由于体内各种毒素的积累,长期使用烟草会导致肝脏损伤和炎症。本研究旨在探讨尼古丁诱导肝损伤的分子机制,caspase级联,和Akt/NF-κB信号通路,以及右泛醇(DEX)的保护作用。对雄性大鼠进行浓度为0.5mg/kg/天的尼古丁和/或浓度为500mg/kg/天的DEX的腹膜内注射8周。治疗期后,对血清样本进行肝功能测试,和组织样本分析Akt的蛋白质水平,NF-κB,Bax,Bcl-xL,Caspase-3和Caspase-9,以及组织病理学改变。此外,进行了氧化应激标志物和促炎细胞因子的评估。尼古丁给药导致IL-6,IL-1β水平升高,MDA,TOS,和氧化应激指数,伴随着降低的TAS水平。此外,尼古丁暴露降低了p-Akt/Akt比率,NF-κB增加,Bax,Caspase-3和Caspase-9蛋白水平,并降低抗凋亡蛋白Bcl-xL水平。DEX治疗显著减轻了这些影响,将参数恢复到与对照组相当的水平。尼古丁诱导的肝损伤导致氧化应激,炎症,和细胞凋亡,Bax/Bcl-xL介导,Caspase-3、Caspase-9和Akt/NF-κB途径。相反,DEX通过NF-κB调节细胞凋亡有效减轻尼古丁诱导的肝损伤,Caspase-3,Caspase-9,Bax抑制,和Bcl-xL激活。
Chronic tobacco use can lead to liver damage and inflammation due to the accumulation of various toxins in the body. This study aimed to investigate the correlation between the molecular mechanisms of nicotine-induced liver injury, the caspase cascade, and the Akt/NF-κB signaling pathway, as well as the protective effects of dexpanthenol (DEX). Male rats were subjected to intraperitoneal injections of nicotine at a concentration of 0.5 mg/kg/day and/or DEX at a concentration of 500 mg/kg/day for 8 weeks. After the treatment period, liver function tests were conducted on serum samples, and tissue samples were analyzed for protein levels of Akt, NF-κB, Bax, Bcl-xL, Caspase-3, and Caspase-9, along with histopathological changes. Additionally, assessments of oxidative stress markers and proinflammatory cytokines were carried out. Nicotine administration led to elevated levels of IL-6, IL-1β, MDA, TOS, and oxidative stress index, accompanied by decreased TAS levels. Moreover, nicotine exposure reduced the p-Akt/Akt ratio, increased NF-κB, Bax, Caspase-3, and Caspase-9 protein levels, and decreased the antiapoptotic protein Bcl-xL levels. DEX treatment significantly mitigated these effects, restoring the parameters to levels comparable to those of the control group. Nicotine-induced liver injury resulted in oxidative stress, inflammation, and apoptosis, mediated by Bax/Bcl-xL, Caspase-3, Caspase-9, and Akt/NF-κB pathways. Conversely, DEX effectively attenuated nicotine-induced liver injury by modulating apoptosis through NF-κB, Caspase-3, Caspase-9, Bax inhibition, and Bcl-xL activation.