l‐borneol promotes neurovascular unit protection in the subacute phase of transient middle cerebral artery occlusion rats: p38‐MAPK pathway activation, anti‐inflammatory, and anti‐apoptotic effect

Abstract Our previous study showed l ‐borneol reduced cerebral infarction in the acute stage after cerebral ischemia, but there is little about the study of subacute phase. We herein investigated the cerebral protective effects of l ‐borneol on neurovascular units (NVU) in the subacute phase after transient middle cerebral artery occlusion (t‐MCAO). The t‐MCAO model was prepared by the line embolus method. Zea Longa, mNss, HE, and TTC staining were used to evaluate the effect of l ‐borneol. We evaluated the mechanisms of l ‐borneol on inflammation, p38 MAPK pathway, and apoptosis, etc. through various technologies. l ‐borneol 0.2, 0.1, 0.05 g·kg −1 could significantly reduce cerebral infarction rate, alleviate the pathological injury, and inhibit inflammation reaction. l ‐borneol could also significantly increase brain blood supply, Nissl bodies, and the expression of GFAP. Additionally, l ‐borneol activated the p38 MAPK signaling pathway, inhibited cell apoptosis, and maintained BBB integrity. l ‐borneol had a neuroprotective effect, which was related to activating the p38 MAPK signaling pathway, inhibiting inflammatory response and apoptosis, and improving cerebral blood supply to protect BBB and stabilize and remodel NVU. The study will provide a reference for the use of l ‐borneol in the treatment of ischemic stroke in the subacute phase.