Chemoprotective and Adjuvant Effects of Immunomodulator Ginsan in Cyclophosphamide-Treated Normal and Tumor Bearing Mice

2007 ◽  
Vol 20 (3) ◽  
pp. 487-497 ◽  
Author(s):  
J.Y. Shim ◽  
Y. Han ◽  
J.Y. Ahn ◽  
Y.S. Yun ◽  
J.Y. Song
Keyword(s):  
Mrna Expression ◽  
Bone Marrow Cells ◽  
Treated Group ◽  
Post Treatment ◽  
Sublethal Dose ◽  
Adjuvant Effect ◽  
Growth And Survival ◽  
Expression Levels ◽  
Tumor Bearing ◽  
Mrna Expression Levels

Ginsan is a polysaccharide extracted from Panax ginseng that is known to have multiple immunomodulatory effects. This study evaluates the chemoprotective effect of ginsan on normal mice and the adjuvant effect on tumor bearing mice in combination with cyclophosphamide (CP). Ginsan (100 mg/kg) was injected 24 h before or after a sublethal dose of a CP treatment. The mice pre-treated with ginsan all died within 10 days whereas up to 53% of the mice post-treated with ginsan increased survival to day 30 compared with only 10% in the CP alone treated group on day 30. The post-treatment of ginsan accelerated the recovery of the bone marrow cells and blood neutrophils by approximately 1.3- and 1.75-fold compared to CP treated control mice at 5 days after CP administration, respectively. These marked differences in activity between the pre- and post-treatment of ginsan with CP was clarified by examining the mRNA expression levels of several cytokines in spleen cells and the self-renewal potential of hematopoietic progenitor cells, CFU-s. The post-treatment with ginsan increased the mRNA expression levels of TNF-α, IL-1β, IL-6, SCF, and GM-CSF with respect to that of the CP alone or ginsan pre-treated group. Similarly, the number of CFU-s was significantly higher in the mice post-treated with ginsan. The inhibition of tumor growth and survival elongation was also observed when ginsan was administered 24 h after the CP treatment. These results show that the post-treatment with ginsan had an immunomodulating and adjuvant effect in combination with CP, which indicates its wide applications in reducing the adverse effects of chemotherapy and improving the general conditions of patients.

Effect of estrogen and progesterone hormones on the expression of angiotensin II receptors in the heart and aorta of male rats.

2020 ◽  
Vol 20 ◽  
Author(s):  
Bahaa Al‑Trad ◽  
Osama Abu-alrob ◽  
Yousf Jaradat ◽  
Mazhar Al-Zoubi ◽  
Almuthanna K. Alkarki ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Protein Expression ◽  
Mrna Expression ◽  
Treated Group ◽  
Estrogen Treatment ◽  
Mrna Levels ◽  
Expression Levels ◽  
Progesterone Treatment ◽  
Enos Mrna ◽  
Mrna Expression Levels

Background: Activation of the Angiotensin II type 1 receptor (AT1R) has been implicated in the pathogenesis of cardiovascular disease while activation of Angiotensin II type 2 receptor (AT2R) leads to effects that are opposite to those mediated by AT1R. The interaction between female sex hormones and the renin angiotensin system was proven to play an essential role in the pathological changes in the cardiovascular system. Objectives: To investigate the direct effect of estrogen and progesterone in arterial and cardiac AT1R and AT2R expression in vivo in male. Method: Male adult rats were assigned into four groups: Group 1 (control), group 2 (progesterone treated group; 10mg/kg), group 3 (estrogen treated group; 20µg/kg) and group 4 (progesterone; 10mg/kg + estrogen; 20µg/kg treated group). All treatments were administrated subcutaneously every second day for 21days. Results: Estrogen treatments increase the left ventricle (LV) protein expression of AT1R and progesterone treatment decreased the LV protein expression of AT2R. In the aorta, estrogen treatment increased the mRNA expression levels of AT1R while progesterone treatment increased the AT2R mRNA expression levels. Estrogen treatment decreases the LV and aortic endothelial nitric-oxide synthase (eNOS) mRNA levels while progesterone treatments decrease the LV eNOS mRNA levels but increase the aortic eNOS mRNA levels. The serum angiotensin II levels were increased by estrogen treatment only. Conclusion: Both estrogen and progesterone treatments appear to have a harmful effect on the male rat hearts, possibly by increasing the protein expression of AT1R (for estrogen), decrease the protein and mRNA expression of AT2R (for progesterone) and decrease the eNOS mRNA levels (for both). However, it seems that progesterone but not estrogen exerts a vascular protective effect in males.

scholarly journals Effect of mir-129 on the Sensitivity Enhancement of Methotrexate and Migration Inhibition in Osteosarcoma Cancer Cells

2021 ◽  
Keyword(s):  
Mrna Expression ◽  
Cancer Cells ◽  
Target Genes ◽  
Osteosarcoma Cells ◽  
Cytotoxic Effects ◽  
Growth And Survival ◽  
Expression Levels ◽  
Cell Death Assay ◽  
Underlying Mechanisms ◽  
Mrna Expression Levels

Background: MicroRNAs have been recently declared to be contributed to the various aspects of osteosarcoma cells, including growth and survival, apoptosis, invasion, and chemoresistance. Objectives: The present study aimed to investigate the potentiating effects of miR-129 on the chemosensitivity of Saose-2 osteosarcoma cells to methotrexate (MTX) and underlying mechanisms. Methods: Saose-2 cells were transfected with miR-129 mimics using Lipofectamine. The cytotoxic effects of miR-129 and MTX on Saose-2 cells were measured using MTT assay. Scratch wound healing assay was used to evaluate cell migration. The apoptosis rate of cancer cells was also measured using ELISA Cell Death Assay and flow cytometry. The mRNA expression levels of target genes were measured using quantitative RT-PCR. Results: miR-129 mimic transfection significantly increased the expression levels of this miRNA in Saose-2 cells (P<0.05). The combination of MTX with miR-129 transfection led to enhanced cytotoxic effects of MTX in lower concentrations. In addition, miR-129 significantly increased MTX-induced apoptosis levels and decreased invasion behavior in Saose-2 cells. The mRNA expression levels of c-Myc, K-Ras, CXCR4, MMP9, and ADAMTS, as main genes involved in chemoresistance and invasion, were downregulated in miR-129 transfected cells. Conclusion: The obtained results revealed the importance of miR-129 in the sensitivity of osteosarcoma cells to MTX and its underlying mechanisms. Therefore, miR-129 might be an appropriate candidate for reversing MTX resistance in osteosarcoma cells.

scholarly journals Candidate Gene Expression Investigation in Children With Attention Deficit Hyperactivity Disorder

2021 ◽  
Author(s):  
Hilal Akalin ◽  
Yakut Erdem ◽  
Nuriye Gokce ◽  
Sevgi Ozmen ◽  
Muhammet Ensar Dogan ◽  
...  
Keyword(s):  
Attention Deficit Hyperactivity Disorder ◽  
Mrna Expression ◽  
Attention Deficit ◽  
Study Groups ◽  
Post Treatment ◽  
Control Group ◽  
Expression Levels ◽  
Hyperactivity Disorder ◽  
Pre Treatment ◽  
Mrna Expression Levels

Abstract Background: In this study, expression level analysis of genes associated with Attention Deficit Hyperactivity Disorder (ADHD) (SLC6A3, SLC6A4, SLC1A2, VMAT2, MAOA, COMT, GLYAT, GRM5, DRD4, TPH1, and ADRA2C) by pre-treatment and post-treatment with Atomoxetine and Methylphenidate was investigated. Methods: Forty-three ADHD diagnosed children and 38 healthy children were included to study. Forty-three patients with ADHD were divided into two groups, of which 35 patients used methylphenidate and 8 patients use atomoxetine. Five main study groups were generated: A control group, a group that includes methylphenidate pre-treatment samples, a group includes methylphenidate post-treatment samples, a group that includes atomoxetine pre-treatment samples and a group that includes atomoxetine post-treatment samples. Blood samples (10 ml each) were taken from everyone in study groups into EDTA tubes and RNA isolation was performed. mRNA expression levels of 11 determined candidate genes were showed via reverse transcription quantitative PCR method. Results: The expression levels of SLC6A3 (DAT) of ADHD diagnosed children were significantly higher than the control group, while the mRNA expression levels of SLC6A4, SLC1A2, VMAT2, MAOA, COMT, GLYAT, and TPH1 genes were significantly lower (t- test, p≤0.01).Conclusion: The expression level differences of these genes were determined to be useful as biomarkers in the diagnosis of ADHD. More patient numbers and studies with different groups are needed to fully reveal the relationship between these genes and the disease and its treatment.

scholarly journals The role of CXCR3 and its ligands expression in Brucellar spondylitis

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xin Hu ◽  
Xiaoqian Shang ◽  
Liang Wang ◽  
Jiahui Fan ◽  
Yue Wang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mrna Expression ◽  
Mononuclear Cells ◽  
Healthy Controls ◽  
Inflammatory Infiltration ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Inflammatory Damage ◽  
Ifn Γ ◽  
Mrna Expression Levels

Abstract Aim Brucellar spondylitis (BS) is one of the most serious complications of brucellosis. CXCR3 is closely related to the severity of disease infection. This research aimed to study the degree of BS inflammatory damage through analyzing the expression levels of CXCR3 and its ligands (CXCL9 and CXCL10) in patients with BS. Methods A total of 29 BS patients and 15 healthy controls were enrolled. Real-Time PCR was used to detect the mRNA expression levels of IFN-γ, CXCR3, CXCL9 and CXCL10 in peripheral blood mononuclear cells (PBMCs) of BS patients and healthy controls. Hematoxylin-Eosin staining was used to show the pathological changes in BS lesion tissues. Immunohistochemistry staining was used to show the protein expression levels of Brucella-Ab, IFN-γ, CXCR3, CXCL9 and CXCL10 in BS lesion tissues. At the same time, ELISA was used to detect the serum levels of IFN-γ, CXCL9 CXCL10 and autoantibodies against CXCR3 in patients with BS. Results In lesion tissue of BS patients, it showed necrosis of cartilage, acute or chronic inflammatory infiltration. Brucella-Ab protein was abundantly expressed in close lesion tissue. And the protein expression levels of IFN-γ, CXCR3 and CXCL10 were highly expressed in close lesion tissue and serum of BS patients. At the same time, the mRNA expression levels of IFN-γ, CXCR3 and CXCL10 in PBMCs of BS patients were significantly higher than those in controls. Conclusion In our research, the expression levels of IFN-γ, CXCR3 and its ligands were significantly higher than those in controls. It suggested that high expression levels of IFN-γ, CXCR3 and its ligands indicated a serious inflammatory damage in patients with BS.

Unilateral labyrinthectomy induced changes on GDNF receptor complex proteins in the rat medial vestibular nuclei

2007 ◽  
Vol 16 (4-5) ◽  
pp. 171-177
Author(s):  
Adrian Lozada ◽  
Kaj Karlstedt ◽  
Pertti Panula ◽  
Antti A. Aarnisalo
Keyword(s):  
Mrna Expression ◽  
Vestibular Nucleus ◽  
Medial Vestibular Nucleus ◽  
Receptor Complex ◽  
Trophic Effect ◽  
Expression Levels ◽  
Protein Levels ◽  
Unilateral Labyrinthectomy ◽  
Ganglion Neurons ◽  
Mrna Expression Levels

In the auditory periphery, GDNF has been shown to have a trophic effect to spiral ganglion neurons, both during development and in adult animals. We have studied the effect of unilateral labyrinthectomy (UL) on protein levels and expression of GDNF multicomponent receptor complex: the ret tyrosine kinase and coreceptor GFRα-1 in the medial vestibular nucleus of the adult rat. GFRα-1 protein levels display an increasing trend in ipsilateral medial vestibular nucleus culminating at 48 h post UL. On the other hand, GFRα-1 mRNA expression levels in ipsi- and contralateral medial vestibular nucleus show a steadily decreasing trend that is significant at 1 week post-lesion. Protein levels for c-Ret isoforms also show an initial bilateral decreasing trend that ceases at 48 h in ipsilateral medial vestibular nucleus but persists on the contralateral side. c-Ret mRNA expression levels show a significant decrease at 4 h post UL followed by another significant decrease 1 week post UL. Our data would suggest that neurotrophins belonging to the GDNF family are involved in this model of post-lesional CNS plasticity.

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