BACKGROUND Ulcer colitis(UC)is a chronic,nonspecific,and noninfectious inflammatory bowel disease.Recently,Toll-like receptors(TLRs)have been found to be closely associated with clinical inflammatory diseases.Achievin...BACKGROUND Ulcer colitis(UC)is a chronic,nonspecific,and noninfectious inflammatory bowel disease.Recently,Toll-like receptors(TLRs)have been found to be closely associated with clinical inflammatory diseases.Achieving complete remission in patients with intermittent periods of activity followed by dormancy is challenging.Moreover,no study has explored the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.AIM To explore the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.METHODS This prospective clinical study included patients who met the exclusion criteria in 2020 and 2021.The patients with UC were divided into two groups(control and experimental).The peripheral blood of the experimental and control groups were collected under aseptic conditions.The expression of TLR4 protein,NF-κB,IL-6,and IL-17 was detected in the peripheral blood of patients in the experimental group and control group before and 1 month after taking the drug.Linear co rrelation analysis was used to analyze the relationship between the expression level of TLR4 protein and the expression levels of downstream signal NF-κB and inflammatory factors IL-6 and IL-17,and P<0.05 was considered statistically significant.RESULTS There were no significant differences in the patient characteristics between the control and experimental groups.The results showed that the expression levels of TLR4 and NF-κB in the experimental group were significantly lower than those in the control group(P<0.05).The levels of IL-6 and IL-17 in the experimental group were significantly lower than those in the control group(P<0.05).The TLR4 protein expression in the experimental group was positively correlated with the expression level of downstream signal NF-κB and was positively correlated with the levels of downstream inflammatory cytokines IL-6 and IL-17(r=0.823,P<0.05).CONCLUSION Kuicolong-yu enema decoction retains traditional Chinese medicine enema attenuates the inflammatory response of UC through the TLR4/NF-κB signaling pathway.展开更多
目的探讨柴朴汤对哮喘小鼠支气管上皮细胞高迁移率族蛋白B1(HMGB1)、Toll样受体4(TLR4)、核因子-κB(NF-κB)及下游炎症介质单核细胞趋化蛋白-1(MCP-1)、白细胞介素-6(IL-6)的影响。方法将小鼠支气管上皮细胞分为对照组(Con组,空白血清...目的探讨柴朴汤对哮喘小鼠支气管上皮细胞高迁移率族蛋白B1(HMGB1)、Toll样受体4(TLR4)、核因子-κB(NF-κB)及下游炎症介质单核细胞趋化蛋白-1(MCP-1)、白细胞介素-6(IL-6)的影响。方法将小鼠支气管上皮细胞分为对照组(Con组,空白血清培养)、Model组(哮喘小鼠血清培养)和Chaipu组(柴朴汤药血清培养)。采用qRT-PCR和Western blotting检测小鼠支气管上皮细胞中HMGB1、TLR4、NF-κB、MCP-1、IL-6的mRNA及蛋白表达情况,ELISA法测定细胞培养液中MCP-1和IL-6的水平。结果与Con组相比,Model组小鼠支气管上皮细胞HMGB1、TLR4、NF-κB、MCP-1、IL-6表达均明显升高(P<0.05);Model组细胞培养液中MCP-1、IL-6也显著升高(P<0.05)。与Model组相比,Chaipu组小鼠支气管上皮细胞HMGB1、TLR4、MCP-1、IL-6 mRNA和蛋白表达降低,NF-κB m RNA表达亦降低(P<0.05);Chaipu组细胞培养液中MCP-1、IL-6也显著降低(P<0.05)。结论柴朴汤可下调哮喘血清诱导的炎症因子的表达,可能与其抑制HMGB1/TLR4/NF-κB炎症通路有关。展开更多
目的探究高迁移率族蛋白1(High Mobility Group Box Protein1, HMGB1)通过(Toll-like Receptor4,TLR4)/核因子κB(Nuclear Factor Kappa-B, NF-κB)/NOD样受体热蛋白结构域相关蛋白3(NOD-like Receptor Thermal Protein Domain Associat...目的探究高迁移率族蛋白1(High Mobility Group Box Protein1, HMGB1)通过(Toll-like Receptor4,TLR4)/核因子κB(Nuclear Factor Kappa-B, NF-κB)/NOD样受体热蛋白结构域相关蛋白3(NOD-like Receptor Thermal Protein Domain Associated Protein 3, NLRP3)信号通路介导内皮细胞焦亡在系统性血管炎中的作用机制。方法 研究于2021年10月—2023年9月在齐齐哈尔医学院附属第三医院开展。取人脐静脉血管内皮细胞进行培养,随机分为对照组和实验组,实验组加入人重组HMGB1,对比对照组与实验组、实验组NLRP3及TLR4表达抑制前后,内皮细胞焦亡相关蛋白的表达水平。结果 系统性血管炎组与健康对照组比较,人脐静脉血管内皮细胞中HMGB1、含半胱氨酸的天冬氨酸蛋白水解酶-1(caspase-1)、白细胞介素-1β(interleukin-1β, IL-1β)、白细胞介素-18(interleukin-18, IL-18)水平升高,差异有统计学意义(P均<0.05)。细胞实验中实验组与对照组比较,caspase-1、IL-1β、IL-18水平升高,差异有统计学意义(P均<0.05)。过表达HMGB1并抑制NLRP3可使NLRP3(2.71±0.59 vs 1.24±0.58)、caspase-1(0.69±0.12 vs 0.40±0.03)、IL-1β[(1.75±0.31)pg/mL vs (1.16±0.12)pg/mL]、IL-18[(0.15±0.04)pg/mL vs (0.09±0.01)pg/mL]水平降低,差异有统计学意义(P均<0.05);过表达HMGB1并抑制TLR4可使TLR4(4.93±1.04 vs 1.96±0.84)、NF-κB(5.62±1.39 vs 2.15±1.04)、NLRP3(2.71±0.59 vs 1.24±0.58)、caspase-1(0.69±0.12 vs 0.40±0.03)、IL-1β[(1.75±0.31)pg/mL vs (1.16±0.12)pg/mL]、IL-18[(0.15±0.04)pg/mL vs (0.09±0.01)pg/mL]水平明显降低,差异有统计学意义(P均<0.05)。结论 HMGB1通过调节TLR4/NF-κB/NLRP3信号通路介导内皮细胞焦亡,进而改善系统性血管炎。展开更多
骨关节炎(osteoarthritis,OA)作为临床常见老年退行性疾病,目前尚无有效治疗手段。研究发现OA是一种慢性低度炎性疾病。损伤相关分子模式HMGB1(high mobility group box-1)在OA病理过程中发挥中心分子作用。HMGB1与固有免疫模式识别受体...骨关节炎(osteoarthritis,OA)作为临床常见老年退行性疾病,目前尚无有效治疗手段。研究发现OA是一种慢性低度炎性疾病。损伤相关分子模式HMGB1(high mobility group box-1)在OA病理过程中发挥中心分子作用。HMGB1与固有免疫模式识别受体TLR4(toll-like receptor 4,TLR4)结合后激活NF-κB信号通路导致OA软骨退变和滑膜炎等免疫炎症反应。通过综述HMGB1介导TLR4/NF-κB信号通路在OA发病机制中的作用,为靶向阻断HMGB1治疗OA提供理论依据和参考。展开更多
【目的】研究苦苣菜水提物对脂多糖(LPS)诱导的小鼠肺炎模型中炎症相关因子及炎症信号通路的影响,探究苦苣菜水提物对小鼠肺炎的抗炎作用。【方法】制备苦苣菜水提物,将昆明小鼠随机分为空白组、模型组、阳性对照组及苦苣菜水提物低、...【目的】研究苦苣菜水提物对脂多糖(LPS)诱导的小鼠肺炎模型中炎症相关因子及炎症信号通路的影响,探究苦苣菜水提物对小鼠肺炎的抗炎作用。【方法】制备苦苣菜水提物,将昆明小鼠随机分为空白组、模型组、阳性对照组及苦苣菜水提物低、中、高浓度组,空白组小鼠不做任何处理,模型组小鼠灌胃0.3 mL生理盐水,阳性对照组小鼠灌胃0.3 mL 5 mg/kg地塞米松,苦苣菜水提物低、中、高浓度组小鼠依次灌胃0.3 mL 100、200和400 mg/mL苦苣菜水提物,持续灌胃给药1周后,空白组小鼠腹腔注射0.3 mL生理盐水,其余组小鼠腹腔注射0.3 mL 30 mg/kg LPS诱导建立小鼠肺炎模型。采用ELISA方法检测各组小鼠血清中白细胞介素-6(IL-6)、IL-10、转化生长因子-β(TGF-β)的含量;利用免疫组织化学(IHC)和Western blotting检测各组小鼠肺中炎症信号通路(HMGB1/TLR4/NF-κB)蛋白的表达水平。【结果】与空白组相比,模型组小鼠血清中IL-6含量显著上调(P<0.05),IL-10、TGF-β含量有所上调,肺脏中HMGB1、TLR4、NF-κB的分布及蛋白表达量极显著上调(P<0.01);与模型组相比,苦苣菜水提物处理组小鼠血清中促炎因子IL-6含量有所下调,抗炎因子IL-10含量有所上调,抗炎因子TGF-β含量极显著上调(P<0.01);在肺脏中HMGB1、TLR4、NF-κB大量分布在肺泡周围的上皮细胞上,与模型组相比,苦苣菜水提物处理组小鼠肺脏中HMGB1、TLR4、NF-κB的分布极显著下调(P<0.01),且表现出剂量依赖效应,HMGB1、TLR4蛋白表达量极显著下调(P<0.01),NF-κB蛋白表达量显著或极显著下调(P<0.05;P<0.01)。【结论】苦苣菜水提物能抑制LPS诱导的肺炎小鼠血清中促炎因子IL-6的分泌及肺脏中信号通路HMGB1、TLR4、NF-κB蛋白的表达,促进小鼠血清中抗炎因子IL-10、TGF-β的分泌,表明苦苣菜水提物具有抗肺炎作用。展开更多
AIM To study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide(LPS)-induced liver injury in vivo and in vitro.METHODS Male β-arrestin 2^(+/+) and β-arrestin 2^(-/-)C57 BL/6 J mice were used ...AIM To study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide(LPS)-induced liver injury in vivo and in vitro.METHODS Male β-arrestin 2^(+/+) and β-arrestin 2^(-/-)C57 BL/6 J mice were used for in vivo experiments, and the mouse macrophage cell line RAW264.7 was used for in vitro experiments. The animal model was established via intraperitoneal injection of LPS or physiological sodium chloride solution. Blood samples and liver tissues were collected to analyze liver injury and levels of pro-inflammatory cytokines. Cultured cell extracts were collected to analyze the production of pro-inflammatory cytokines and expression of key molecules involved in the TLR4/NF-κB signaling pathway.RESULTS Compared with wild-type mice, the β-arrestin 2 knockout mice displayed more severe LPS-induced liver injury and significantly higher levels of proinflammatory cytokines, including interleukin(IL)-1β, IL-6, tumor necrosis factor(TNF)-α, and IL-10. Compared with the control group, pro-inflammatory cytokines(including IL-1β, IL-6, TNF-α, and IL-10) produced by RAW264.7 cells in the β-arrestin 2 si RNA group were significantly increased at 6 h after treatment with LPS. Further, key molecules involved in the TLR4/NF-κB signaling pathway, including phosphoIκBα and phosho-p65, were upregulated.CONCLUSION β-arrestin 2 can protect liver tissue from LPS-induced injury via inhibition of TLR4/NF-κB signaling pathwaymediated inflammation.展开更多
Objective:To investigate the clinical efficacy of dexmedetomidine in the regulation of TLR4/My D88/NF-κB in the prevention of paroxysmal sympathetic over-excitation (PSH) in patients with severe head injury. Methods:...Objective:To investigate the clinical efficacy of dexmedetomidine in the regulation of TLR4/My D88/NF-κB in the prevention of paroxysmal sympathetic over-excitation (PSH) in patients with severe head injury. Methods:One hundred patients with severe head injury who were admitted to our hospital from September 2016 to May 2019 were enrolled. The randomized digital table method was divided into 50 cases in the study group and the control group. Patients in the study group were given dexmedetomidine at a dose of 1.0 μg/kg before anesthesia induction, followed by infusion at 0.4 μg / (kg·h), and the control group was injected with the same amount of normal saline. The incidence of PSH, clinical symptoms, imaging findings, mechanical ventilation time, tracheal intubation/incision duration, ICU hospitalization time, total length of hospital stay, and GCS scores three months after discharge were compared between the two groups. At the same time, the fluorescence intensity, TLR4, NF-κB expression level and tumor necrosis factor-α (TNF-α) expression levels in peripheral blood CD14+ monocytes of the two groups were detected. Results:The incidence of PSH was significantly lower in the study group than in the control group at 7 and 3 months (P<0.05). The total length of hospital stay, duration of ICU hospitalization, intraoperative tracheotomy, and mechanical ventilation time were significantly lower in the study group than in the control group. And the GCS score was higher than the control group, and the difference was statistically significant (P<0.05). In addition, the imaging results showed that there were some differences in the location of imaging lesions between the two groups. The proportion of lesions in the ventricular system and surrounding areas was higher in the control group than in the study group (P<0.05). And the T14-T3 CD14+ PBMC MyD88 fluorescence intensity, TLR4 and NK-κB positive expression rate were significantly higher than those of T0 (P<0.05), but the MyD88 fluorescence intensity, TLR4 and NK-κB positive expression rate in the study group were significantly lower than those in the control group at T1~T3 (P<0.05). The levels of serum TNF-α in T1~T3 groups were significantly higher than those in T0 (P<0.05), but the levels of serum TNF-α in T1~T3 in the study group were significantly lower than those in the control group (P< 0.05). Conclusions:Dexmedetomidine can reduce the oxidative stress response in patients with severe head injury by inhibiting TLR4/My D88/NF-κB signaling pathway, thus effectively reducing the risk of PSH and improving the prognosis of patients.展开更多
基金reviewed and approved by the Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Anhui Hospital Institutional Review Board(2022AH-022).
文摘BACKGROUND Ulcer colitis(UC)is a chronic,nonspecific,and noninfectious inflammatory bowel disease.Recently,Toll-like receptors(TLRs)have been found to be closely associated with clinical inflammatory diseases.Achieving complete remission in patients with intermittent periods of activity followed by dormancy is challenging.Moreover,no study has explored the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.AIM To explore the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.METHODS This prospective clinical study included patients who met the exclusion criteria in 2020 and 2021.The patients with UC were divided into two groups(control and experimental).The peripheral blood of the experimental and control groups were collected under aseptic conditions.The expression of TLR4 protein,NF-κB,IL-6,and IL-17 was detected in the peripheral blood of patients in the experimental group and control group before and 1 month after taking the drug.Linear co rrelation analysis was used to analyze the relationship between the expression level of TLR4 protein and the expression levels of downstream signal NF-κB and inflammatory factors IL-6 and IL-17,and P<0.05 was considered statistically significant.RESULTS There were no significant differences in the patient characteristics between the control and experimental groups.The results showed that the expression levels of TLR4 and NF-κB in the experimental group were significantly lower than those in the control group(P<0.05).The levels of IL-6 and IL-17 in the experimental group were significantly lower than those in the control group(P<0.05).The TLR4 protein expression in the experimental group was positively correlated with the expression level of downstream signal NF-κB and was positively correlated with the levels of downstream inflammatory cytokines IL-6 and IL-17(r=0.823,P<0.05).CONCLUSION Kuicolong-yu enema decoction retains traditional Chinese medicine enema attenuates the inflammatory response of UC through the TLR4/NF-κB signaling pathway.
文摘目的探讨柴朴汤对哮喘小鼠支气管上皮细胞高迁移率族蛋白B1(HMGB1)、Toll样受体4(TLR4)、核因子-κB(NF-κB)及下游炎症介质单核细胞趋化蛋白-1(MCP-1)、白细胞介素-6(IL-6)的影响。方法将小鼠支气管上皮细胞分为对照组(Con组,空白血清培养)、Model组(哮喘小鼠血清培养)和Chaipu组(柴朴汤药血清培养)。采用qRT-PCR和Western blotting检测小鼠支气管上皮细胞中HMGB1、TLR4、NF-κB、MCP-1、IL-6的mRNA及蛋白表达情况,ELISA法测定细胞培养液中MCP-1和IL-6的水平。结果与Con组相比,Model组小鼠支气管上皮细胞HMGB1、TLR4、NF-κB、MCP-1、IL-6表达均明显升高(P<0.05);Model组细胞培养液中MCP-1、IL-6也显著升高(P<0.05)。与Model组相比,Chaipu组小鼠支气管上皮细胞HMGB1、TLR4、MCP-1、IL-6 mRNA和蛋白表达降低,NF-κB m RNA表达亦降低(P<0.05);Chaipu组细胞培养液中MCP-1、IL-6也显著降低(P<0.05)。结论柴朴汤可下调哮喘血清诱导的炎症因子的表达,可能与其抑制HMGB1/TLR4/NF-κB炎症通路有关。
文摘目的探究高迁移率族蛋白1(High Mobility Group Box Protein1, HMGB1)通过(Toll-like Receptor4,TLR4)/核因子κB(Nuclear Factor Kappa-B, NF-κB)/NOD样受体热蛋白结构域相关蛋白3(NOD-like Receptor Thermal Protein Domain Associated Protein 3, NLRP3)信号通路介导内皮细胞焦亡在系统性血管炎中的作用机制。方法 研究于2021年10月—2023年9月在齐齐哈尔医学院附属第三医院开展。取人脐静脉血管内皮细胞进行培养,随机分为对照组和实验组,实验组加入人重组HMGB1,对比对照组与实验组、实验组NLRP3及TLR4表达抑制前后,内皮细胞焦亡相关蛋白的表达水平。结果 系统性血管炎组与健康对照组比较,人脐静脉血管内皮细胞中HMGB1、含半胱氨酸的天冬氨酸蛋白水解酶-1(caspase-1)、白细胞介素-1β(interleukin-1β, IL-1β)、白细胞介素-18(interleukin-18, IL-18)水平升高,差异有统计学意义(P均<0.05)。细胞实验中实验组与对照组比较,caspase-1、IL-1β、IL-18水平升高,差异有统计学意义(P均<0.05)。过表达HMGB1并抑制NLRP3可使NLRP3(2.71±0.59 vs 1.24±0.58)、caspase-1(0.69±0.12 vs 0.40±0.03)、IL-1β[(1.75±0.31)pg/mL vs (1.16±0.12)pg/mL]、IL-18[(0.15±0.04)pg/mL vs (0.09±0.01)pg/mL]水平降低,差异有统计学意义(P均<0.05);过表达HMGB1并抑制TLR4可使TLR4(4.93±1.04 vs 1.96±0.84)、NF-κB(5.62±1.39 vs 2.15±1.04)、NLRP3(2.71±0.59 vs 1.24±0.58)、caspase-1(0.69±0.12 vs 0.40±0.03)、IL-1β[(1.75±0.31)pg/mL vs (1.16±0.12)pg/mL]、IL-18[(0.15±0.04)pg/mL vs (0.09±0.01)pg/mL]水平明显降低,差异有统计学意义(P均<0.05)。结论 HMGB1通过调节TLR4/NF-κB/NLRP3信号通路介导内皮细胞焦亡,进而改善系统性血管炎。
文摘【目的】研究苦苣菜水提物对脂多糖(LPS)诱导的小鼠肺炎模型中炎症相关因子及炎症信号通路的影响,探究苦苣菜水提物对小鼠肺炎的抗炎作用。【方法】制备苦苣菜水提物,将昆明小鼠随机分为空白组、模型组、阳性对照组及苦苣菜水提物低、中、高浓度组,空白组小鼠不做任何处理,模型组小鼠灌胃0.3 mL生理盐水,阳性对照组小鼠灌胃0.3 mL 5 mg/kg地塞米松,苦苣菜水提物低、中、高浓度组小鼠依次灌胃0.3 mL 100、200和400 mg/mL苦苣菜水提物,持续灌胃给药1周后,空白组小鼠腹腔注射0.3 mL生理盐水,其余组小鼠腹腔注射0.3 mL 30 mg/kg LPS诱导建立小鼠肺炎模型。采用ELISA方法检测各组小鼠血清中白细胞介素-6(IL-6)、IL-10、转化生长因子-β(TGF-β)的含量;利用免疫组织化学(IHC)和Western blotting检测各组小鼠肺中炎症信号通路(HMGB1/TLR4/NF-κB)蛋白的表达水平。【结果】与空白组相比,模型组小鼠血清中IL-6含量显著上调(P<0.05),IL-10、TGF-β含量有所上调,肺脏中HMGB1、TLR4、NF-κB的分布及蛋白表达量极显著上调(P<0.01);与模型组相比,苦苣菜水提物处理组小鼠血清中促炎因子IL-6含量有所下调,抗炎因子IL-10含量有所上调,抗炎因子TGF-β含量极显著上调(P<0.01);在肺脏中HMGB1、TLR4、NF-κB大量分布在肺泡周围的上皮细胞上,与模型组相比,苦苣菜水提物处理组小鼠肺脏中HMGB1、TLR4、NF-κB的分布极显著下调(P<0.01),且表现出剂量依赖效应,HMGB1、TLR4蛋白表达量极显著下调(P<0.01),NF-κB蛋白表达量显著或极显著下调(P<0.05;P<0.01)。【结论】苦苣菜水提物能抑制LPS诱导的肺炎小鼠血清中促炎因子IL-6的分泌及肺脏中信号通路HMGB1、TLR4、NF-κB蛋白的表达,促进小鼠血清中抗炎因子IL-10、TGF-β的分泌,表明苦苣菜水提物具有抗肺炎作用。
基金Supported by the National Natural Science Foundation of China,No.81470848the Breeding Foundation for Young Pioneers’Research of Sun Yat-sen University,No.14ykpy27
文摘AIM To study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide(LPS)-induced liver injury in vivo and in vitro.METHODS Male β-arrestin 2^(+/+) and β-arrestin 2^(-/-)C57 BL/6 J mice were used for in vivo experiments, and the mouse macrophage cell line RAW264.7 was used for in vitro experiments. The animal model was established via intraperitoneal injection of LPS or physiological sodium chloride solution. Blood samples and liver tissues were collected to analyze liver injury and levels of pro-inflammatory cytokines. Cultured cell extracts were collected to analyze the production of pro-inflammatory cytokines and expression of key molecules involved in the TLR4/NF-κB signaling pathway.RESULTS Compared with wild-type mice, the β-arrestin 2 knockout mice displayed more severe LPS-induced liver injury and significantly higher levels of proinflammatory cytokines, including interleukin(IL)-1β, IL-6, tumor necrosis factor(TNF)-α, and IL-10. Compared with the control group, pro-inflammatory cytokines(including IL-1β, IL-6, TNF-α, and IL-10) produced by RAW264.7 cells in the β-arrestin 2 si RNA group were significantly increased at 6 h after treatment with LPS. Further, key molecules involved in the TLR4/NF-κB signaling pathway, including phosphoIκBα and phosho-p65, were upregulated.CONCLUSION β-arrestin 2 can protect liver tissue from LPS-induced injury via inhibition of TLR4/NF-κB signaling pathwaymediated inflammation.
基金Nanchong city school cooperative research project in 2018(No.18SXHZ0445).
文摘Objective:To investigate the clinical efficacy of dexmedetomidine in the regulation of TLR4/My D88/NF-κB in the prevention of paroxysmal sympathetic over-excitation (PSH) in patients with severe head injury. Methods:One hundred patients with severe head injury who were admitted to our hospital from September 2016 to May 2019 were enrolled. The randomized digital table method was divided into 50 cases in the study group and the control group. Patients in the study group were given dexmedetomidine at a dose of 1.0 μg/kg before anesthesia induction, followed by infusion at 0.4 μg / (kg·h), and the control group was injected with the same amount of normal saline. The incidence of PSH, clinical symptoms, imaging findings, mechanical ventilation time, tracheal intubation/incision duration, ICU hospitalization time, total length of hospital stay, and GCS scores three months after discharge were compared between the two groups. At the same time, the fluorescence intensity, TLR4, NF-κB expression level and tumor necrosis factor-α (TNF-α) expression levels in peripheral blood CD14+ monocytes of the two groups were detected. Results:The incidence of PSH was significantly lower in the study group than in the control group at 7 and 3 months (P<0.05). The total length of hospital stay, duration of ICU hospitalization, intraoperative tracheotomy, and mechanical ventilation time were significantly lower in the study group than in the control group. And the GCS score was higher than the control group, and the difference was statistically significant (P<0.05). In addition, the imaging results showed that there were some differences in the location of imaging lesions between the two groups. The proportion of lesions in the ventricular system and surrounding areas was higher in the control group than in the study group (P<0.05). And the T14-T3 CD14+ PBMC MyD88 fluorescence intensity, TLR4 and NK-κB positive expression rate were significantly higher than those of T0 (P<0.05), but the MyD88 fluorescence intensity, TLR4 and NK-κB positive expression rate in the study group were significantly lower than those in the control group at T1~T3 (P<0.05). The levels of serum TNF-α in T1~T3 groups were significantly higher than those in T0 (P<0.05), but the levels of serum TNF-α in T1~T3 in the study group were significantly lower than those in the control group (P< 0.05). Conclusions:Dexmedetomidine can reduce the oxidative stress response in patients with severe head injury by inhibiting TLR4/My D88/NF-κB signaling pathway, thus effectively reducing the risk of PSH and improving the prognosis of patients.
