Preservation of the blood–brain barrier (BBB) function is a potential protective strategy against cerebral ischemic injuries. CD151 has a beneficial effect in maintaining vascular stability and plays a role in pro-angiogenesis. Both vascular stability and angiogenesis can affect BBB function. Therefore, we aimed to examine the action of CD151 in regulating BBB permeability after cerebral ischemic injury in the present study. Using a transient focal cerebral ischemia (tFCI) rat model, we established that CD151 overexpression in the brain mitigated the leakage of endogenous IgG at 6–24 h after tFCI in vivo. Moreover, we found that CD151 can decrease the diffusion of macromolecules through monolayer brain microvessel endothelial cells (BMVECs) after glucose and oxygen deprivation (OGD)–reoxygenation in vitro. Furthermore, overexpression of CD151 in BMVECs suppressed OGD–reoxygenation-induced F-actin formation and RhoA activity. However, while preserving BBB integrity after tFCI, CD151 overexpression did not affect the post-stroke outcomes. Taken together, the present study demonstrated that CD151 overexpression in the brain protects BBB permeability at early phase after tFCI. CD151 may be a potential target for early BBB protection in ischemic stroke.

保护血脑屏障（BBB）功能是预防脑缺血性损伤的潜在保护策略。 CD151 对维持血管稳定性具有有益作用，并在促血管生成中发挥作用。血管稳定性和血管生成都会影响血脑屏障功能。因此，本研究旨在探讨CD151在脑缺血损伤后调节BBB通透性的作用。使用短暂性局灶性脑缺血 (tFCI) 大鼠模型，我们确定在体内 tFCI 后 6-24 小时，大脑中 CD151 的过度表达可减轻内源性 IgG 的渗漏。此外，我们发现在体外葡萄糖和缺氧（OGD）复氧后，CD151可以减少大分子通过单层脑微血管内皮细胞（BMVEC）的扩散。此外，BMVEC 中 CD151 的过度表达抑制了 OGD 复氧诱导的 F-肌动蛋白形成和 RhoA 活性。然而，在 tFCI 后保持 BBB 完整性的同时，CD151 过度表达并不影响中风后的结果。综上所述，本研究表明，大脑中 CD151 过度表达可保护 tFCI 后早期的 BBB 通透性。 CD151可能是缺血性中风早期BBB保护的潜在靶点。