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2017 ; 14
(1
): 122
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Sac-1004, a vascular leakage blocker, reduces cerebral ischemia-reperfusion
injury by suppressing blood-brain barrier disruption and inflammation
#MMPMID28645333
Zhang H
; Park JH
; Maharjan S
; Park JA
; Choi KS
; Park H
; Jeong Y
; Ahn JH
; Kim IH
; Lee JC
; Cho JH
; Lee IK
; Lee CH
; Hwang IK
; Kim YM
; Suh YG
; Won MH
; Kwon YG
J Neuroinflammation
2017[Jun]; 14
(1
): 122
PMID28645333
show ga
BACKGROUND: Blood-brain barrier (BBB) breakdown and inflammation are critical
events in ischemic stroke, contributing to aggravated brain damage. The BBB
mainly consists of microvascular endothelial cells sealed by tight junctions to
protect the brain from blood-borne substances. Thus, the maintenance of BBB
integrity may be a potential target for neuroprotection. Sac-1004, a pseudo-sugar
derivative of cholesterol, enhances the endothelial barrier by the stabilization
of the cortical actin ring. RESULTS: Here, we report on the protective effects of
Sac-1004 on cerebral ischemia-reperfusion (I/R) injury. Treatment with Sac-1004
significantly blocked the interleukin-1?-induced monolayer hyperpermeability of
human brain microvascular endothelial cells (HBMECs), loss of tight junctions,
and formation of actin stress fiber. Sac-1004 suppressed the expression of
adhesion molecules, adhesion of U937 cells, and activation of nuclear factor-?B
in HBMECs. Using a rat model of transient focal cerebral ischemia, it was shown
that Sac-1004 effectively ameliorated neurological deficits and ischemic damage.
In addition, Sac-1004 decreased BBB leakage and rescued tight junction-related
proteins. Moreover, the staining of CD11b and glial fibrillary acidic protein
showed that Sac-1004 inhibited glial activation. CONCLUSIONS: Taken together,
these results demonstrate that Sac-1004 has neuroprotective activities through
maintaining BBB integrity, suggesting that it is a great therapeutic candidate
for stroke.
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