I'm quite sure your doctor will not allow you to get carbon monoxide on your own by smoking cigarettes. Do not try this by yourself.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0154781
Abstract
Cerebral
ischemia and neurodegenerative diseases lead to impairment or death of
neurons in the central nervous system. Stem cell based therapies are
promising strategies currently under investigation. Carbon monoxide (CO)
is an endogenous product of heme degradation by heme oxygenase (HO)
activity.
Administration of CO at low concentrations produces several
beneficial effects in distinct tissues, namely anti-apoptotic and
anti-inflammatory. Herein the CO role on modulation of neuronal
differentiation was assessed. Three different models with increasing
complexity were used: human neuroblastoma SH-S5Y5 cell line, human
teratocarcinoma NT2 cell line and organotypic hippocampal slice cultures
(OHSC). Cell lines were differentiated into post-mitotic neurons by
treatment with retinoic acid (RA) supplemented with CO-releasing
molecule A1 (CORM-A1). CORM-A1 positively modulated neuronal
differentiation, since it increased final neuronal production and
enhanced the expression of specific neuronal genes: Nestin, Tuj1 and
MAP2. Furthermore, during neuronal differentiation process, there was an
increase in proliferative cell number (ki67 mRNA expressing cells) and a
decrease in cell death (lower propidium iodide (PI) uptake, limitation
of caspase-3 activation and higher Bcl-2 expressing cells). CO
supplementation did not increase the expression of RA receptors. In the
case of SH-S5Y5 model, small amounts of reactive oxygen species (ROS)
generation emerges as important signaling molecules during CO-promoted
neuronal differentiation. CO’s improvement of neuronal differentiation
yield was validated using OHSC as
ex vivo model. CORM-A1
treatment of OHSC promoted higher levels of cells expressing the
neuronal marker Tuj1. Still, CORM-A1 increased cell proliferation
assessed by ki67 expression and also prevented cell death, which was
followed by increased Bcl-2 expression, decreased levels of active
caspase-3 and PI uptake. Likewise, ROS signaling emerged as key factors
in CO’s increasing number of differentiated neurons in OHSC. In
conclusion, CO’s increasing number of differentiated neurons is a novel
biological role disclosed herein.
CO improves neuronal yield due to its
capacity to reduce cell death, promoting an increase in proliferative
population. However, one cannot disregard a direct CO’s effect on
specific cellular processes of neuronal differentiation. Further studies
are needed to evaluate how CO can potentially modulate cell mechanisms
involved in neuronal differentiation. In summary,
CO appears as a
promising therapeutic molecule to stimulate endogenous neurogenesis or
to improve
in vitro neuronal production for cell therapy strategies.
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