Results
3.1. D-allose protects
the brain from MCAO/R-induced injury in vivo
In this study, we used the MCAO/R) model in C57BL/6J male mice aged 8-12
weeks, which truly mimicked human IS, to assess the neuroprotective
effect of D-allose. Compared with the Sham group, mice in the MCAO/R
group showed strong neurological deficits, obvious infarct volume and
brain edema (P <0.01, Fig1 A-C), suggesting serious
brain injury was induced by the MCAO/R model. As the results showed in
Fig.1 D-F, in the MCAO/R and MCAO/R+NS group, transient MCAO/R produced
an evident-defined infarct, brain edema and well neurological deficits,
0.4mg/g D-allose which given intraperitoneal injection within 5min after
reperfusion significantly reduced brain infarct volume by 30%, brain
edema by 4% and improve NSS score by 45% at 48 h after MCAO/R.
Moreover, the presence of D-allose significantly decreased these
apoptosis markers, Bax, cleaved Caspase 3 and cleaved Caspase1 level, as
well as the rate of apoptosis-positive neurons in the ipsilateral
cortex, which was examined by using Western blot and TUNEL staining
(P <0.01, Fig1 G-H). Meanwhile, as shown in Fig. 1 I-K,
some classical inflammatory cytokines, IL-1β, IL-6 and TNF-α levels are
increased markedly in mice subjected to MCAO/R. D-allose treatment
significantly reduced the production levels of IL-1β, IL-6 and TNF-α
which compared with that in the MCAO/R group (P <
0.01). Together, these results suggested that D-allose could protect the
brain from MCAO/R-induced apoptosis and inflammation, as well as
provides a potential for clinical trials of IS treatment with
D-allose in the future.