Effect of remote limb ischemic post‐conditioning on the expression of miR‐21‐5p/PirB in the brain of rats with focal cerebral ischemia

Abstract

Cerebral ischemia causes great damage to ischemic brain regions. Remote limb post-conditioning (RLIPostC) has neuroprotective effects on cerebral ischemia.Paired immunoglobulin receptor B (PirB) has been confirmed to affect the cerebral ischemia injury. Therefore, this study investigated the mechanism of RLIPostC on cerebral ischemia injury. The middle cerebral artery occlusion (MCAO) model was established in rats, followed by RLIPostC (by blocking the blood flow in the distal limb for 10 min after MCAO, and restored for 10 min, three cycles), or in vivo lentivirus infection of miR-21-5p agomir, sh-PirB and oe-PirB. The locomotor abilities were assessed using the foot fault test and balance beam walking test at 48 h, 7 and 21 days after operation, and neurological function was measured on day 21. The cerebral infarct area, Nissl bodies and the pathology of brain tissues were examined using histological staining, followed by the assessment of miR-21-5p and PirB levels and the binding relationship between miR-21-5p and PirB. miR-21-5p was poorly expressed in MCAO rats. Both RLIPostC and overexpression of miR-21-5p reduced motor dysfunction, neurological function score, cerebral infarction area and brain edema; increased Nissl bodies in MCAO rats and thus alleviated the brain damage caused by cerebral ischemia. RLIPostC promoted miR-21-5p expression. PirB was highly expressed in cerebral ischemia, and miR-21-5p targeted PirB. Overall, RLIPostC promotes miR-21-5p expression and then inhibits PirB to alleviate cerebral ischemia injury, which provides theoretical basis for basic research on motor dysfunction and neuron injury after cerebral ischemia and the development of neuroscience.

Intracerebral hirudin injection alleviates cognitive impairment and oxidative stress and promotes hippocampal neurogenesis in rats subjected to cerebral ischemia

“…Middle cerebral artery occlusion can induce cerebral ischemia-like conditions in rodents and is widely used to induce cerebral ischemia injury in vivo. [31][32][33] Therefore, hirudin was intracerebroventricularly injected into middle cerebral artery occlusion-subjected rats. In the current study, we found that occlusion resulted in motor and cognitive dysfunction, while administration of hirudin alleviated motor impairment, improved spatial learning and memory capacity and neurological functions, and reduced cerebral infarction.…”

“…Hirudin is a bioactive ingredient originating from leeches, and its effects on oxidative stress and neurogenesis in ischemic stroke remain uncertain. Middle cerebral artery occlusion can induce cerebral ischemia‐like conditions in rodents and is widely used to induce cerebral ischemia injury in vivo 31–33 . Therefore, hirudin was intracerebroventricularly injected into middle cerebral artery occlusion‐subjected rats.…”