Effects of propofol on the mRNA expression of toll-like receptor 4 in BV-2 cells during mimic ischemia-reperfusion injury in vitro

Zhang, Qing; Sun, Peng; Zhang, Shihai; Tian, Yuan; Zhang, Jinghui

doi:10.1007/s11596-008-0622-7

Cited by 5 publications

(2 citation statements)

References 8 publications

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“…Although propofol increased the expression of immune cells compared with inhaled anesthetic agents, it significantly increased the apoptosis of lipopolysaccharidetreated mononuclear cells and lymphocytes (25)(26)(27). Many studies have supported a protective effect of propofol against injury through TLR4 (28)(29)(30)(31)(32). The difference in results between propofol and midazolam in the present study was remarkable, although both are GABAergic drugs.…”

Section: Discussioncontrasting

confidence: 44%

The effect of repetitive exposure to intravenous anesthetic agents on the immunity in mice

et al. 2020

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Introduction: This study was designed to assess the effect of repetitive exposure to intravenous anesthetic agents on the immunity in mice. Materials and Methods: The mice were divided into six groups: three intravenous anesthetic agents groups (dexmedetomidine, midazolam and propofol groups), and three corresponding control groups (CD, CM, and CP groups). The intravenous injections were administered once per day for 5 days. The immunity of mice was checked after the last intravenous injection. Histopathology and immunochemistry of liver and kidneys were evaluated. Cytokine levels in the blood was also checked. vs. evaluated with cytokine levels in the blood. Results: Cluster of differentiation (CD)4 + T cells were significantly less expressed in dexmedetomidine and propofol groups, compared with the corresponding control groups [34.08 ± 5.63% in the dexmedetomidine group vs. 59.74 ± 8.64% in the CD group, p < 0.05; 25.28 ± 7.28% in the propofol group vs. 61.12 ± 2.70% in the Cp group, p < 0.05]. Apoptosis of CD4 + T cells was increased significantly in dexmedetomidine and propofol groups, compared with the corresponding control groups. Histopathological findings of liver and kidneys did not show any specific differences of any of three intravenous anesthetic agents groups with their corresponding control groups, although immunohistochemical examination indicated significantly lower expression of Toll-like receptor-4 from liver and kidneys in dexmedetomidine and propofol groups. The cytokine levels were not different between the groups. Conclusion: Repetitive exposure to dexmedetomidine and propofol reduced the expression of CD4 + T cells but did not induce any significant liver or kidney injuries.

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Section: Discussioncontrasting

confidence: 44%

The effect of repetitive exposure to intravenous anesthetic agents on the immunity in mice

et al. 2020

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“…The expression of TLRs has been detected in microglia as well as astrocytes, and their expression has been shown to be modulated by a variety of internal or external stimuli, including TLR agonists, hypoxia, and proinflammatory cytokines [2 -4], suggesting direct involvement of TLRs in the regulation of CNS inflammation. In both in vivo and in vitro studies, our previous data demonstrated that TLR4 and TLR2 might be involved in brain damage and in inflammation triggered by ischemic injury [5][6][7][8]. They may activate a nuclear factor-kappa B (NF-κB) signaling pathway, thereby resulting in the transcription of many pro-inflammatory genes encoding cytokines, chemokines, proteins of the complement system and aggravating brain damage.…”

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confidence: 99%

TLR4 signaling induced TLR2 expression in the process of mimic cerebral ischemia/reperfusion in vitro

Sun

Zhang

Han

et al. 2010

Sci. China Life Sci.

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Both TLR4 and TLR2 participated in the mediation of the inflammatory injury in the process of partial cerebral ischemia/reperfusion. However, it still remains unclear whether a crosstalk exists between TLR2 and TLR4 in ischemic cerebral damage. In the present study, we investigated the effect of TLR4 signaling on TLR2 expression during mimic cerebral I/R in vitro. BV-2 cells were cultured and treated with ischemia/reperfusion, then transfected with the plasmid pEGFP-H1/TLR4-siRNA, the plasmid pEGFP-H1/control sequence-siRNA and the blank plasmid, respectively. Interestingly, the expression of TLR2 and TLR4 mRNA and protein, NF-kappaB p65 mRNA and supernatant TNF-alpha level were significantly higher in ischemia/reperfusion treated cells than those lack of ischemia/reperfusion treatment, and as compared with those in ischemia/reperfusion treated cells without transfection, no significant differences about the above mentioned gene and protein expression were found in the blank plasmid tranfected cells and the plasmid pEGFP-H1/control sequence-siRNA transfected cells respectively, while the expression levels in the plasmid pEGFP-H1/TLR4-siRNA transfected cells were significantly lower. Additionally, in order to determine the effects of pyrrolidinediethyldithiocarbamate (PDTC), an NF-kappaB inhibitor, on the TLR4-induced TLR2 expression in BV-2 cells treated with ischemia/reperfusion, it was found that TLR4 and TLR2 mRNA expressions in PDTC pretreated cells were significantly lower in comparison with normal saline pretreated cells and non-pretreated cells. The data suggested that TLR2 activation, signaled by TLR4 and regulated by NF-kappaB, might be directly involved play an important role in ischemia/reperfusion induced brain damage.

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Research progress of propofol in alleviating cerebral ischemia/reperfusion injury

Zheng,

Xiao,

Han

et al. 2024

Pharmacol. Rep

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Effects of propofol on the mRNA expression of toll-like receptor 4 in BV-2 cells during mimic ischemia-reperfusion injury in vitro

Cited by 5 publications

References 8 publications

The effect of repetitive exposure to intravenous anesthetic agents on the immunity in mice

The effect of repetitive exposure to intravenous anesthetic agents on the immunity in mice

TLR4 signaling induced TLR2 expression in the process of mimic cerebral ischemia/reperfusion in vitro

Research progress of propofol in alleviating cerebral ischemia/reperfusion injury

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