College of Basic Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong 510120, P.R. China.
Mol Med Rep. 2021 Nov;24(5). doi: 10.3892/mmr.2021.12431. Epub 2021 Sep 13.
Stroke is one of the main causes of disease‑related mortality worldwide. Buyang Huanwu Decoction (BHD) has been used to protect against stroke and stroke‑induced disability for several years in China. Studies have shown that BHD can relieve neuronal damage in rats with cerebral ischemia/reperfusion (I/R) injury. However, the mechanism remains unclear. A middle cerebral artery occlusion and reperfusion (MCAO‑R) model was used in the present study. The animals were treated with BHD (5, 10 and 20 g/kg) or rapamycin. Infarct size and modified neurological severity score were calculated on day 5 following MCAO‑R surgery. Cellular changes around the ischemic penumbra were revealed by hematoxylin and eosin and Nissl staining. The protein expression levels of nestin, brain‑derived neurotrophic factor (BDNF), doublecortin on the X chromosome (DCX) and autophagy‑related proteins (beclin 1, LC3‑II and p62) in the peri‑ischemic area of the brain were detected. The results demonstrated that post‑surgical treatment with BHD reduced the brain infarct size and improved neurological deficits in MCAO‑R rats. BHD protected against MCAO‑R‑induced neuronal impairment and promoted neurogenesis, increased the protein expression of nestin, BDNF and DCX and markedly enhanced autophagy by increasing beclin 1 and LC3‑II and decreasing p62. Meanwhile, BHD promoted the expression of sirtuin 1 (SIRT1), an important regulator of autophagy. In conclusion, the present study suggested that post‑surgical treatment with BHD could protect rat brains from I/R injury, potentially through the SIRT1/autophagy pathway.
中风是全球疾病相关死亡率的主要原因之一。补阳还五汤 (BHD) 已在中国用于预防中风和中风引起的残疾多年。研究表明,BHD 可以减轻脑缺血/再灌注 (I/R) 损伤大鼠的神经元损伤。然而,其机制尚不清楚。本研究采用大脑中动脉闭塞再灌注 (MCAO-R) 模型。动物用 BHD (5、10 和 20 g/kg) 或雷帕霉素治疗。MCAO-R 手术后第 5 天计算梗死面积和改良神经严重程度评分。苏木精和伊红及尼氏染色显示缺血半影区周围的细胞变化。检测大脑缺血半影区周围的巢蛋白、脑源性神经营养因子 (BDNF)、X 染色体上的双皮质素 (DCX) 和自噬相关蛋白 (beclin 1、LC3-II 和 p62) 的蛋白表达水平。结果表明,BHD 术后治疗可减少 MCAO-R 大鼠的脑梗死面积,改善神经功能缺损。BHD 可防止 MCAO-R 诱导的神经元损伤,促进神经发生,增加巢蛋白、BDNF 和 DCX 的蛋白表达,并通过增加 beclin 1 和 LC3-II 、减少 p62 显著增强自噬。同时,BHD 促进了自噬重要调节因子 SIRT1 的表达。综上所述,本研究表明,BHD 术后治疗可保护大鼠大脑免受 I/R 损伤,可能通过 SIRT1/自噬途径。