摘要
目的本实验主要基于NF-κB通路探讨天麻素对脑缺血所致肝损伤大鼠的作用原理和机制。方法对40只健康SD成年雄性大鼠进行随机分组:正常对照组(NORM)、假手术组(SHAM)、脑缺血模型组(MCAO)和天麻素治疗组(GAS)。除正常对照组外,其余组别均采用栓塞大鼠右侧大脑中动脉的方法复制局灶性脑缺血模型。造模成功后,天麻素治疗组大鼠给予天麻素注射液每日10 mg/kg腹腔内注射,持续2周;假手术组大鼠每日给予等量的生理盐水腹腔内注射,持续2周;脑缺血模型组大鼠不予任何治疗。称取大鼠的肝脏重量和体质量计算肝脏指数;采用HE染色法对各组大鼠肝组织进行病理变化测定;采用Western Blot法对各组大鼠肝组织中肿瘤坏死因子-α(TNF-α)和核因子-κB p65(NF-κB p65)的蛋白表达水平进行测定。结果与正常对照组和假手术组相比,脑缺血模型组和天麻素治疗组的肝组织显示出显著的水肿和炎性损伤,并且肝组织中的NF-κB p65和TNF-α的蛋白表达水平也明显上升;与脑缺血模型组相比,天麻素治疗组肝组织的炎性损伤程度有所缓解,其肝组织中NF-κB p65与TNF-α的蛋白表达水平也有所下降。结论脑缺血能够导致肝组织炎性损伤,NF-κB信号通路中的NF-κB p65和TNF-α可能参与了炎性反应的发生过程;天麻素能减轻脑缺血大鼠的肝损伤,其机制可能是抑制了NF-κB信号通路中炎性因子的表达,从而发挥对肝损伤的修复作用。
Objective To investigate the mechanism of action of gastrodin on liver injury induced by cerebral ischemia in rats via the NF-κB pathway.Methods Forty healthy adult male SD rats were randomly divided into four groups:normal control group(NORM),sham operation group(SHAM),cerebral ischemia model group(MCAO,induced by middle cerebral artery occlusion)and gastrodin treatment group(GAS).Except for the NORM group,focal cerebral ischemia models were established by occluding the right middle cerebral artery in the other groups.After successful modeling,rats in the GAS group received daily intraperitoneal injections of gastrodin at a dose of 10 mg/kg for 2 weeks.Rats in the SHAM group received daily intraperitoneal injections of an equal volume of saline for 2 weeks,while rats in the MCAO group received no treatment.The liver weight and body weight of rats were measured to calculate the liver index.HE staining was used to determine the pathological changes of liver tissues in each group.Western Blot analysis was performed to measure the protein expression levels of tumor necrosis factor-α(TNF-α)and nuclear factor-κB p65(NF-κB p65)in liver tissues of rats in each group.Results Compared with the NORM group and SHAM group,the liver tissue of the MCAO group and the GAS group showed significant edema and inflammatory injury,accompanied by increased protein expression levels of NF-κB p65 and TNF-α in liver tissues.Compared with the MCAO group,the degree of inflammatory injury in the liver tissues of the GAS group was alleviated,and the protein expression levels of NF-κB p65 and TNF-α in the liver tissues were also decreased.Conclusion Cerebral ischemia can lead to inflammatory injury in liver tissues,and NF-κB p65 and TNF-α in the NF-κB signaling pathway may be involved in the occurrence of the inflammatory response.Gastrodin can alleviate liver injury in rats with cerebral ischemia,and its mechanism may be to inhibit the expression of inflammatory factors in the NF-κB signaling pathway,thus playing a role in repairing liver injury.
作者
陈昭莹
胡蓉
李凤舜
产翠翠
CHEN Zhaoying;HU Rong;LI Fengshun;CHAN Cuicui(School of Clinical Medicine,Wannan Medical College,Wuhu 241002,Anhui,China;School of Basic Medical Sciences,Wannan Medical College,Wuhu 241002,Anhui,China)
出处
《右江民族医学院学报》
2025年第1期56-60,共5页
Journal of Youjiang Medical University for Nationalities
基金
安徽省大学生创新创业训练计划项目(S202310368021)。
