses was started from the eighth week and was continued until the 21st week. The length of the colonic crypt was measured through histology appearance using Hematoxylin-eosin (HE) staining while the immunohistochemical method was used to observe apoptotic activity through the enhancement of caspase-3 expression. The results showed that the increase in EPE dosage also increased the crypt colon length compared to the positive control group. The administration of 1.00 mg/20gBW EPE significantly increased cell apoptosis which can be observed through caspase-3 expression compared to the positive control group (p<0.05). Based on these data, the extract of EPE can be developed as phytotherapy for chemopreventive.    

Anti-inflammatory Effect of Alcoholic Extract of Nigella sativa L on Bovine Fibroblast-like synoviocyte and THP-1

2018 ◽  
Vol 9 (02) ◽  
pp. 20181-20191 ◽  
Author(s):  
Dr Maghsoudi, Hossein ◽  
Samaneh Haj-allahyari
Keyword(s):  
Nigella Sativa ◽  
Pcr Analysis ◽  
Control Group ◽  
Alcoholic Extract ◽  
Iranian Traditional Medicine ◽  
Tnf Α ◽  
Radiocarpal Joint ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Due to the side effects of current therapies for osteoarthritis one of the alternative medicine is using herbal medicine such as Nigella sativa .L which in Iranian traditional medicine has been used as a treatment option. The purpose of this study is evaluating the effect of alcoholic extract of Nigella sativa (AENS) on pro-inflammatory cytokines in Bovine Fibroblast-like BFLs (BFLS) and THP-1. BFLS cells were isolated from Radiocarpal joint. After evaluating of LC50 (27 µg/mL), both cells (5x105 (cells\wel)) were incubated at 37 ° C and 5% CO2 and 90% humidity for 72 hours with AENS (6.13 μg\ml as a media LC50). One set of cells was activated for 1h with LPS for RT-PCR analysis of COX-2, INOS, IL-1β, TNF-α expression and another set of cells was activated for 24h, cells supernatant were analyzed for PGE-2 and nitrite content. The present study demonstrates that AENS reduced expression levels of COX-2, INOS, TNF-α in control group. Reduced expression of COX2 and INOS was significantly along with the reducing production of NO and PGE2.Also, AENS decreased the expression of TNF-α and iL-1β in control group. Our results showed that the anti-inflammatory effect of AENS not only has anti-inflammatory effect on the BFLS cells but also related to the THP-1 that are active in the synovial membrane.

scholarly journals Investigation of the Therapeutic Effects of Chloroquine in Adriamycin-Induced Hepatotoxicity

2021 ◽  
Vol 5 (1) ◽  
pp. 8-14
Author(s):  
Ali Tuğrul Akin ◽  
Emin Kaymak ◽  
Emel Öztürk ◽  
Derya Karabulut ◽  
Nurhan Kuloğlu ◽  
...  
Keyword(s):  
Therapeutic Agent ◽  
Chemotherapeutic Agent ◽  
Control Group ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Cancer Types ◽  
Anti Inflammatory ◽  
Group 2 ◽  
Histopathological Score ◽  
Liver Tissues

AbstractThe aim of this study is to investigate the therapeutic effects of Chloroquine (CLQ) against Adriamycin (ADR) induced hepatotoxicity. ADR is a chemotherapeutic agent used in the treatment of many cancer types, but it causes hepatotoxicity. CLQ is used as an anti-inflammatory drug in the treatment of malaria, rheumatoid arthritis, and pneumonia caused by Covid-19. Rats were divided into four groups: Control group, ADR group (2 mg/kg Adriamycin, one in three days for 30 days, i.p.), CLQ group (50 mg/kg Chloroquine, per day for 30 days, i.p.), ADR+CLQ (2 mg/kg Adriamycin, one in three days for 30 days, i.p. and 50 mg/ kg Chloroquine, per day for 30 days, i.p.). Animals were sacrificed, and liver tissues were extracted for further examinations. Histopathological changes in liver tissues were scored and IL-17 immunostaining was performed to determine the expression levels among experimental groups. Bodyweights in the ADR group decreased significantly compared to the Control group and CLQ group. Furthermore, bodyweight in ADR+CLQ group was significantly higher compared to ADR group. The histopathological score was significantly higher in ADR group when compared to Control and CLQ group while CLQ administrations reduced the damage induced by ADR in the ADR+CLQ group. IL-17 immunoreactivity was considerably increased in the ADR group. On the other hand, IL-17 expressions of ADR+CLQ were substantially less compared to ADR group. We suggest that CLQ can be used as a therapeutic agent to reduce the detrimental effects of ADR, thanks to its anti-inflammatory properties.

Negative correlation between caspase-3 and COX-2 expression in colon cancer

2012 ◽  
Vol 32 (1) ◽  
pp. 68-74
Author(s):  
Tahany M. Shams ◽  
Maha M. Atwa ◽  
Mohamed E. Shams
Keyword(s):  
Colon Cancer ◽  
Negative Correlation ◽  
Caspase 3 ◽  
Cox 2

scholarly journals The Combined Use of Phenothiazines and Statins Strongly Affects Doxorubicin-Resistance, Apoptosis, and Cox-2 Activity in Colon Cancer Cells

2019 ◽  
Vol 20 (4) ◽  
pp. 955 ◽  
Author(s):  
Kamila Środa-Pomianek ◽  
Krystyna Michalak ◽  
Anna Palko-Łabuz ◽  
Anna Uryga ◽  
Piotr Świątek ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Colon Cancer Cells ◽  
Phenothiazine Derivatives ◽  
Component Mixture ◽  
P Glycoprotein ◽  
Novel Approach ◽  
Combined Use ◽  
Cox 2

Since none of the multidrug resistance (MDR) modulators tested so far found their way into clinic, a novel approach to overcome the MDR of cancer cells has been proposed. The combined use of two MDR modulators of dissimilar mechanisms of action was suggested to benefit from the synergy between them. The effect of three phenothiazine derivatives that were used as single agents and in combination with simvastatin on cell growth, apoptosis induction, activity, and expression of cyclooxygenase-2 (COX-2) in doxorubicin-resistant colon cancer cells (LoVo/Dx) was investigated. Treatment of LoVo/Dx cells by phenothiazine derivatives combined with simvastatin resulted in an increase of doxorubicin cytotoxicity and its intracellular accumulation as compared to the treatment with phenothiazine derivatives that were used as single agents. Similarly, LoVo/Dx cells treated with two-component mixture of modulators showed the reduced expression of ABCB1 (P-glycoprotein) transporter and COX-2 enzyme, both on mRNA and protein level. Reduced expression of anti-apoptotic Bcl-2 protein and increased expression of pro-apoptotic Bax were also detected. Additionally, COX-2 activity was diminished, and caspase-3 activity was increased to a higher extent by phenothiazine derivative:simvastatin mixtures than by phenothiazine derivatives themselves. Therefore, the introduction of simvastatin strengthened the anti-MDR, anti-inflammatory, and pro-apoptotic properties of phenothiazines in LoVo/Dx cells.

scholarly journals IN SILICO DOCKING STUDIES ON KAEMPFERITRIN WITH DIVERSE INFLAMMATORY AND APOPTOTIC PROTEINS FUNCTIONAL APPROACH TOWARDS THE COLON CANCER

2017 ◽  
Vol 9 (9) ◽  
pp. 199
Author(s):  
Mydhili Govindarasu ◽  
Mariyappan Palani ◽  
Manju Vaiyapuri
Keyword(s):  
Colon Cancer ◽  
Cytochrome P450 ◽  
Amino Acid ◽  
Protein Kinase ◽  
Caspase 3 ◽  
Tnf Α ◽  
Different Types ◽  
Inflammatory Proteins ◽  
Cox 2 ◽  
Apoptotic Proteins

Objective: The objective of this research was to formulate the binding energies and interaction of amino acid residues in kaempferitrin with different types of apoptotic and inflammatory proteins of colon cancer.Methods: AutoDock Vina and MGL tool were used for docking calculations. Both programs require the pdbqt input files and allow for flexibility of all the torsional bonds of small molecules. Discovery Studio Visualizer v3.5 was used for removal of water molecules and ligands and the pymol program was used to do analysis of the docking with various apoptotic proteins BAX, Bcl-2, COX-2, Protein kinase B.Results: In our study was developed binding energy scoring function of kaempferitrin docked with different types of inflammatory proteins and apoptotic proteins. Binding score values for-6.9 (BAX),-7.2 (Bcl-2),-7.3 (caspase-3),-8.8 (Cox-2),-7.4 (Cytochrome P450),-6.7 (Proteinase kinase B),-8.0 (TNF-α) and-7.2 (VEGF) kcal/mol, respectively. Amino acid interaction of kaempferitrin with proteins for ARG-25, LEU-52, ASN-54, PHE-55, GLU-17, LYS-14, TRP-22, THR-21 GLY-16 (Protein Kinase B), ASP-102, ASN-48, GLN-52, ASP-104 (BAX), GLU-176, TRP-173, GLU-132, PHE-135 (Bcl-2), SER-249, ASP-2, ASN-208, GLN-217, LEU-242 (Caspase 3), TYR-55, HIS-39, SER-49, GLU-322, GLY-326 (COX-2), SER-95, LEU-94, ARG-82, VAL-123, ALA-96 (TNF-α), ASP-414, LYS-322, GLU-326, GLU-416, GLU-438, ALA-439, GLU-437 (Cytochrome P450) and LEU-47, GLN-46, CYS-61, CYS-60, ASP-63, GLU-67, GLY-65, LEU-66 (VEGF) respectively.Conclusion: The results obtained in this research work clearly indicated the docking scores of apoptotic and Inflammatory proteins imply that kaempferitrin is an effective inhibitory compound for colon cancer.

scholarly journals Metabonomic Profiling in Study Protective Effect of Sea Buckthorn Sterol on Acute Liver Injury Induced By Carbon Tetrachloride in Rats

2021 ◽  
Author(s):  
Changting Sheng ◽  
Yang Guo ◽  
Jing Ma ◽  
Eun-Kyung Hong， ◽  
Benyin Zhang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Aspartic Acid ◽  
Acute Liver Injury ◽  
Sea Buckthorn ◽  
Control Group ◽  
Expression Levels ◽  
Cox 2 ◽  
Liver Tissues

Abstract Objective: To study the effect and protection mechanism of sea buckthorn sterol on acute liver injury induced by carbon tetrachloride (CCl4) in rats. Methods: CCl4 was used to make a rat model of acute liver injury. The rats were divided into six groups including blank control group, model control group, bifendate treated positive control group, low-, medium-, and high-doses of sea buckthorn sterol treated groups. The enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), gamma-glutamyl transpeptidase (γ-GT), and catalase (CAT) were investigated. Total antioxidant capacity (T-AOC), total protein (TP), and the content of malondialdehyde (MDA), the level of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in liver tissues were determined. HE staining was used for the observation of inflammatory changes of liver tissues. The endoplasmic reticulum and mitochondria in liver tissues were observed by electron microscope. Wide range of targeted technologies were used for the detection of the full-spectrum metabolome, and metabolome differences among samples were investigated by means of the combination of UPLC-MS/MS detection platform, self-built database, and multivariate statistical analysis. Transcriptomics were studied using the RNA-SEQ method. Based on comparison results, gene expression levels were analyzed, and differentially expressed genes were identified according to their expression levels in different samples. Results: After the treatment of sea buckthorn sterol, the activities of SOD, GSH-Px, CAT, T-AOC, and TP in liver tissues were increased, while the activities of γ-GT, COX-2, and PGE2 were decreased, and the content of MDA was also reduced. Sea buckthorn sterol can reduce the inflammatory lesions in liver tissues, and the damage of the structure of endoplasmic reticulum and mitochondria of liver cells were significantly alleviated compared with the model group. The levels of L-malic acid, 7Z, 10Z, 13Z, 16Z, 19Z-docosapentaenoic acid, creatine, N-acetyl-l-alanine, N-acetyl-aspartic acid, trigonelline, 4-guanidine butyric acid, N-amidine L-aspartic acid, CE(16:1), CE(18:2), PE(16:1/16:0), DG(16:0/18:02/0:0), TG(14:0/18:0/20:4), TG(16:0/18:0/20:4), TG(16:0/16:1/22:5), N-glycine-l-leucine, and FFA(6:0) were significantly restored after the treatment of sea buckthorn sterol. Sea buckthorn sterol could participate in the citric acid cycle, arginine and proline metabolism, alanine, aspartate and glutamate metabolism, niacin and niacinamide metabolism, fat digestion and absorption, and glycerophospholipid metabolism. Besides, the expressions of Cyp1a1, Noct, and Tubb6 could be regulated by sea buckthorn sterol, and thus the metabolic damage by CCl4 was reduced. Conclusion: Sea buckthorn sterol could improve liver function in the animal model of CCl4-induced acute liver injury in rats. The mechanism of liver protection is likely related to the regulation of metabolic disorders, anti-lipid peroxidation, and inhibition of inflammatory response.

Effect of Bee Venom on an Experimental Cellular Model of Alzheimer’s Disease

2020 ◽  
Vol 48 (08) ◽  
pp. 1803-1819
Author(s):  
Yong Ho Ku ◽  
Jae Hui Kang ◽  
Hyun Lee
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mrna Expression ◽  
Caspase 3 ◽  
Bee Venom ◽  
Control Group ◽  
Cellular Model ◽  
Expression Levels ◽  
Cox 2 ◽  
Mrna Expression Levels

Alzheimer’s disease (AD) is a neurodegenerative disease and is characterized by the deposition of the [Formula: see text]-Amyloid peptide ([Formula: see text]A), which causes the inflammation of neurons. Bee venom (BV) elicits a strong anti-inflammatory response, and therefore we conducted an in vitro experiment to study the efficacy of BV in an AD cellular model. To mimic AD, the U87MG cell line was incubated for 168 hours with 2.5 [Formula: see text]M [Formula: see text]A. Changes were confirmed by microscopy, and peptides were measured under stain-free conditions using homo-tomography. Sulforhodamine B analysis was performed to analyze the cell viability. Real-Time quantitative polymerase chain reaction (qPCR) analysis was conducted to analyze mRNA expression levels of pro-inflammatory cytokines (NF-[Formula: see text]B, COX-2, TNF-[Formula: see text], IL-1), and Western blot was performed to measure the Caspase-3 protein levels. BV showed no cytotoxicity at concentrations below 10 [Formula: see text]g/mL. The NF-[Formula: see text]B mRNA levels were not significantly different between the BV group and the control group. The amount of [Formula: see text]A accumulation in the BV group decreased significantly. The mRNA expression levels of COX-2, TNF-[Formula: see text], and IL-1 were significantly reduced using 10 [Formula: see text]g/mL of BV compared to those in the control group. Additionally, Caspase-3 levels were also reduced compared to those of the control group when BV was used at a concentration of 10 [Formula: see text]g/mL. BV could inhibit apoptosis and inflammatory responses in an AD cellular model. In addition, it prevented cell accumulation of [Formula: see text]A, an important pathogenic mechanism in AD.

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