Placental apoptotic markers are associated with placental morphometry

Placenta ◽  
2021 ◽  
Author(s):  
Vaishali Kasture ◽  
Deepali Sundrani ◽  
Karuna Randhir ◽  
Girija Wagh ◽  
Sadhana Joshi
Keyword(s):  
2021 ◽  
pp. 096032712110134
Author(s):  
S Rahi ◽  
R Gupta ◽  
A Sharma ◽  
S Mehan

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disease characterized by cognitive and sensorimotor impairment. Numerous research findings have consistently shown that alteration of Smo-Shh (smoothened-sonic hedgehog) signaling during the developmental process plays a significant role in ASD and triggers neuronal changes by promoting neuroinflammation and apoptotic markers. Purmorphamine (PUR), a small purine-derived agonist of the Smo-Shh pathway, shows resistance to hippocampal neuronal cell oxidation and decreases neuronal cell death. The goal of this study was to investigate the neuroprotective potential of PUR in brain intoxication induced by intracerebroventricular-propionic acid (ICV-PPA) in rats, with a focus on its effect on Smo-Shh regulation in the brain of rats. In addition, we analyze the impact of PUR on myelin basic protein (MBP) and apoptotic markers such as Caspase-3, Bax (pro-apoptotic), and Bcl-2 (anti-apoptotic) in rat brain homogenates. Chronic ICV-PPA infusion was administered consecutively for 11 days to induce autism in rats. In order to investigate behavioral alterations, rats were tested for spatial learning in the Morris Water Maze (MWM), locomotive alterations using actophotometer, and beam crossing task, while Forced Swimming Test (FST) for depressive behavior. PUR treatment with 5 mg/kg and 10 mg/kg (i.p.) was administered from day 12 to 44. Besides cellular, molecular and neuroinflammatory analyses, neurotransmitter levels and oxidative markers have also been studied in brain homogenates. The results of this study have shown that PUR increases the level of Smo-Shh and restores the neurochemical levels, and potentially prevents morphological changes, including demyelination.


Author(s):  
Sarina Levy-Mendelovich ◽  
Shraga Aviner ◽  
Nechama Sharon ◽  
Hagit Miskin ◽  
Joanne Yacobovich ◽  
...  

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 120
Author(s):  
Maged E. Mohamed ◽  
Mohamed S. Abduldaium ◽  
Nancy S. Younis

Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on isoproterenol (ISO)-induced MI in rat models and explored part of the underlying molecular mechanisms. Methods: Rats were divided into five groups; groups I and II served as normal and linalool control groups, Group III administered ISO alone; groups V and VI received two different doses of Linalool and were challenged by ISO. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Results: Linalool limited the infarcted area size and diminished the elevated cardiac enzymes. Linalool escalated HO-1 and Nrf2, both nuclear and cytosol fractions, and reduced Keap 1. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses.


Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e85-e86
Author(s):  
Vaishali Kasture ◽  
Dr. Deepali Sundrani ◽  
Dr. Girija Wagh ◽  
Dr. Sadhana Joshi
Keyword(s):  

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