中医学报2025，Vol.40Issue(6)：1311-1317,7.DOI:10.16368/j.issn.1674-8999.2025.06.211
肉桂醛通过抑制IRAK4/TAK1信号通路发挥对创伤性脑损伤大鼠的神经保护作用
Neuroprotective Effects of Cinnamaldehyde on Traumatic Brain-injured Rats by Inhibiting IRAK4/TAK1 Signaling Pathway
摘要
Abstract
Objective:To investigate the neuroprotective effects of cinnamaldehyde(CA)on traumatic brain injury(TBI)in rats based on the interleukin-1 receptor-associated kinase-4(IRAK4)/transforming growth factor β activated kinase 1(TAK1)signaling pathway.)signaling pathway to investigate the neuroprotective mechanism of cinnamaldehyde(CA)in traumatic brain injury(TBI)rats.Methods:A rat TBI model was established and randomly divided into a model group(TBI),a CA low-dose group(L-CA group,25 mg·kg-1),a CA medium-dose group(M-CA group,50 mg·kg-1),and a CA high-dose group(H-CA group,75 mg·kg-1),with 12 rats in each group;and 12 normally reared rats were used as a sham operation group(Sham).The rats in each group were injected intraperitoneally with drugs or saline for 7 d.The neurological function of the rats was assessed by the modified neurological deficit se-verity score(mNSS score),the water content of the brain tissue was measured by gravimetry,the pathological morphology of the brain tissue was observed by HE staining,the apoptosis rate of the brain tissue was measured by TUNEL staining,and the interleukin-1β(IL-1β),IL-6,tumor necrosis factor-α(TNF-α)content in rat brain tissues,and the expression levels of p-IRAK4/IRAK4 and p-TAK1/TAK1 in rat brain tissues were detected by Western blot.Results:Compared with the Sham group,the mNSS scores of rats in the TBI group were elevated at 6 h,1 d,3 d,and 7 d after modeling(P＜0.05);compared with the TBI group,the mNSS scores of rats in the L-CA group,M-CA group,and H-CA group were decreased at 1 d,3 d,and 7 d after modeling(P＜0.05).Compared with the Sham group,the water content of the brain tissue of rats in the TBI group was increased(P＜0.05);compared with the TBI group,the water content of the brain tissue of rats in the L-CA,M-CA and H-CA groups was decreased(P＜0.05).In the TBI group,there was obvious edema in the brain tissue,some cell nuclei were consolidated,and many inflammatory cells were infiltrated;in the L-CA,M-CA and H-CA groups,the pathological damage was significantly reduced compared with that in the TBI group.Com-pared with the Sham group,the apoptosis rate of rat brain tissue in the TBI group increased(P＜0.05);compared with the TBI group,the apoptosis rate of rat brain tissue in the L-CA,M-CA and H-CA groups decreased(P＜0.05).Compared with the Sham group,the content of IL-1β,IL-6 and TNF-α in the brain tissue of rats in the TBI group was increased(P＜0.05);compared with the TBI group,the content of IL-1β,IL-6 and TNF-α in the brain tissue of rats in the L-CA group,the M-CA group and the H-CA group was decreased(P＜0.05).The levels of p-IRAK4/IRAK4 and p-TAK1/TAK1 in the brain tissue of rats in the TBI group were increased compared with those in the Sham group(P＜0.05);and the levels of p-IRAK4/IRAK4 and p-TAK1/TAK1 in the brain tissue of rats in the L-CA group,the M-CA group and the H-CA group were decreased compared with those in the TBI group(P＜0.05).Conclusion:CA may exert neuroprotective effects on TBI rats by inhibiting the IRAK4/TAK1 signaling pathway and attenu-ating inflammatory response and apoptosis.关键词
肉桂醛/创伤性脑损伤/IRAK4/TAK1信号通路/神经功能/细胞凋亡/炎症反应Key words
cinnamaldehyde/traumatic brain injury/IRAK4/TAK1 signaling pathway/neurological function/apoptosis/inflammatory re-sponse分类
医药卫生引用本文复制引用
韩福新,武伟男,张蕊..肉桂醛通过抑制IRAK4/TAK1信号通路发挥对创伤性脑损伤大鼠的神经保护作用[J].中医学报,2025,40(6):1311-1317,7.基金项目
陕西省重点研发计划一般项目(2022SF-205) （2022SF-205）
西安市人民医院科研孵化基金项目重点培育项目(ZD-12) （ZD-12）
