scholarly journals THE EFFECT OF RECOMBINANT VASCULAR ENDOTHELIAL GROWTH FACTOR 121 ON NITRIDE OXIDE LEVEL IN MICE (Mus musculus) MODEL OF PREECLAMPSIA

2017 ◽  
Vol 53 (3) ◽  
pp. 191
Author(s):  
Soetrisno Soetrisno ◽  
Isharyadi Isharyadi ◽  
Sri Sulistyowati

Preeclampsia is a multifactorial syndrome in pregnancy whose cause is still unknown. Several proangiogenic and antiangiogenic mediators such as Vascular Endothelial Growth Factor (VEGF) and Nitrite Oxide (NO) play important roles in preventing preeclampsia. VEGF can increase NO level that lowers maternal blood pressure, improves endothelial function and reduces placental hypoxia in preeclampsia. Recombinant VEGF 121 is expected to be an option in the prevention and treatment of preeclampsia. This experimental study used mice (Mus musculus) as the model. The objective of this study was to observe the effect of recombinant VEGF 121 in increasing the level of nitric oxide in mice (Mus musculus) model of preeclampsia. This was an experimental analytical study with Randomized Control Trial (RCT) design. The study enrolled 27 pregnant mice (Mus musculus) which met the restriction criteria divided into 3 groups. The first group (K1) were 9 normal pregnant mice. The second group (K2) were 9 pregnant mice of preeclampsia model without treatment. The third group (K3) were 9 pregnant mice of preeclampsia model receiving recombinant VEGF 121 therapy. The independent variable was the administration of recombinant VEGF 121 and the dependent variable was the serum NO level. Statistical analysis was performed by using anova statistics. NO level in the first group (K1) was 1.746±0.347, with minimum value of 1.00 µM, and maximum value of 2.28 µM, CI (1.479-2.013).  NO level in second group (K2) was 1.167±0.380, with minimum value of 0.64 µM, and maximum value of 1.94 µM, CI (0.875-1.460). NO level in the third group (K3) was 2.164±0.556, with minimum value of 1.56 µM, and maximum value of 5.96 µM, CI (1.842-2.486). With anova statistical test, there were significant differences between K1 group and K2 group (p value=0.004<0.05), K1 group and K3 group (p value=0.000<0.05) as well as K2 group and K3 group (p value=0.029<0.05). In conclusion, Recombinant VEGF 121 increased the level of nitric oxide in mice (Mus musculus) model of preeclampsia significantly.

2012 ◽  
Vol 32 (5) ◽  
pp. 884-895 ◽  
Author(s):  
Fabricio Simão ◽  
Aline S Pagnussat ◽  
Ji Hae Seo ◽  
Deepti Navaratna ◽  
Wendy Leung ◽  
...  

Resveratrol may be a powerful way of protecting the brain against a wide variety of stress and injury. Recently, it has been proposed that resveratrol not only reduces brain injury but also promotes recovery after stroke. But the underlying mechanisms are unclear. Here, we tested the hypothesis that resveratrol promotes angiogenesis in cerebral endothelial cells and dissected the signaling pathways involved. Treatment of cerebral endothelial cells with resveratrol promoted proliferation, migration, and tube formation in Matrigel assays. Consistent with these pro-angiogenic responses, resveratrol altered endothelial morphology resulting in cytoskeletal rearrangements of β-catenin and VE-cadherin. These effects of resveratrol were accompanied by activation of phosphoinositide 3 kinase (PI3-K)/Akt and Mitogen-Activated Protein Kinase (MAPK)/ERK signaling pathways that led to endothelial nitric oxide synthase upregulation and increased nitric oxide (NO) levels. Subsequently, elevated NO signaling increased vascular endothelial growth factor and matrix metalloproteinase levels. Sequential blockade of these signaling steps prevented resveratrol-induced angiogenesis in cerebral endothelial cells. These findings provide a mechanistic basis for the potential use of resveratrol as a candidate therapy to promote angiogenesis and neurovascular recovery after stroke.


Biochimie ◽  
2001 ◽  
Vol 83 (6) ◽  
pp. 515-522 ◽  
Author(s):  
Kyril Turpaev ◽  
Dmitry Litvinov ◽  
Vera Dubovaya ◽  
Andrey Panasyuk ◽  
Dmitry Ivanov ◽  
...  

2018 ◽  
Vol 315 (3) ◽  
pp. H482-H491 ◽  
Author(s):  
Eunhee Chung ◽  
Kaylan M. Haizlip ◽  
Leslie A. Leinwand

During pregnancy, the heart undergoes significant and numerous changes, including hypertrophy, that are usually described as physiological and reversible. Two aspects of the cardiac response to pregnancy are relatively understudied: advanced maternal age and multiple pregnancies (multiparity). Repeated breeder (RB) mice that have undergone five to seven consecutive pregnancies were euthanized 21 days after the weaning of their last pups and compared with age-matched primiparous, one-time pregnant (O1P) mice. The ages of the older mouse groups were similar (12 ± 1 mo). Pregnancy at a later age resulted in reduced fertility (40%); resorption was 29%, maternal mortality was 10%, and mortality of the pups was 17%. Contractile function as indicated by percent fractional shortening was significantly decreased in O1P and RB groups compared with the old nonpregnant control (ONP) group. There was no pathological induction of the fetal program of gene expression, with the exception of β-myosin heavy chain mRNA, which was induced in O1P compared with ONP mice ( P < 0.05) but not in RB mice. MicroRNA-208a was significantly increased in O1P compared with ONP mice ( P < 0.05) but significantly decreased in RB compared with ONP mice ( P < 0.05). mRNA of genes regulating angiogenesis (i.e., vascular endothelial growth factor-A) were significantly downregulated, whereas proinflammatory genes [i.e., interleukin-6, chemokine (C-C motif) ligand 2, and Cd36] were significantly upregulated in O1P ( P < 0.05) but not in RB mice. Overall, our results suggest that rather than multiparity, pregnancy in advanced age is a much more stressful event in both pregnant dams and fetuses, as evidenced by increased mortality, lower fertility, downregulation of angiogenesis, upregulation of inflammation, and cardiac dysfunction. NEW & NOTEWORTHY Pregnancy in older mice significantly decreases cardiac function, although repeated breeder mice demonstrated increased wall hypertrophy and dilated chamber size compared with one-time pregnant mice. Interestingly, many of the molecular changes were altered in one-time pregnant mice but not in repeated breeder mice, which may contribute to adverse pregnancy outcomes in a first pregnancy at a later age.


Author(s):  
Ayodeji Folorunsho Ajayi ◽  
Busuyi David Kehinde ◽  
Olubodun Micheal Lateef ◽  
Bolaji Aderibigbe Akorede

Objective: Nitric oxide (NO), prostaglandin E2 (PgE2), and vascular endothelial growth factor (VEGF) are fundamental regulators of epithelial restitution and angiogenesis. They play important roles in ulcer healing. Insights into their possible changes during gastric ulcer healing putting age into consideration could give a guide to the proper management of ulcers in the aging population. This study, therefore, examined alterations in the concentrations of PgE2, NO, and VEGF in the gastric mucosa of rats of different ages after induction of ulcer and during healing.Methods: Male Wister rats (aged 3, 6, and 18 months old) were divided into three groups according to their ages. The ulcer was induced using the acetic acid ulcer model. Healing indices studied on days 3, 7, and 14 were the macroscopic dimension of ulcer, stomach tissue concentration of PgE2, NO, and VEGF, with the immunohistochemical expression of VEGF.Results: Outcome of this study showed 100%, 88.36%, and 62.30% area of mucosa healed in 3-, 6-, and 18-month-old rats respectively, on day 14 post-induction of ulcer. PgE2, NO, and VEGF concentrations were inversely proportional to age during healing. Immunohistochemical staining showed that younger rat (3 and 6 months old) had higher expression of VEGF throughout the healing period.Conclusion: It was therefore concluded that the slower rate of healing in older rats could be due to reduced gastroprotection, epithelial restitution, and angiogenesis as age increases.


Sign in / Sign up

Export Citation Format

Share Document