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Table 1
Studies describing the use of EPO and its analogues in experimental stroke models
MCAOt (rat)
MCAOp (rat)
MCAOt (mouse)
MCAOp (mouse)
Erythropoietin (EPO)
Sirén et al. (
64
)
Sadamoto et al. (
82
)
Fletcher et al. (
79
)
Bernaudin et al. (
57
)
Yu et al. (
80
)
Brines et al. (
56
)
Wakida et al. (
87
)
Aluclu et al. (
81
)
Ding et al. (
86
)
Li et al. (
84
)
Esneault et al. (
48
)
Wang et al. (
66
,
91
)
Villa et al. (
83
)
Li et al. (
85
)
Carbamylated EPO (CEPO)
Leist et al. (
89
)
Wang et al. (
91
)
Villa et al. (
83
)
IgG-EPO fusion protein
Fu et al. (
88
)
Fu et al. (
92
)
Asialoerythropoietin
Price et al. (
77
)
Erbayraktar et al. (
63
)
Carnasep (darbepoetin alfa)
Belayev et al. (
90
)
Villa et al. (
83
)
EPO-S100E
SIOG-I-EPO
Villa et al. (
83
)
Gan et al. (
78
)
MCAO
Middle cerebral artery occlusion,
MCAOt
(temporary),
MCAOp
(permanent)
the age of rat on the brain ischemic damage is still controversial
(
32, 33
). In any case, aging is associated with reduction in
angiogenesis and degradation of some neurological function
that could impact stroke evolution and outcomes. Furthermore,
stroke remains a disease of the elderly in human; therefore, the
use of young animals should be discarded from experimental
studies.
2. The strain should be carefully chosen. Different strains could
have a different intrinsic response to ischemic brain injury,
due to differences in genetic background (
34, 35
). For exam-
ple, the stroke-prone rat derived from the SHR is susceptible
to develop larger and much less variable infarcts following
MCAO (
36, 37
). This strain of rat has a genetic susceptibility
to stroke independent of hypertension (
38
). This unique
strain may provide a model to investigate genetic susceptibil-
ity to stroke. Furthermore, differences in intracranial and
intracerebral vascular anastomoses could result in a larger
infarct volume in some strains (
32
). If the genetic background
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