Objective To investigate the effect of atractylenolide Ⅲ (A Ⅲ) on stroke in spontaneously hypertensive rats by regulating microRNA-296-5p(miR-296-5p)expression.

Methods The spontaneously hypertensive rats (SHR) were given 0.9% sodium chloride solution freely for 2 months, and then fed with 1% sodium chloride solution to establish the stroke model of SHR. The rat models were randomly grouped into Model group, A Ⅲ low-dose group (A Ⅲ-L group), A Ⅲ high-dose group (A Ⅲ-H group), positive drug nimodipine group (Nim group), miR-296-5p agonist group(miR-296-5p agomir group), agomir NC group, A Ⅲ-H+miR-296-5p agomir group, and A Ⅲ-H+agomir NC group, with 12 in each group. The changes in neurological symptom scores, average arterial pressure, survival time, and platelet adhesion rate were detected and recorded; hematoxylin and eosin (HE) staining was applied to detect pathological changes in the CA1 region of the rat hippocampus; quantitative reverse transcription polymerase chain reaction (qRT-PCR) was applied to detect the expression of miR-296-5p in the hippocampal CA1 region.

Results Compared with the NC group, the Model group showed increases in neurological symptom score, mean arterial pressure, platelet adhesion rate, miR-296-5p expression, shortened survival time, and severe pathological damage to the hippocampal CA1 area (P < 0.05); compared with the Model group, the neurological symptom scores, mean arterial pressure, platelet adhesion rate, and miR-296-5p expression in the A Ⅲ-L, A Ⅲ-H, and Nim groups decreased, the survival time was prolonged, and the pathological damage in the CA1 area of the hippocampus was alleviated(P < 0.05); compared with Model group and agomir NC group, neurological symptom score, mean arterial pressure, platelet adhesion rate and miR-296-5p expression of rats in the miR-296-5p agomir group were increased, survival time was shortened, and pathological damage in hippocampal CA1 region was aggravated (P < 0.05). compared with the A Ⅲ-H group and the AⅢ-H+agomir NC group, the neurological symptom score, average arterial pressure, platelet adhesion rate and miR-296-5p expression of rats were increased, the survival time was shortened, and the pathological damage in hippocampal CA1 region was serious in the AIII-H+miR-296-5p agomir group (P < 0.05).

Conclusion A Ⅲ may treat SHR stroke by inhibiting the expression of miR-296-5p.