Abstract
Methylophiopogonanone A (MO-A), an active homoisoflavonoid of the Chinese herb Ophiopogon japonicus which has been shown to have protective effects on cerebral ischemia/reperfusion (I/R) injury, has been demonstrated to have anti-inflammatory and anti-oxidative properties. However, little is known about its role in cerebral I/R injury. Therefore, in this study, by using a middle cerebral artery occlusion (MCAO) and reperfusion rat model, the effect of MO-A on cerebral I/R injury was examined. The results showed that MO-A treatment reduced infarct volume and brain edema, improved neurological deficit scores, reversed animal body weight decreases, and increased animal survival time in the stroke groups. Western blotting showed that MO-A suppressed MMP-9, but restored the expression of claudin-3 and claudin-5. Furthermore, transmission electron microscopy were monitored to determine the blood–brain barrier (BBB) alterations in vitro. The results showed that MO-A markedly attenuated BBB damage in vitro. Additionally, MO-A inhibited ROS production in ECs and MMP-9 release in differentiated THP-1 cells in vitro, and suppressed ICAM-1 and VCAM-1 expression in ECs and leukocyte/EC adhesion. In conclusion, our data indicate that MO-A has therapeutic potential against cerebral I/R injury through its ability to attenuate BBB disruption by regulating the expression of MMP-9 and tight junction proteins.
Highlights
Ischemic stroke, a complex devastating disease, is caused by drastic disruption of cerebral blood flow, resulting in a deficiency of glucose and oxygen and triggering a multi-step pathophysiological ischemic cascade
The results showed that there was no infarct in sham animals, but significant ischemic injury following transient middle cerebral artery occlusion (MCAO)
Neurological scores were measured at 6 hours, 24 hours, 3 days and 7 days (Fig 2C), and animal body weights were measured at day 1, 3 and 7 (Fig 2D)
Summary
A complex devastating disease, is caused by drastic disruption of cerebral blood flow, resulting in a deficiency of glucose and oxygen and triggering a multi-step pathophysiological ischemic cascade. The results showed that there was no infarct in sham animals, but significant ischemic injury following transient MCAO (model group).
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