If this does this, where is the protocol and the distribution method to get this delivered to all stroke hospitals?
But your doctor should already be using Candesartan on you.
generic drug candesartan (brand name: ATACAND®) Blood Pressure Drug Helps Alzheimer's June 2018
This line from there is instructive:
The scientists found that candesartan prevented glutamate-induced neuronal death.
The latest here:
Candesartan Reduces Neuronal Apoptosis Caused by Ischemic Stroke via Regulating the FFAR1/ITGA4 Pathway
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Associated Data
Abstract
Ischemic stroke (IS) is a general term for necrosis of brain tissue caused by stenosis, occlusion of arteries supplying blood to the brain (carotid artery and vertebral artery), and insufficient blood supply to the brain. Cerebral ischemia is the main kind of IS causing cell damage. However, the underlying mechanism still needs to be clarified further. In this study, it was demonstrated that FFAR1 was a hub gene in IS. The expression of FFAR1 was increased in PC12 cells with OGD/R treatment. FFAR1 deficiency inhibited cell viability and induced cell apoptosis, which was reversed by FFAR1 overexpression. Moreover, candesartan, as a compound targeting FFAR1, facilitated cell viability and reduced cell apoptosis. The expression of ITGA4 was also high in OGD/R-PC12 cells as FFAR1. Furthermore, FFAR1 deficiency retarded the increasing of cell viability and inhibition of cell apoptosis by downregulation of Bax and Cleaved Caspase-3 in OGD/R-PC12 cells with candesartan treatment. In conclusion, candesartan may regulate neuronal apoptosis through FFAR1/ITGA4 axis.
1. Introduction
In recent years, with the development of the economy and the improvement of living standards, stroke has become an important factor threatening health [1]. The main reason is cerebral ischemia, which subsequently causes damage to cell and apoptosis [2, 3]. At present, there are many studies on ischemic stroke, but its intrinsic molecular mechanism and treatment methods still need to be explored extensively. Cerebral ischemia causes cell apoptosis, which can lead to the irreversible death of neuronal cells [4]. Therefore, there is an urgent need for early prevention and effective treatment to reduce the occurrence and harm of stroke.
In recent years, more and more evidences have shown that FFA has multiple functions, including as an energy source and as a natural ligand for the group of orphan G protein-coupled receptors (GPCR) and free fatty acid receptors (FFAR), which participates in the interweaving of metabolism and immunity in many aspects, such as the regulation of inflammation and the secretion of peptide hormones. So far, several FFARs activated by FFAs with different chain lengths have been identified and characterized. In particular, FFAR1 (GPR40) and FFAR4 (GPR120) are activated by long-chain saturated fatty acids and unsaturated fatty acids. It is reported that the long-chain fatty acid receptor GPR40 has a significant inhibitory effect on poststroke central pain (one of the complications of cerebral ischemia and neuropathic pain syndrome) and has an antinociceptive effect. At the same time, some research has showed that it played an important role in astrocytes [5–7]. In addition, the overexpression of ITGA4 on MSCs enhanced transendothelial migration in vitro and improved the safety of intracarotid artery transplantation into stroke rats [8].
Candesartan, also known as candesartan cilexetil C8 intermediate, is an active metabolite derived from the hydrolyte of candesartan cilexetil. Candesartan is an antagonist of angiotensin II AT1 receptor. It antagonizes the vasoconstriction of angiotensin II by binding to vascular smooth muscle AT1 receptors, thereby reducing peripheral vascular resistance [9–11]. This drug is used to treat essential hypertension.
In this study, oxygen-glucose deficiency (OGD) was used to stimulate PC12 cells to establish in vitro cell models. We discussed the effects of candesartan and FFAR1/ITGA4 signal axis on PC12 cells with OGD.
More at link.
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