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目的:探讨糖皮质激素诱导的肿瘤坏死因子相关蛋白配体(GITRL)在脂多糖(LPS)诱导的Kupffer细胞(KCs)凋亡中的作用。方法:分离BALB/c小鼠的KCs,转染对照siR-NA或者GITRL siRNA 24 h后,分四组培养,分别为对照(Control)组:仅加入培养液;地塞米松(Dex)组:加入Dex10μmol/L;LPS组:加入LPS 1 mg/L;LPS+Dex组:加入LPS 1 mg/L和Dex 10μmol/L。24 h后用免疫细胞化学法检测GITRL蛋白的表达,应用Annexin V/PI双染标记和流式细胞术检测KCs的凋亡率。结果:LPS刺激增加了KCs GITRL的表达(P<0.05),然而地塞米松处理降低了LPS诱导的GITRL表达。LPS刺激诱导了KCs的凋亡,但是沉默GITRL基因或者地塞米松处理抑制了LPS诱导的凋亡(P<0.05)。结论:LPS可以诱导小鼠KCs的凋亡,其作用可能依赖于GITRL信号的转导。
AIM: To investigate the role of glucocorticoid-induced tumor necrosis factor-related protein ligand (GITRL) in the apoptosis of Kupffer cells (KCs) induced by lipopolysaccharide (LPS). Methods: The KCs of BALB / c mice were isolated and transfected with siR-NA or GITRL siRNA for 24 h. The cells were divided into four groups: Control group: only medium; Dex group: LPS group: adding LPS 1 mg / L; LPS + Dex group: adding LPS 1 mg / L and Dex 10 μmol / L. GITRL protein expression was detected by immunocytochemistry 24 h later. The apoptosis rate of KCs was detected by Annexin V / PI double staining and flow cytometry. Results: LPS stimulation increased the GITRL expression of KCs (P <0.05), however, dexamethasone treatment reduced the expression of GITRL induced by LPS. LPS stimulation induced KCs apoptosis, but silencing of GITRL gene or dexamethasone inhibited LPS-induced apoptosis (P <0.05). CONCLUSION: LPS can induce the apoptosis of KCs in mice and its effect may depend on the transduction of GITRL signal.