Kang Le, Miao Mingsan, Bai Ming, Tian Shuo
College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450046, China.
Office for Scientific Research, Henan University of Chinese Medicine, Zhengzhou 450046, China.
Saudi J Biol Sci. 2017 Dec;24(8):1798-1802. doi: 10.1016/j.sjbs.2017.11.015. Epub 2017 Nov 10.
To study the protective effect of total flavonoid in rabdosia rubescens on BIT model by brain ischemic tolerance (hereinafter BIT) model of mice.
BIT model is used to block bilateral common carotid arteries and to copy BIT model of mice. After 10 min of transient ischemia for rats in preconditioning group, the mice in the nimodipine group and naoluotong capsule group were given the total flavonoid in rabdosia rubescens (300 mg/kg, 150 mg/kg, 75 mg/kg) for gavage, sham operation group, ischemia/reperfusion injury (hereinafter IRI) group and BIT group were fed with the same volume of 0.5% sodium carboxymethyl cellulose (CMC) once a day for 5 days. After administration for 1 h on day 5 (120 h), the rats in the other groups except for the sham operation group were treated with blood flow block for 30 min and reperfusion for 22 h. The serum NSE level were measured and the brain NO content and NOS activity changes was measured to observe the histopathological changes of brain tissue.
BIT models of mice and in rats were both successfully replicated. The total flavonoid in rabdosia rubescens can decrease the mortality of mice, decrease serum NSE level, increase the content of NO and the activity of NOS in the brain tissue of mice, and improve the pathological damage of cortex and hippocampus of mice.
The total flavonoid in rabdosia rubescens can stimulate an endogenous protective mechanism by inducing the release of low levels of cytokines NO and NOS, which reduces the release of serum NSE, relieves the brain tissue ischemia-reperfusion injury, and further improves the protection effect of ischemic preconditioning on brain injury. The damage of brain tissue ischemia and reperfusion, and further improve the ischemia Protective effect of preconditioning on brain injury.
通过小鼠脑缺血耐受(以下简称BIT)模型研究冬凌草总黄酮对BIT模型的保护作用。
采用BIT模型阻断双侧颈总动脉复制小鼠BIT模型。预处理组大鼠短暂缺血10分钟后,尼莫地平组和脑络通胶囊组小鼠分别给予冬凌草总黄酮(300mg/kg、150mg/kg、75mg/kg)灌胃,假手术组、缺血/再灌注损伤(以下简称IRI)组和BIT组每天灌胃等体积的0.5%羧甲基纤维素钠(CMC),连续5天。第5天(120小时)给药1小时后,除假手术组外,其他组大鼠进行血流阻断30分钟再灌注22小时。检测血清NSE水平,测定脑组织NO含量及NOS活性变化,观察脑组织病理组织学变化。
成功复制小鼠和大鼠的BIT模型。冬凌草总黄酮可降低小鼠死亡率,降低血清NSE水平,提高小鼠脑组织中NO含量及NOS活性,改善小鼠皮质和海马的病理损伤。
冬凌草总黄酮可通过诱导低水平细胞因子NO和NOS释放激发内源性保护机制,减少血清NSE释放,减轻脑组织缺血再灌注损伤,进而提高缺血预处理对脑损伤的保护作用。减轻脑组织缺血再灌注损伤,进一步提高缺血预处理对脑损伤的保护作用。