scholarly journals Investigation of the Pathogenesis and Treatment Efficiency of Bevacizumab-Induced Hypertension in the Rat Model

2019 ◽  
Vol 5 (1) ◽  
pp. 16
Author(s):  
Mehmet Ali Balci ◽  
Musa Özgür Özyiğit ◽  
Volkan İpek ◽  
İlker Mustafa Kafa ◽  
Ender Kurt
Keyword(s):  
Blood Pressure ◽  
Renal Injury ◽  
Female Rats ◽  
Control Group ◽  
Vascular Endothelial ◽  
Treatment Efficiency ◽  
Bevacizumab Treatment ◽  
Induced Hypertension ◽  
Software Pack ◽  
Endothelial Growth Factor

Bevacizumab is known to reduce Vascular Endothelial Growth Factor (VEGF) to undetectable levels when used in conjunction with chemotherapy. Hypertension is a frequent adverse effect of bevacizumab, although its mechanism(s) remain unclear. In this study, our aim was to examine the pathogenesis of bevacizumab-induced hypertension and to investigate the treatment efficacy of valsartan. A total of 24 Wistar Albino female rats were included in the study. Rats were divided into three groups with 8 rats in each, as follows: The control group, bevacizumab group and bevacizumab + valsartan group. Blood pressure, blood urea nitrogen and serum creatinine levels were measured, urine samples were collected for 24 hours statistical analyses were performed using IBM SPSS 20 software pack. Nephrectomy specimens in bevacizumab and bevacizumab + valsartan groups exhibited varying degrees of renal injury. Although valsartan was able to reduce the bevacizumab-induced rise in blood pressure, it could not prevent the development of nephropathy. Conclusions these findings suggest that hypertension occurring secondary to bevacizumab treatment in rats may be associated with mechanisms involving renal injury.

Fetal growth restriction in hypothyroidism is associated with changes in proliferative activity, apoptosis and vascularisation of the placenta

2012 ◽  
Vol 24 (7) ◽  
pp. 923 ◽  
Author(s):  
Juneo F. Silva ◽  
Paula N. Vidigal ◽  
Daniele D. Galvão ◽  
Jankerle N. Boeloni ◽  
Philipe Pimenta Nunes ◽  
...  
Keyword(s):  
Proliferative Activity ◽  
Fetal Death ◽  
Fetal Weight ◽  
Female Rats ◽  
Control Group ◽  
Vascular Endothelial ◽  
Immunohistochemical Expression ◽  
Endothelial Growth Factor ◽  
Control Protein ◽  
Cell Division Control

The objective of this study was to evaluate fetal weight, histomorphometric changes and proliferative activity, apoptosis and angiogenesis of the placenta in rats with hypothyroidism. Thirty-six adult female rats were divided into two groups with 18 animals each: control and hypothyroidism. Hypothyroidism was induced by daily administration of propylthiouracil (1 mg/animal). The administration began five days before becoming pregnant and the animals were sacrificed at 14 or 19 days of gestation. The control group received a placebo. The number and weight of fetuses and the rate of fetal death was determined, as well as the morphometric characteristics, the immunohistochemical expression of cell division control protein 47 (CDC)-47 and vascular endothelial growth factor (VEGF) and the number of apoptotic cells in the placental disk. The data were analysed by Mann–Whitney U test. Hypothyroidism reduced the weight of fetuses and of the uterus and placenta (P < 0.05), altered the thickness of the placental labyrinth and spongiotrophoblast (P < 0.05), increased the population of glycogen cells in the spongiotrophoblast (P < 0.05), interfered with the vascular development of the placental labyrinth and decreased VEGF expression (P < 0.05), reduced the expression of CDC-47 and cellularity and increased the apoptotic rate in the placental disk (P < 0.05). We conclude that hypothyroidism affects fetal weight by altering the proliferative activity, apoptosis and vascularisation of the placenta.

Effect of HylocereusPolyrhizus Rind Extract Toward Interleukin-1β, Vascular Endothelial Growth Factor Expression, Endometriosis Implant Area

2017 ◽  
Vol 9 (08) ◽  
Author(s):  
YanuarEka P. ◽  
Hendy Hendarto ◽  
Widjiati .
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Treatment Group ◽  
Negative Control Group ◽  
Negative Control ◽  
Control Group ◽  
Vascular Endothelial ◽  
Mice Model ◽  
Endothelial Growth Factor ◽  
Fruit Rind

Retrograde menstruation lead to I Kappa B Kinase (IKK) fosforilation in peritoneum macrophage and cause secretion of proinflammatory cytokine interleukin1β then stimulate endometriosis cell to produce Vascular Endothelial Growth Factor which lead to increasing of endometriosis lession seen as endometriosis implant area. Cytokine secretion was inhibited through prevention of NF-κB activation by dragon red fruit rind extract (Hylocereuspolyrhizus). The aim of this reserach is to know the effect of dragon red fuit rind extract with 0,25; 0,5; and 1 mg/g bodyweight dosage toward IL-1β, VEGF expression and implant area in endometriosis mice model. The design of this experiment was randomized post test only control group design.Endometrios mice model were made in 14 days and split into two group, positive control group and treatment group after two week negative control group and postive control group were given Na-CMC 0,5% solution consequetively, and treatment group were given dragon red fruit extract with different dosage. Signification number for IL-1β is p>0,05, signification number for VEGF is p>0,05, and implant area signification number is p>0,05. Administration of dragon red fruit rind extract can decrease IL-1β, VEGF, and implant area.

Investigation of Targeting Relationship between Micro-Rna-22 and Vegfr3 in Lung Squamous Cell Carcinoma

2020 ◽  
Vol 23 ◽  
Author(s):  
Zheng Dong ◽  
Qing-Hua Xu ◽  
Yuan-Bin Zhu ◽  
Yong-Feng Wang ◽  
Jie Xiong ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lung Squamous Cell Carcinoma ◽  
Luciferase Reporter ◽  
Control Group ◽  
Vascular Endothelial ◽  
Luciferase Reporter Gene ◽  
Endothelial Growth Factor

Aims : The present study explored the clinical significance of microRNA-22 (miR-22) expression in lung squamous cell carcinoma and to explore the targeting relationship with vascular endothelial growth factor receptor 3 (VEGFR3). Methods: A total of 49 patients with lung squamous cell carcinoma who underwent surgical treatment was selected. The expression of miR-22 was detected by fluorescence quantitative real-time PCR (qPCR), the expression of VEGFR3 was detected by Western blotting assays, and D240 labeled microlymphatic vessels density (MLVD) was detected immunohistochemistry (IHC). Lung squamous cell carcinoma cell line SK-MES-1 was selected and the targeting relationship between miR-22 and VEGFR3 was analyzed by double luciferase reporter gene assay. Western blotting assays were used to detect the expression of vascular endothelial growth factor-D (VEGF-D) and D240 in the blank control group, empty vector transfection group, miR-22 transfection group, miR-22 and VEGFR3 co-transfection group. Results: The expression range of miR-22 in lung squamous cell carcinoma was 0.8-3.5. The expression of miR-22 in lung squamous cell carcinoma was significantly different by tumor maximum diameter, lymph node metastasis, vascular invasion and TNM stage. The expression of miR-22 was linked to survival time. There was a negative correlation between miR-22 and VEGFR3, miR-22 and MLVD. Double luciferase reporter gene assays showed that miR-22 reduced the luciferase activity of pGL3-VEGFR3-WT transfected cells. Compared with the control group, the expression of VEGF-D and D2-40 in the miR-22 transfection group was significantly decreased. However, VEGF-D and D240 in the miR-22 and VEGFR3 cotransfection group reversed the changes. Conclusion: We assumed that the abnormal expression of miR-22 in lung squamous cell carcinoma may be involved in the development and progression of lung squamous cell carcinoma. MiR-22 negatively regulated the target gene VEGFR3 to mediate lymphangiogenesis. The expression of miR-22 may also be linked to the prognosis of the disease.

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