The Mechanism of Taurine Protection Against Endoplasmic Reticulum Stress in an Animal Stroke Model of Cerebral Artery Occlusion and Stroke-Related Conditions in Primary Neuronal Cell Culture - Advances in Experimental Medicine and Biology - page 233

Fig. 23.2 Effect of taurine on ATF4 (from the PERK pathway) in neuronal cell cultures under
hypoxia/reoxygenation condition and in rat MCAO stroke model. Taurine does not alter activity of
the PERK pathway in primary neuronal cell culture and MCAO model. Norm normoxia, Hyp
hypoxia (0.3% O 2 ) for 20 h, reoxygenation for 20 h, Ta u + Hyp neurons were treated with 10 mM
taurine for 1 h, then hypoxia for 20 h, reoxygenation for 20 h, MCAO middle cerebral artery occlu-
sion for 2 h followed by 4 days reperfusion, MCAO + taurine middle cerebral artery occlusion for
2 h followed by 4 days reperfusion, taurine was injected 24 h after reperfusion subcutaneously and
injection continued for 4 days. ( a ) ATF4 expression analyzed by Western blot in primary neuronal
cell culture. The bar graphs reflect the densitometric data from the experiment of ATF4 Western
blot results with arbitrary units. ( b ) ATF4 expression analyzed by Western blot in MCAO rats in
the core area. The values in bar graph represent mean ± SEM, ( n = 3, ** p < 0.01 versus norm)

conditions and in the core of the infarct of MCAO rats with and without taurine treat-
ment by Western blot analysis (Fig. 23.3 ). The results showed that phosphorylated
IRE1 is highly expressed in cortical neurons under hypoxia/reoxygenation and in the
core of the infarct in MCAO rat brain. Taurine decreases the expression of p-IRE1 to
normal condition both in primary neuronal culture under hypoxia/reoxygenation lev-
els (Fig. 23.3c ) and in the core of the infarct of MCAO rats (Fig. 23.3d ), demonstrat-
ing that taurine significantly inhibits the IRE1 pathway in ER stress.

23.3.3 Taurine Can Decrease Apoptosis by Downregulation

of Apoptotic Markers and Caspase-12 in Primary
Neuronal Culture Induced by Hypoxia/Reoxygenation
and in the Core of the Brain of MCAO

The Bcl-2 family plays crucial roles in the regulation of the mitochondrial pathways
of apoptosis during experimental stroke. Bax is a member of the Bcl-2 family which