局解手术学杂志2024，Vol.33Issue(12)：1033-1038,6.DOI:10.11659/jjssx.12E023050
木犀草苷对缺氧缺血性脑病大鼠脑损伤的影响及机制
Effect and mechanism of luteolin on brain injury in rats with hypoxia-ischemia encephalopathy
摘要
Abstract
Objective To investigate the effects of luteolin on brain injury and Toll like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB)signaling pathway in rats with hypoxia-ischemia encephalopathy(HIE).Methods A total of 60 male rats were randomly divided into the normal control(NC)group,the model group,the low-dose group(25 mg/kg luteolin),the high-dose group(50 mg/kg luteolin),and the high-dose+lipopolysaccharide(LPS)group(50 mg/kg luteolin+0.5 mg/kg TLR4 agonist LPS),with 12 rats in each group.HIE model was constructed by ligation of common carotid artery and hypoxia.Neurological severity score(NSS)was used to detect the cerebral nerve function of rats in each group.Serum tumor necrosis factor-α(TNF-α)and brain-derived neurotrophic factor(BDNF)levels were detected by ELISA assay.HE staining was used to detect the pathological changes of brain tissue.The levels of malondialdehyde(MDA)and superoxide dismutase(SOD)in brain tissue of rats were detected by kit.TTC staining was used to detect cerebral infarction in rats.Western blot was used to detect the expression of TLR4,nuclear factor-kappa B(NF-κB),p-NF-κB,activated cleaved cysteine aspartate proteinase 3(Cleaved Caspase-3)protein in brain tissue.Results Compared with the model group,the NSS,levels of TNF-α and MDA,volume of cerebral infarction,and expression of TLR4,p-NF-κB/NF-κB and Cleaved Caspase-3 in low-dose group and high-dose group were decreased(P<0.05),BDNF and SOD levels were increased(P<0.05),the histopathological damage of hippocampus was obviously alleviated,the structure was gradually clear,and the number of nerve cells was normal.Compared with the high-dose group,the levels of the above indexes were inversely expressed in the high-dose+LPS group(P<0.05),and the histopathological damage in the hippocampus was aggravated.Conclusion Luteolin can improve brain injury and inhibit TLR4/NF-κB signaling pathway in HIE rats,and the inhibition of TLR4/NF-κB signaling pathway may be the mechanism of luteolin in improving brain injury.关键词
木犀草苷/Toll样受体4/核因子-κB/缺氧缺血性脑病Key words
luteolin/Toll-like receptor 4/nuclear factor-kappa B/hypoxia-ischemia encephalopathy分类
医药卫生引用本文复制引用
杨畅,金海涛,张雯..木犀草苷对缺氧缺血性脑病大鼠脑损伤的影响及机制[J].局解手术学杂志,2024,33(12):1033-1038,6.基金项目
武汉市中医药科研项目(WZ22C65) （WZ22C65）
