Nitric Oxide (NO) plays an important role for regulation of cellular and vascular response of inflammation and initiates killing mechanism in the host-defense reactions. NO production is regulated through inducible nitric oxide synthase (iNOS) pathway in response to infections and injurious agents besides pro-inflammatory cytokines secreted by the host. Evaluation of NO pathway is one of the major targets which can evaluate various immunomodulators for their therapeutic interaction on innate immune system. Lipopolysaccharide (LPS) and concavalin A (ConA) are used as standard mitogen for peripheral blood mononuclear cells and splenocyte of mammalian and avian cell culture. During the present investigation ZnCl(2) has been explored as standard mitogen and result was comparable with standard mitogen. The result has been evaluated on the basis of relative mRNA expression of iNOS and interferon gamma and nitrite assay. Observation indicated significantly higher expression of both biomolecules in comparison to control, LPS, ConA treated group. This study indicated that, ZnCl(2) can also be used as standard stimulant for molecular mining of innate immunity.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11033-009-9708-yDOI Listing

Publication Analysis

Top Keywords

nitric oxide
12
standard mitogen
12
mitogen result
8
zinc chloride
4
chloride alternative
4
alternative stimulant
4
stimulant vitro
4
vitro study
4
study nitric
4
oxide production
4

Similar Publications

A preclinical study on effect of betanin on sodium fluoride induced hepatorenal toxicity in wistar rats.

J Complement Integr Med

January 2025

Department of Basic Medical Sciences, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Background: Excessive fluoride exposure leads to increased oxidative stress and lipid peroxidation, causing harmful effects on the metabolic organs in the human body. Betanin, a pigment obtained from beetroot, is seen to have powerful anti-inflammatory and antioxidant. The study was conducted to determine the role of betanin in fluoride induced hepato-renal toxicity in Wistar rats.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

PCM Consulting, Pathways Connectivity Maps Inc., Mountain View, CA, USA.

Background: High-throughput assays have attracted significant attention in Alzheimer's Disease (AD) research, especially for enabling rapid diagnostics screening for factors at the molecular level contributing to the disease recurrence. With advances in laboratory automation, there is a growing need for quality pre-clinical data. Assays such as Microarrays, Proteomics, or AI are all dependent on high-quality input data that serve as a starting point.

View Article and Find Full Text PDF

Background: Stiffening of the large arteries is a hallmark feature of vascular aging and is associated with cognitive impairment and Alzheimer's disease pathology. Increased large artery stiffness leads to higher-than-normal pulse pressure in the cerebral circulation, damaging endothelial cells. It is known that short-term exposure to stiffer large arteries causes cerebral artery endothelial dysfunction and hypoperfusion in young mice.

View Article and Find Full Text PDF

Background: Nitric oxide (NO) is involved in synaptic transmission and cerebral plasticity, playing a role in the memory process. However, in states of brain inflammation, hypoxia, or ischemia, there is induction of inducible nitric oxide synthase (iNOS) expression by astrocytes and pyramidal cells in the brain. Under conditions of chronic activation, there is a decoupling of iNOS dimers, leading to a massive generation of superoxide anion and peroxynitrite, O2.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

The Ohio State University, Columbus, OH, USA.

Background: Microglia, the innate immune cells of the brain, are a principal player in Alzheimer's Disease (AD) pathogenesis. Their surveillance of the brain leads to interaction with the protein aggregates that drive AD pathogenesis, most notably Amyloid Beta (Aβ). Aβ can elicit attempts from microglia to clear and degrade it using phagocytic machinery, spurring damaging neuroinflammation in the process.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!